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SFU- semester 1 > Psych 280 FInal > Flashcards

Psych 280 FInal Flashcards

0
Q

Motivation

A

A drive state that initiates homeostatic behaviour

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1
Q

Homeostasis

A

Active process of maintaining a more or less stable, balanced environment in the body

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2
Q

Obligatory losses

A

Unavoidable loss of a regulated variable (energy/water/temp) as a consequence of processes necessary for life

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3
Q

Are humans endotherms or ectotherms?

A

Endotherms, bc we make our own heat inside our bodies like all mammals
Ectotherms get their heat from outside their body (lizards and snakes) and need to be close to hear sources

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4
Q

What do ectotherms rely on for oxygen?

A

Bursts of intense anaerobic muscular activity (activity initiated by chemical reactions that postpone the requirement for oxygen) so after a bit they need rest and regain the oxygen that was lost

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5
Q

What evolutionary trait has helped endotherms with generating heat?

A

A greater capacity for oxygen utilization to generate heat through metabolism (no oxygen debt)

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6
Q

The homeostatic mechanisms that regulate temperature/body fluids/metabolism are what type of systems?

A

Negative feedback systems=deviation from desired value (set point) triggers a compensatory action of the system
Negative bc restoring desired value stops the response

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7
Q

Set zone for body temp of mammals

A

36-38 C

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8
Q

When does a mammals body temp go up or down?

A

Down during sleep

Up to produce a fever to fight infection

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9
Q

Dangers of a high fever?

A

Proteins lose their correct shape, link together and malfunction (denaturing)
Eventually it can cause brain centres that regulate heart rate and breathing to die killing the person

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10
Q

Dangers of body temp too low?

A

Chemical reactions in body occur too slowly and ice crystals can disrupt cell membranes, killing the cell

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11
Q

“Antifreeze” of some fishes and beetles consists of what?

A

Special protein molecules that suppress the formation of ice crystals/prevent damage to membranes

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12
Q

Hypothalamus’ role (hint: lesions)

A

Sense and controls body temp
Lesion experiments eventually showed that diff hypothalamic sites controlled two diff thermoregulatory systems
Lesions in POA (preoptic area) = no physiological responses to cold (shivering/constriction) but didn’t interfere with behaviours like pressing levers to control heating lamps
Lesions in lateral hypothalamus = no behavioural regulation of temp but didn’t interfere with physiological responses
EXAMPLE OF REDUNDANCY

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13
Q

Describe 3 levels of hierarchy of thermoregulatory circuits

A

Spinal level
Brainstem
Hypothalamus

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14
Q

Endotherms and ectotherms both behaviourally regulate body temp in 3 ways

A

1-Changing exposure of body surface (huddling/extending limbs)
2-changing external insulation
3-changing surroundings

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15
Q

What are the three basic elements of mammalian thermoregulatory systems?

A 
Afferents (skin surface/body core/hypothalamus or POA)
Neural regions (spinal cord/brainstem/hypothalamus or POA) 
Effectors (behavioural responses and automatic responses)
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16
Q

Which homeostatic system is the most complex?

A

Food intake/energy balance bc food supplies not only energy but nutrients

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17
Q

What are nutrients? Which can we only get thru diet?

A

Chemicals required for the effective functioning/growth/maintenance of the body
We don’t know all nutritional requirements for humans
We have 20 amino acids but 9 only found in diet (essential amino acids)
Also need some fatty acids and 15 vitamins and lots of minerals

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18
Q

How is energy made in the body?

A

Released when chemical bonds if complex molecules are broken and smaller, simpler compounds form as a result

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19
Q

Basal metabolism

A

Consumption of energy to fuel processes such as heat production, maintenance of membrane potentials and other basic life-sustaining functions of the body
Consumes 55% of food energy in a meal

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20
Q

Metabolic studies show that animals lose what percent of energy from a meal in what

A

33% of energy in food: digestion
55%: basal metabolism
12%: active behavioural processes

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21
Q

Basal metabolism rule (relates energy expenditure to body weight)

A

Kcal/day=70 x weight0.75

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22
Q

Food deprivation affects what even more than body weight?

A

Metabolic rate

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23
Q

What part of the cell is responsible for basal metabolic rate?

A

Mitochondria

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24
Q

Benefit of calorie reduction in diet of animals

A

Slowing aging of body and brain bc pair of genes for transcription factors (substances that control other genes) that are involved in food deprivation and control production of hormones and trophic factors (substances that promote cell growth/survival) important for longevity

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25
Q

What happens to the body during caloric restriction?

A

Ubiquitous protein called SIRT1 (marker for increased longevity in diff animals) is increased
20 years of this has shown slower aging and prevented disease and early death in rhesus monkeys

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26
Q

What is the most immediate source of energy in the body?

A

Complex carbohydrates that are rapidly broken down into simple sugars that cell can use

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27
Q

Principle sugar used by body for energy

A

Glucose

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28
Q

Describe short-term storage of glucose

A

Glucose converted into more complicated molecule called glycogen and stored as reserve fuel (liver and skeletal muscles) = GLYCOGENESIS promoted by pancreatic hormone INSULIN
Second pancreatic hormone GLUCAGON turns glycogen back into glucose = GLYCOGENOLYSIS (triggered when concentrations of glucose drop too low)

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29
Q

Describe long-term storage of glucose

A

Fats (lipids=large molecules consisting of fatty acids and glycerol that are insoluble in water) deposited in fat-storing cells that form adipose tissue
Some come from food and others synthesized in body from surplus sugars/other nutrients
During prolonged food deprivation, fat converted to glucose (=GLUCONEOGENESIS) and secondary form of fuel called ketones as well which is used by body/brain

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30
Q

Best way to lose weight

A

Diet low in carbs and high in proteins/fats which ups good cholesterols while decreasing fats
Questionable as high fat diets are shown as bad
Diet + exercise

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31
Q

2 things insulin is important for

A

1- converting glucose into glycogen

2- enabling the body to use glucose

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32
Q

What are glucose transporters and what do they do?

A

Specialized proteins that span the cell membrane and transport glucose molecules into the cell for use

Interact with insulin in order to function

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33
Q

What are the three diff mechanisms that stimulate insulin release?

A

1- sensory stimuli from food evokes a conditioned release of insulin in anticipation of glucose arrival in the blood (=cephalic phase of insulin release)
Cephalic means coming from the head
2- DIGESTIVE PHASE: Food entering stomach/intestines makes them release gut hormones, and some of those stimulate the pancreas to release insulin. Also digestive tract’s taste-receptive cells stimulate insulin release too
3- ABSORPTIVE PHASE: glucodetectors (special cells found in liver) detect glucose entering bloodstream and signal pancreas to release insulin

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34
Q

Once insulin is released, two things can happen

A

Body makes use of some of the glories immediately

Extra glucose is converted into glycogen which is stored in liver/muscles

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35
Q

Describe system that informs the brain of circulating glucose levels and contributes to hunger

A

1- liver communicated with pancreas via nervous system
2- info from glucodetectors in liver travels via vagus nerve to the nucleus of the solitary tract (NST) in the brainstem
3- then info relayed to hypothalamus

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36
Q

What causes diabetes mellitus? Describe

A

Cause: lack of insulin

It’s excessive glucose in the urine caused by failure of insulin to signal to body to absorb the glucose

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37
Q

Type 1 diabetes

A

Juvenile-onset diabetes
Pancreas stops producing insulin
Brain can still make use of glucose from food, the rest of the body can’t
Forced to use energy from fatty acids which means lots of leftover glucose in bloodstream (some of which is secreted in urine)

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38
Q

What’s happens if person with type 1 diabetes untreated?

A

Eats a lot
Loses weight bc body can’t make efficient use of digested food
Reliance on fatty acids causes damage to tissues
Drink and urinate a lot to get rid of extra glucose
Missing insulin replaced by injections

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39
Q

What’s the cause of type 2 diabetes? Describe

A

Adult-onset diabetes
Reduced sensitivity to insulin
Usually associated with obesity
Leads to further health problems

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40
Q

What are the signals for satiety or hunger?

A

High or low levels of insulin secreted by amount of food in pipeline
Glucose levels
Both integrated with other sources of info to decide whether to initiate hunger

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41
Q

Hypoglycemia

A

High insulin levels directing much of the glucose out of circulation and into storage

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42
Q

What three things is the hypothalamus vital for

A

Regulation of metabolic rate
Food intake
Body weight

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43
Q

Describe lesions in rats that created extreme satiety or hunger

A

Bilateral regions of ventromedial hypothalamus (VMH) = WEIGHT GAIN/HYPERPHAGIA
Legions of the lateral hypothalamus (LH) = WEIGHT LOSS/APHAGIA

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44
Q

Describe inconsistencies in dual-centre hypothesis for appetite

A

VMH lesioned animals = period of rapid weight gain but then stabilized at new, higher body weight and would only eat amount of food necessary to maintain that weight
LH lesioned animals = first kept alive via feeding tube soon resumed spontaneous eating to maintain new, lower body weight

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45
Q

Arcuate nucleus

A

Arc-shaped hypothalamic nucleus implicated in appetite control

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46
Q

What happens when mice receive two copies of the gene called obese (ob)?

A

They regulate their body weight at a high level
They have larger and more fat cells compared to ob/+ (normal) mice
They maintain their obesity even when given a gross diet or when required to work hard for their food
They have defective genes for the peptide leptin

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47
Q

Leptin

A

Peptide hormone released by fat cells then protein secreted into bloodstream; ob gene product

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48
Q

Where are leptin receptors found?

A

ObR found in choroid plexus, the cortex, and several hypothalamic nuclei

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49
Q

What happens when animals have defects in the gene that encodes ObR?

A

Become obese

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50
Q

Describe ghrelin (where it comes from, and what it’s named for)

A

Endrocrine cells of the stomach release ghrelin into the bloodstream
Named after it’s effects in growth hormone secretion (GH-releasing)
Appetite STIMULANT

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51
Q

How are ghrelin levels affected by fasting and eating a meal?

A

RISE during fasting

DROP after eating a meal

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52
Q

Oddity of an obese person’s ghrelin levels?

A

Obese subjects have lower baseline levels of ghrelin before eating but after a meal they never go down (as well as their leptin levels)
Ghrelin mechanism unresponsive to feeding and always slightly elevated = constant hunger

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53
Q

Describe PYY3-36

A

Peptide hormone
Comes from intestines
Acts on hypothalamic appetite control mechanisms to lessen appetite

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54
Q

Describe levels of PYY3-36 before and after eating

A

Low levels in the blood before eating

Levels rise quickly after eating

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55
Q

What do injections of PYY3-36 do to appetite?

A

Systematic injections lessen appetite (also injections directly into Arcuate nucleus of hypothalamus in rats)

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56
Q

What levels of PYY3-36 are associated with obesity?

A

Lower than normal levels

Post meal increases in this peptide linked to feeling full in normal weight people

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57
Q

How does PYY3-36 interact with ghrelin?

A

Acts in opposition to ghrelin = acts as an appetite stopper for hypothalamus, working together on the arcuate appetite

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58
Q

Describe the Arcuate appetite system

A

Has TWO SETS of ARCUATE NEURONS with OPPOSITE EFFECTS (named accordingly to types of hormones/nuerotransmitters they produce)
Set 1- produce peptide NEUROPEPTIDE Y (NPY) and AGOUTI-RELATED PEPTIDE (AgRP) thus known as NPY/AgRP neurons which STIMULATE APPETITE while REDUCING METABOLISM = WEIGHT GAIN
Set 2- POMC/CART neurons bc they produce pro-opiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART) which INHIBIT APPETITE and INCREASE METABOLISM = WEIGHT LOSS

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59
Q

Two main functions of projections from the POMC/CART neurons and NPY/AgRP neurons

A

Some projections stay within Arcuate = 2 sets of neurons INFLUENCE each other’s ACTIVITY thru RECIPROCAL CONNECTIONS
Some projections leave the Arcuate = MAKE CONTACT with other NEURONS in other HYPOTHALAMIC SITES
This is how FOOD INTAKE is MODULATED by the Arcuate system

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60
Q

What’s the diff between what ghrelin/PYY3-36 do to appetite and what leptin/insulin do?

A

Ghrelin and PYY3-36 provide faster, hour to hour hunger signals from the gut
Act primarily on the appetite-stimulating NPY/AgRP neurons of the Arcuate
More specifically:
Ghrelin STIMULATES the cells = INCREASE in appetite
PYY3-36 INHIBITS cells = REDUCES appetite

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61
Q

Describe the two hypothalamic sites that are the primary targets of the projections of the Arcuate

A

1- OREXIGENIC neurons of the LATERAL HYPOTHALAMUS act to INCREASE appetite/food intake
2- ANOREXIGENIC neurons of the PARAVENTRICULAR NUCLEUS (PVN) act to DECREASE appetite/food intake

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62
Q

What is released when appetite-suppressing POMC/CART neurons of the Arcuate go to the LH?

A
  • They release a-melanocyte-stimulating hormone (a-MSH) which is a PEPTIDE HORMONE belonging to a small family of substances called MELANOCORTINS (derived from POMC)
  • Acts on specific MELANOCORTIN TYPE 4 RECEPTORS (MC4Rs) located on LH neurons
  • decreases the LH’s appetite stimulating activity = net decrease in feeding
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63
Q

Describe how NPY/AgRP neurons are essential for increases in feeding (thru PVN and LH)

A
  • Via INHIBITORY ACTION on ANOREXIGENIC PVN NEURONS, NPY released by the NPY/AgRP neurons = INCREASED appetite
  • AgRP competes with a-MSH for MC4R binding and when the a-MSH signal is blocked, AgRP COUNTERS the appetite-suppressing effects of a-MSH and instead produces an INCREASE in feeding behaviour via LH
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64
Q

What is Orexin and what does it do

A
  • Peptide produced by hormones in LH
  • participates in control of feeding
  • direct injection into hypothalamus of rats causes 6x feeding
  • regulated by circulating leptin
  • involved in sleep disorder narcolepsy
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65
Q

Describe the nucleus of the solitary tract (NST) and what it does with feeding

A
  • Appetite signals from the hypothalamus converge here
  • part of the common pathway for feeding behaviour
  • reviews/integrates appetite signals from diff sources (including hypothalamus)
  • info about nutrient levels is conveyed thru body to NST via vagus nerve (thanks to peptide cholecystokinin (CCK) which inhibits appetite by acting on vagus nerve after eating)
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66
Q

Describe endocannabinoid system

A
  • regulator for appetite/feeding
  • can stimulate hunger
  • act in brain and periphery
  • could affect mesolimbic dopamine reward system
  • act directly on hypothalamic appetite mechanisms while inhibiting satiety signals from gut
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67
Q

What is epigenetic transmission

A

Passage of epigenetic modifications of a gene from one generation to the next

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68
Q

Is alteration of leptin signals an effective strategy for appetite control?

A

No, bc only a tiny amount of obese people have abnormal leptin levels or MORE than thin people

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69
Q

How could cannabinoid antagonist drugs effectively suppress appetite? Name an example of a drug

A

-By causing “anti-munchies” (reverse of hunger experienced by marijuana users
-example: RIMONABANT interferes with signalling via CB1 cannabinoid receptors, effectively lessens appetite/feeding behaviour = weight loss
BUT causes mood problems

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70
Q

Describe two types of drugs that can be designed to target some of the signalling systems that have to do with the Arcuate appetite controller

A
  • a-MSH activity effectively reduces hunger so drugs that activate the MC4R MELANOCORTIN receptor could be effective appetite suppressants
  • treatment with PYY3-36 (via nasal spray) or something that mimics it can act directly on Arcuate neurons to reduce appetite
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71
Q

Describe metabolic rate and how it affects obesity

A
  • Metabolic rate increases = extra calories expended in the form of heat
  • controlled by thyroid hormones (thyroxine specifically) but treating people with thyroxine has cardiovascular side effects
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72
Q

Two ways that metabolic rate can be increased by drugs

A
  • drugs that increase energy utilization by selectively activating TRB thyroid hormone receptors (which avoids side effects cause by TRa receptors)
  • drugs that increase activity of mitochondrion-rich brown fat which burns energy faster to generate heat (possible to make regular “white” fat tissue to behave like brown fat and start burning stored energy at a high rate)
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73
Q

Describe how inhibition of fat tissue could happen in weight loss

A

-You can interfere with the formation of new fat tissue (needs to add new blood vessels which is a process called angiogenesis, so blocking this process could lessen fat formation)

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74
Q

Describe reduced absorption treatment

A

One of the only approved weight loss meds out there, ortlistat (Xenical) works by interfering with the digestion of fat
Bad side effect: intestinal discomfort

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75
Q

Describe 3 types of anti-obesity surgery

A
  • liposuction: popular, but only kinda successful and usually temporary results
  • bariatric procedures: bypass part f intestinal tract or stomach in order to reduce volume/absorption capacity of digestive system, changes appetite control hormones indirectly, no bad side effects except for surgery risks
  • less invasive surgical procedures: user study, includes use of gastric stimulators that activate feelings of fullness to reduce appetite, inserting weights into stomachs of mice works as well
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76
Q

Anorexia nerviosa

A

Anorexia- no appetite
Nerviosa- nervous system related
-their insulin levels go up higher in the presence of food than regular, which shows that they could have exaggerated hunger but not consciously be able to perceive it
-mismatch between physiological and cognition
-abnormal levels of agouti-related peptide (AgRP) = abnormal hypothalamic appetite system
-hereditary
-abnormalities in serotonergic neurotransmission and weird functioning of dopamine reward system = predisposition

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77
Q

Bulimia (bulimia nerviosa)

A

gorge themselves then vomit/take laxatives to avoid weight gain
Might not look emancipated

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78
Q

Binge eating

A
  • Strong pleasure associated with food activates opiate and dopaminergic reward mechanisms = like drug addiction
  • associated with mutation of gene encoding in the MC4R receptor (failing to receive a-MSH message to feel full)
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79
Q

Electroencephalography (EEG)

A

Recording and study of gross electrical activity in the brain recorded by large electrodes placed on the scalp

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80
Q

Electro-oculography (EOG)

A

Electrical recording of eye movements

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81
Q

Electromyography (EMG)

A

Electrical recording of muscle activity

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82
Q

What are the three measurements (“graphy”s) used in studying sleep

A

EEG
EOG
EMG

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83
Q

Describe the two classes of sleep

A

Slow-wave sleep (SWS): sleep which is defined in stage 1 to 3 and defined by presence of slow wave EEG activity
+
Rapid eye movement (REM) sleep: also called paradoxical sleep; characterized by small amplitude, fast EEG waves, no postural tension

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84
Q

What is desynchronized EEG?

A

AKA beta activity; pattern of EEG activity that is a mix of many diff high frequencies with low amplitude

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85
Q

What’s your EEG rhythm when you close your eyes and relax?

A

Regular oscillation at frequency of 8-12 hertz = ALPHA RHYTHM

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86
Q

What happens when you go from relaxed mode into sleep?

A

Time spent in alpha rhythm decreases, EEG shows events of much smaller amplitude and irregular frequency, as well as sharp waves called VERTEX SPIKES (leads into stage 1 sleep)

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87
Q

Stage 1 sleep

A
  • heart rate slows
  • muscular tension lessens
  • eyes may roll about slowly
  • lasts only several mins
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88
Q

Stage 2 sleep

A
  • SLEEP SPINDLES (waves of 12-14 hertz occurring in periodic bursts)
  • K COMPLEXES (sharp negative EEG potential)
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89
Q

Stage 3 sleep

A
  • large amplitude, slow waves (DELTA WAVES)

- divided into early and late (late when delta waves are present more than half the time)

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90
Q

After about an hour (progression thru all stages with a brief return to stage 2) what happens?

A

You see pattern of small amplitude, high frequency activity similar to pattern of someone who’s awake but skeletal muscles are totally relaxed/limp
REM SLEEP
Breathing/pulse rates irregular
Vivid dreams

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91
Q

Why are muscles flaccid during REM sleep?

A

Brainstem regions stop motoneurons

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92
Q

Describe average sleep time for adults and what it’s made up of

A
  • 7 to 8 hours
  • half in stage 2
  • REM 20%
  • repeat cycles of 90 to 110 minutes about four or five times each night
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93
Q

What’s the diff between REM stage dreams and other stage dreams?

A

REM stage: visual imagery, story with odd perceptions

Other stages: just thinking

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94
Q

Diff between night terror and nightmare?

A

Nightmare: long scary dream that makes you wake up from REM sleep
Night terror: sudden arousal from stage 3 SWS w/ intense fear and autonomic activation, can’t remember it, only remember crushing feeling on chest

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95
Q

Symptoms of sleep deprivation

A
  • hallucinations (like schizophrenia)
  • irritability
  • difficulty concentrating
  • episodes of disorientation
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96
Q

Fatal familial insomnia

A
  • Inherited disorder in which humans sleep normally at the beginning of life but later stop sleeping
  • damage is not to single organ system but diffuse bacterial infections
  • degeneration of thalamus
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97
Q

Describe sleep recovery

A

First night: biggest diff found in stage 3 sleep (increased, which leads to decrease of stage 2)
NEVER COMPLETELY MAKES UP FOR SLEEP LOSS
Second night: REM sleep shows greatest recovery, more intense with greater number of rapid eye movements

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98
Q

What are the four main functions of sleep

A

Conservation
Niche adaptation
Body restoration
Memory consolidation

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99
Q

How does sleep conserve energy?

A

Reduces activity thus metabolic rate

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100
Q

How does sleep enforce niche adaptation?

A

Makes creatures nocturnal or diurnal to help them survive according to ecological niche

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101
Q

How does sleep restore the body?

A

Wards off illness/diseases by restoration/building of materials used during time awake such as proteins; growth hormone released

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102
Q

Describe sleep aiding memory consolidation

A

SWS aids in consolidation of memory, specifically declarative memory (that can be stated or described)
REM sleep may help consolidation of non declarative memory
Patterns of neuronal activity seen while task is being learned awake, recreated during SWS where brain “rehearses” the material

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103
Q

Sleep is an active state mediated by which four interacting neural systems?

A

1- FOREBRAIN system (displays SWS by itself)
2- BRAINSTEM system (activates the forebrain into wakefulness)
3- PONTINE system (triggers REM sleep)
4- HYPOTHALAMIC system (affects the other 3 brain regions to determine whether brain will be awake or asleep)

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104
Q

How do general anaesthetics work?

A

Barbiturates and anesthetic gases that make people unconscious
Produce slow waves in EEG that resemble SWS
Some are glutamate antagonists which block neuronal excitation in brain
All are noncompetitive agonists at GABA A receptors and boost their inhibitory effect on neurons
= brain system normally uses GABA to inhibit neural activity and promote SWS

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105
Q

Isolated brain

A

Experimental preparation where animals brainstem is separated from the spinal cord from a cut below the medulla; has helped show that the forebrain promotes slow wave sleep (SWS) and also that wakefulness/SWS/rem sleep are all controlled within the brain

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106
Q

Isolated forebrain

A

Cut in the midbrain (higher on the brainstem than isolated brain)
Does not show REM sleep so proves that forebrain can generate SWS with no contributions by lower brain regions

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107
Q

Where is the constant SWS seen in the cortex of the isolated forebrain generated?

A

By the basal forebrain in the ventral frontal lobe and anterior hypothalamus

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108
Q

At sleep onset, what do neurons of the basal forebrain do?

A

Become active and release GABA To stimulate GABA A receptors in the nearby tuberomammillary nucleus in the posterior hypothalamus and if left alone, this system could keep the cortex asleep forever but brainstem system eventually wakes the forebrain up

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109
Q

What part of the brain awakes the forebrain and how?

A

Reticular formation=diffuse group of cells whose axons and dendrites go in mang directions (extending from medulla to thalamus)
Electrical stimulation awakes animals rapidly

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110
Q

What is the pons role in sleep?

A
  • triggers REM sleep
  • region ventral to the locus coeruleus stop REM sleep and with electrical/pharmacological stimulation of this region with cholinergic agonists can induce or prolong REM sleep
  • some neurons here only active during REM sleep
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111
Q

What are the jobs of the pontine REM sleep center?

A

-stop motoneurons to keep them from firing (GABA and glycine, both inhibitory transmitters, make powerful inhibitory post synaptic potentials in spinal motoneurons that stop them from reaching threshold/producing an action potential = dreamer has flaccid muscles

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112
Q

What part of the pons disables the motor system during sleep?

A

Small lesions ventral to locus coeruleus

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113
Q

Narcolepsy

A

Disorder that involves frequent, intense episodes of sleep, which can last from 5-30 minutes every 90 minutes and occur at anytime during usual waking hours, have normal nighttime sleep, enter REM within first few minutes of sleep

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114
Q

Cataplexy

A

Sudden loss of muscle tone, leading to collapse of the body without losing consciousness
Triggered by intense emotional stimuli like anger or laughter

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115
Q

What’s the mutant gene responsible for cataplexy and what parts of the brain are affected?

A

Receptors for NEUROPEPTIDE hypocretin lost 90% which causes inappropriate activation of cataplexy pathway that should only happen during REM sleep
Neural degeneration of amygdala and close by forebrain structures

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116
Q

Neurons that produce hypocretin are found where? And where do they send their axons to release the hypocretin?

A

Found in the hypothalamus
Send their axons to 3 parts of the brain involved in sleep: basal forebrain, reticular formation and locus coeruleus
Also project axons to hypothalamic tuberomammillary nucleus (inhibited by basal forebrain to induce SWS)

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117
Q

Treatments for narcolepsy (3)

A

GHB (xyrem; concerns about abuse)
Modafilin (provigil; good for narcoleptic attacks and people with ADHD for attention)
Modafinil (debated but studies show it’s no more effective than caffeine)

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118
Q

Sleep paralysis

A
  • common symptom of narcolepsy
  • inability to move or talk just before falling asleep or just after waking up
  • only lasts a short time
  • hypothesis: results when pontine center continues to impose paralysis for a short time after waking from REM period
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119
Q

What are 2 children sleep disorders?

A

Night terrors
Sleep enuresis (bed wetting)
-associated with SWS, treatment is reducing amount of stage 3 sleep/rem time and increasing stage 2 sleep or nasal spray of hormone vasopressin which decreases urine production

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120
Q

What is the scientific name for sleepwalking and what stage of sleep?

A

Somnambulism

Occurs during stage 3 SWS and more common during first half of night

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121
Q

REM behavioural disorder (RBD)

A
  • Characterized by acting out organized behaviour while asleep
  • begins after age 50 and more common in men
  • lesion near locus coeruleus so not paralyzed during REM
  • early symptom of dementia and Parkinson’s disease
  • can be controlled by anti anxiety drugs (benzodiazepines)
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122
Q

What’s it called when you’re sleeping and you don’t think you ever slept?

A

Sleep state misconception

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123
Q

Scientific name for having a hard time falling asleep

A

Sleep-onset insomnia

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124
Q

Scientific name for difficulty staying asleep due to drugs/neurological/psychiatric factors?

A

Sleep-maintenance

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125
Q

What are the two types of sleep apnea?

A

Obstructive apnea: progressive relaxation of muscles of chest, diaphragm, throat cavity

Central apnea: changes in the pacemaker respiratory neurons of brainstem

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126
Q

How does apnea lead to brain damage?

A

Interruptions in oxygen kill neurons in the hippocampus and impair learning ability

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127
Q

What’s the machine used to treat sleep apnea?

A

Continuous positive airway pressure (CPAP) machine that maintains air pressure in airways and prevents collapse of those airways

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128
Q

Cause of sudden infant death syndrome (SIDS)

A

Sleep apnea as a result of immaturity of systems that pace respiration
Abnormalities in brainstem serotonin systems

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129
Q

Drugs used to treat sleep disorders

A

Scopolamine and atropine in the past
Barbiturates developed by bayer
Benzodiazepine triazolam (halcion, ambien, sonata, lunesta) bind to GABA receptors which inhibit broad regions of brain

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130
Q

How do current sleeping pills fall short of being a suitable remedy?

A
  • continued use causes non effectiveness

- persistent drowsiness

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131
Q

What is an organ specialized to receive certain stimuli called?

A

Sensory receptor organ

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132
Q

What do the receptor cells in sensory receptor organs do?

A

Detect certain kinds of stimuli and concert them into the language of the nervous system aka electrical signals

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133
Q

How does info from sensory receptors travel?

A

Sensory receptor organs to brain via action potentials that travel along axons

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134
Q

Scientific name for the type of stimulus to which a given sensory organ is particularly adapted to

A

Adequate stimulus

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135
Q

What frequency can’t humans hear?

A

Frequencies above 20,000 cycles per second aka ultrasonic sound

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136
Q

Describe specific nerve energies

A

Doctrine that receptors and neural channels for the different senses are independent and operate in their own special ways, producing one particular sensation each
Ex: no matter how eye is stimulated (light, electrical shock, etc) result is always visual

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137
Q

Describe the concept of labeled lines (senses)

A

Particular neurons are labeled for distinctive sensory experiences; actions potentials travel along separate nerve tracts depending on what sense they correspond with

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138
Q

Describe sensory transduction

A
  • detection of energy in receptor cells

- receptor cell converts that energy into change in electrical potential across it’s membrane

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139
Q

What are the six main receptors in the skin and what do they do?

A 
Free nerve endings: pain/temp
Merkel's disk: touch
Meissner's corpuscule: touch
Hair follicle receptor: touch
Pacinian (or lamellated) corpuscule; vibration/pressure
Ruffini's ending: stretch
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140
Q

Receptor potential

A

Aka generator potential; local change in resting potential of a receptor cell that mediates between the impact of stimuli and the initiation of nerve impulses

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141
Q

Describe Pacinian corpuscule

A
  • Detects vibration
  • found in skin/muscle
  • axon surrounded by structure that looks like a tiny onion because it has layers of tissue
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142
Q

4 steps of excitatory events in the Pacinian corpuscule

A

1- outside stimulation deforms the corpuscule
2- deformation of the corpuscule stretches the tip of the axon
3- stretching the axon opens up gated ion channels in the membrane, which allows sodium ions to enter
4- when the receptor potential reaches threshold amplitude, the axon produces one or more action potentials

143
Q

Do sensory organs and peripheral sensory pathways convey limited/distorted or accurate info to the brain?

A

Limited/distorted

144
Q

What are the six aspects of sensory processing

A 
Coding
Adaptation 
Pathways
Suppression 
Receptive fields
Attention
145
Q

Describe coding (senses)

A

-Through coding, the pattern of electrical activity in the sensory system must convey information about the original stimulus
-Neural code action potentials
Similarities: size and duration
Differences: number and frequency and rhythm

146
Q

Describe stimulus intensity

A

A single receptor can’t represent an entire range but multiple receptor cells working together provide a broader range for coding the intensity of a stimulus
As strength of stimulus increases, new neurons are recruited

147
Q

Range fractionation (senses)

A

Takes place when different receptor cell are specialists in particular segments or “fractions” of an intensity scale
Requires different receptors and neurons that have different thresholds to fire

148
Q

Somatosensory

A

Referring to body sensation, specifically touch and pain sensation; helps us figure out where the feeling is coming from

149
Q

How are cells distributed in the visual and touch systems?

A

In an orderly map like manner, with a higher concentration of sensitive parts like the lips and the middle of the eye than less sensitive parts like the skin of the back or the periphery of the eye

150
Q

What’s the difference between tonic and phasic receptors in adaptation?

A

Tonic receptors: little or no decrease in frequency of action potentials as stimulation is maintained (show little adaptation)
Phasic receptors: rapid decreasing of the frequency of action potentials when stimulus is maintained (show a lot of adaptation)

151
Q

What happens when the corpuscule is removed from the Pacinian corpuscule?

A

Same constant stimulus applied to the uncovered sensory nerve fibre makes a continuing discharge of action potentials (no adaptation)

152
Q

What is top-down processing? (Senses

A

Higher brain venters (cortex and thalamus etc) modulate sensory information by suppressing info from some centres and amplifying it in others
Happens with pain, sound, etc

153
Q

Sensory pathway

A

Chain of neural connections starting at sensory receptor cells than going to spinal cord to brainstem to thalamus to primary sensory cortical areas (cerebral cortex) and out to other parts of brain

154
Q

Receptors field (senses)

A

Receptive field of a sensory neuron is a region that a stimulus can alter it’s firing rate

155
Q

What’s the difference between the primary sensory cortex and the secondary (or non primary) sensory cortex?

A

Primary: main source of input to other fields of same modality, even though these fields also have direct thalamic inputs; info is sent back and forth thru subcortical loops
Secondary: received and sends back info

156
Q

Difference between primary somatosensory cortex (S1) and secondary somatosensory cortex (S2)?

A

S1: gyrus just behind the central sulcus where sensory receptors on the body surface are mapped; primary cortex for receiving touch and pain info in the parietal lobe
S2: region of cortex that receives direct projections from S1; measures both sides of the body in registered overlay

157
Q

Cingulate cortex (senses)

A

Portion of cortex along and just above corpus callosum; implicated in motivational aspects of attention

158
Q

What type of cell provides a mechanism for inter sensory interactions?

A

Polymodal cells

159
Q

Describe transduction of sound

A

Small vibrations of air molecules become sounds from the outer parts of the auditory system has been shaped thru evolution to capture biologically important sound vibrations and direct them into the inner ear where mechanical force of sound is transducer into neural activity

160
Q

What are the two parts of the external ear

A

Pinnae and ear canal

161
Q

What is the frequency range important for speech perception?

A

2000-5000 hz

162
Q

What 5 parts make up the middle ear?

A

-tympanic membrane (eardrum): sound waves hit it and makes it vibrate with with the same frequency of the sound
-ossicles
1) malleus
2) incus
3) stapes
Concentrate the mechanical forces of vibrating air particles into oval window
-oval window: connects eardrum to inner ear

163
Q

What are the two muscles between the ossicles and what do they do?

A

Tensor tympani: attached to malleus, connected to tympanic membrane
Stapedius: connected to stapes

Improve auditory perception and protect delicate inner ear from loud damaging sounds

164
Q

What are the cochlea’s three canals?

A

1- scala vestibuli (vestibular canal)
2- scala media (middle canal)
3- scala tympani (tympanic canal)

165
Q

What are the 3 principle components that convert sound into neural activity?

A

Organ of Corti:
1- the sensory cells aka hair cells
2- elaborate frame of supporting cells
3- terminations of auditory fibres

166
Q

What’s the base of the organ of Corti called and what does it do?

A

Basilar membrane

Separates scala tympani from scala media and vibrates in response to sound

167
Q

Describe how cochlea converts vibrational energy into waves of fluid

A

1- Stapes move in and out as result of sound waves hitting ear drum which makes waves in fluid of scala vestibuli
2- causes basilar membrane to ripple (different parts have stronger or weaker reactions depending on the frequency of the sound; high=greater effect at base and low=greater effect at apex
3- hair cells transduce movements of basilar membrane into electrical signals

168
Q

How are hair cells arranged in the organ of Corti?

A

Two sets of hair cells; inner hair cells=single row of about 3500 that’s closest to the center of the coiled cochlea
Outer hair cells=12000 in three rows

169
Q

What are stereocilia?

A
  • Each hair cell has about 50-200 of these stuff hairs
  • heights increase across hair cell so the tops form a slope
  • outer hair cells extend enough to create indentations in the bottom of the tectorial membrane (which is at the top of the organ of Corti)
170
Q

The organ of Corti has 4 types of synapses and nerve fibres, what are they?

A

2 afferents: convey messages from hair cell to brain
2 efferents: convey messages from brain to hair cells
IHC associated with many auditory nerve fivers, OHC not

171
Q

What do outer hair cells do?

A
  • They don’t detect sound; they push on the tectorial membrane in response to commands from the brain via the efferent nerve fibers
  • They change their length to fine-tune organ of Corti so we can differ between sounds that are very familiar in frequency
  • depolarization=shorten, polarization=lengthen
172
Q

How do inner hair cells transduce sound into neural activity?

A

1-sounds make basilar membrane vibrate
2-vibrations bend cilia (hairs) that press on tectorial membrane
3- movements of hair cell bundles cause changes in ionic channels of the stereocilia
4- fine fibres called TIP LINKS run along tips of stereocilia which generate hair cell potentials by opening ion channels when they move
5- causes inrush of potassium (K+) and calcium (ca2+) ions
6- hair cell is depolarized
7- rapid increase in calcium at the base of the inner hair cell
8- synaptic vesicles at the base fuse with the presynaptic membrane and release transmitter contents (glutamate) from base of hair cell
9- stimulates afferent nerve fiber to trigger action potentials in the afferent axons
10- action potentials reach brain via vestibulocochlear nerve (cranial nerve Vlll)

173
Q

What’s the vestibulocochlear nerve made up of?

A

30 000-50 000 auditory fibres from cochlea make up it’s auditory part, and these fibres are afferent and carry messages from inner hair cells, stimulating several nerve fibres

174
Q

Describe the paths that output of the cochlear nuclei travel on

A

1- cochlear nuclei to both superior olivary nuclei (so they both receive input from left and right cochlear nuclei)
2- cochlear nuclei to inferior colliculi (parallel paths converge there bc primary auditory center of midbrain; then outputs of inferior colliculi go to medial geniculate nuclei of the thalamus; at least 2 diff pathways from there to go to auditory cortical areas

175
Q

What is tonotropic organization?

A

Major organizational feature in auditory systems where neurons are arranged as an orderly map of stimulus frequency, w/ cells responsive to high frequencies located far away from those responsive to low frequencies

176
Q

Brain imaging studies confirmed that random sounds vs speech sounds activate diff parts of brain. Explain.

A

Random sounds: primary auditory cortex (located on upper surface of temporal lobes)
Speech sounds: more specialized auditory areas

177
Q

Minimal discriminate frequency difference

A

Smallest change in frequency that can be detected reliably between two tones (usually 2hz until 2000hz then larger differences are required)

178
Q

Difference between pitch and frequency

A

Frequency: physical property of sound
Pitch: solely related to the subjective sensory experience of sounds
-changes don’t always relate back to one another

179
Q

What two mechanisms give us the ability to discriminate pitches?

A

Place coding=pitch is encoded in physical location of activated receptors along length of basilar membrane; activation of receptors near base of cochlea (narrow/high frequencies) signals TREBLE and activation of receptors near base of apex (wide/low frequencies) signals BASS

Temporal coding=idea that the frequency of the sound is directly encoded in the firing pattern of auditory neurons

180
Q

What are the two ways in which frequency properties of sound are coded?

A

1- according to the distribution of excitation among cells

2- according to the temporal pattern of discharge in cells projecting to auditory cortex

181
Q

Diff between ultrasound and infrasound

A 
Ultrasound= high frequency sound (above 20,000 hz for a human)
Infrasound= very low frequency sound (below threshold for human hearing which is 20 hz)
182
Q

What’s the difference between onset disparity and ongoing phase disparity

A

Onset disparity= latency difference between the two ears for the beginning of a sound

Ongoing phase disparity= difference between ears for arrival of the peaks and troughs of sound wave

183
Q

What are the two kinds of binaural cues that signal the location of a sound source in the horizontal plane? (Duplex theory)

A

Intensity differences=perceived differences in loudness between two ears, which can be used to localize a sound source

Latency differences=differences between two ears in the time of arrival of a sound, which the nervous system can use to localize sound sources (onset disparity/ongoing phase disparity)

184
Q

What effect does the frequency have in how we perceive the location of the sound source?

A

Low frequency= no intensity differences between ears so times of arrival are the only cues, and in very low frequencies, you can’t tell at all
High frequency= sound shadow cast by head changes the intensity a lot

185
Q

What brain systems analyze binaural cues?

A

Brainstem mechanisms that relieve info from both ears and use arrays of bipolar neurons to find out where sound is coming from via left/right auditory signals
Mammals specifically: superior olivary nucleus is the primary sound localization nucleus in the mammalian brain and its divisions, the lateral superior olive (LSO) which processes intensity differences and the medial superior olive (MSO) which process latency differences, compare info from both systems to determine where sound is coming from (equal time for two signals to arrive on each side would cancel each other out etc)

186
Q

What is spectral filtering?

A

Structure of external ear make some sounds louder and some weaker depending on where the sound is coming from
Gives info about ELEVATION not LOCATION

187
Q

What are the three categories of deafness?

A

Conduction deafness: disorder of outer/middle ear prevent vibrations from reaching the cochlea (ex: ossicles fuse together)

Sensorineural deafness: hearing lost caused by many different types of problems like infections, exposure to loud sounds, diseases, etc

Central deafness: hearing loss caused by brain lesions such as a stoke; includes word deafness (don’t recognize words) and cortical deafness (don’t recognize verbal or nonverbal sounds)

188
Q

Mutations of what gene cause 50% of congenital or onset hearing loss?

A

GJB2 which encodes protein connexin-26 (formation of electrical synapses)

189
Q

What is the ototoxic antibiotic and what was is used to treat?

A

Streptomycin; tuberculosis

190
Q

How do loud noises damage hearing?

A

Damages the cochlea; hair cells receive most of the damage and cilia appear shattered and broken like a forest of fallen trees

191
Q

Tinnitus

A

A sensation of noises or hearing ringing sounds that aren’t there

192
Q

What are cochlear implants

A

Directly stimulates the auditory nerve with electrical impulses; needed bc hair cell loss

193
Q

Can hair cells be regenerated?

A

Maybe bc three proof:
1- fishes and birds= supporting cells crowded around Corti remain capable of dividing/differentiating into hair cells in adulthood
2- guinea pigs= insertion of Atoh1 (Math1) gene into cochlea equals hearing in 8 weeks
3- deletion of Rb1 gene lets hair cells divide and reproduce themselves

194
Q

What is the vestibular system?

A

Tells the brain about gravity, movement and where your body is in space

195
Q

Where is the vestibular system and what does it contain?

A
  • It’s part of the inner ear, attached to the cochlea in a cave in the temporal bone
  • parts: three semicircular canals (tubes filled with fluid) that are connected to utricle (sac like structure) and beside that is the saccule (small fluid filled sac)
196
Q

What are the three different planes of head movement to which the ear canals are oriented?

A

Nodding up and down (pitch; around y-axis)
Shaking side to side (yaw; around the z-axis)
Tilting left or right (roll; around x-axis)

197
Q

Describe the process of perceiving motion in the ear

A

When the hair cells in the ampulla move in the cupula determines how the fluid in the semicircular canals will move and together this signals the brain that the head has moved

198
Q

Otoliths (ear)

A

Small bony crystals in the gelatinous membrane that increase the sensitivity of the receptors in the ear to movement

199
Q

What system did our vestibular system evolve from?

A

Lateral-line system of fish/amphibians; informs the animal of water motion in relation to the surface of their body or prey

200
Q

Vestibular nuclei

A

Nuclei in the brainstem that receive info from vestibular organs through cranial nerve Vlll (the vestibulocochlear nerve)

201
Q

Vestibulo-ocular reflex (VOR)

A

Six muscles that control the movement of each eye have to counter the movements of the head as they happen using a high speed network in the brainstem that uses vestibular info about head rotations to move the eyes in compensation

202
Q

What are the two theories of why we experience motion sickness?

A

1- sensory conflict theory= body feels bad when it receives contradictory sensory messages (especially vestibular info vs visual info)
2- stimulation that activates a system that originally evolved to rid the body of swallowed poison

203
Q

What are the five basic tastes that humans can detect?

A 
Sweet
Salty
Umami
Bitter
Sour
204
Q

What allows us to sense so many flavours?

A

Being able to detect over 10,000 different smells and discriminate as much as 5000

205
Q

What are the specialized receptor cells on the tongue? Describe

A

Lumps of tissue called papillae that increase surface area and on their sites are the taste buds

Three types of papillae:

  • circumvallate papillae/foliate papillae= contain taste buds in it’s sides
  • fungiform papillae= 6 taste buds in each and look like mushrooms

Each taste bud has a cluster of 50-150 taste receptor cells with openings at the end called taste pores which detect tastants (things that have a taste)

Taste cells constantly replaced

206
Q

How are the 5 tastes detected? Describe briefly

A 
Salty/sour= taste cells stimulated by simple ions that act on the ion channels in the membranes of the taste cells
Sweet/bitter= special receptor molecules perceive them and they are communicated by secondary messengers 
Umami= at least two types of receptor proteins are involved
207
Q

Describe how salty flavours are detected

A

1- Sodium ions (Na+) from salty foods enter the sodium channel in cell membrane
2- taste cell is depolarized
3- neurotransmitters (that stimulates the afferent neurons that relay the info to the brain) are released

208
Q

What is the salt receptor other than the sodium channel?

A

Variant of receptor TRPV1 (transient receptor potential vallinoid type 1) can have sensitivity to sodium as well as potassium (k+) and calcium (ca2+)

209
Q

How is the sour flavour detected?

A

-Nobody is really sure
-we know that acids all release hydrogen ions (H+)
-theories: acid-sensing ion channels (resembling ionotropic receptors)
Ex: potassium channel is blocked by hydrogen, which doesn’t allow release of potassium ions from the taste cells and causes depolarization/neurotransmitter release
The necessary ion channel is PKD2L1 (also necessary for sensing carbonation)

210
Q

How are sweet flavours detected?

A
  • specialized G protein coupled receptors on molecules of membrane of taste cells are stimulated (just like with umami and bitter flavours) = intercellular activation of second messengers
  • receptors = T1R and T2R (function like slow metabolic receptors and produce gustducin)
  • when members T1R2 and T1R3 combine, they make a receptor that detects sweetness
  • for other types of sweeteners, both are combined
211
Q

Tastes that T1R and T2R detect?

A 
T1R= sweet/umami
T2R= bitter
212
Q

How are bitter tastes detected?

A

Members of T2R family of G protein-coupled receptors = bitter receptors

  • 30 members
  • each bitter sensing taste cell produces all types (or almost) T2R bitter receptors so good at detecting them but bad at telling the diff between them
213
Q

What is the chemical that 25% people can’t taste (bitter) in the USA?

A

PTC (related to PROP)

214
Q

Describe supertasters

A

Heightened sensitivity to bitter tastes and have a preference to stronger sweet tastes
Have 425 fungiform papillae

215
Q

How are umami tastes detected?

A

-detected by at least two receptors, 1=variant of metabotropic glutamate receptor (responds to amino acid glutamate) 2=T1R1+T1R3 receptors (responds to all 20 amino acids)

216
Q

Describe the gustatory system

A

Taste receptor cells -> afferent fibres (go along 3 diff cranial nerves=facial, vagus, glossopharyngeal) -> brainstem nuclei (synapse with second order gustatory neurons that project to) -> thalamus (ventral posterior medial nucleus) -> cerebral cortex

217
Q

What part of the cerebral cortex is part of the gustatory system

A

Gustatory cortex (anterior insula/frontal operculum)

218
Q

What are the two theories of how taste info is encoded to the brain?

A

1- pattern coding (relative activity across across groups of axons from diff taste receptor cells)
2- labeled lines (concept that each nerve input “line” only send one type of info to brain)

219
Q

Anosmia

A

Odor blindness

220
Q

Describe the parts of the inner nose involved in olfactory system

A
  • Sheet of cells called the olfactory epithelium lines the dorsal portion of the nasal cavities including the septum
  • this contains three types of cells: supporting cells, basal cells and olfactory receptor cells
  • each olfactory receptor cell has a long, thin dendrite that extends to the outer layer of the epithelium (mucosal surface) which has many cilia that come out of the dendritic knob
  • at the other end, the cell has a fine unmyelinated axon that runs to the olfactory bulb
221
Q

What happens if the olfactory epithilium is damaged?

A

It can regenerate and can reconnect to the olfactory bulb

222
Q

Describe the olfaction transduction process (5 steps)

A

1- odourant molecule ATTACHES TO specific receptor protein
2- receptor-odourant complex ACTIVATES G protein, which COMBINES with molecule of GTP, UNATTACHING GDP
3- G protein alpha subunit DISSOCIATES+ACTIVATES adenyl cyclase, PRODUCING cAMP
4- cyclic AMP (second messenger) ACTIVATES gated cation channel. Na+ and Ca2+ ions ENTER the cell, DEPOLARIZING it and OPENING chloride channels = further depolarization
5- receptor protein RETURNS to unbound state

223
Q

How many olfactory receptor genes does the human genome have? How many are fully functional?

A

1000; 350 (the rest accumulated mutations and don’t work anymore bc not necessary)

224
Q

How many odours can we discriminate?

A

5000

225
Q

Describe the olfactory bulb

A
  • Anterior part of the brain (front)
  • organized in spherical neural circuits called glomeruli which is where the axon terminals of olfactory neurons synapse on the dendrites of the specialized mitral cells (sharpens smells)
226
Q

What do olfactory receptor proteins do?

A

Help guide the innervating axons to their matching glomeruli

227
Q

What is the only sensory modality that doesn’t need to pass through the thalamus to get to the cortex?

A

Olfactory

228
Q

Where does output from the olfactory bulb go?

A

Axons from mitral cells go to brain regions like prepyriform and entorhinal cortex, amygdala, hypothalamus

229
Q

Describe the system that detects pheromones

A

The vomeronasal system (detects odour trails that animals secrete)

  • receptors in vomeronasal organ (VNO) of epithelial cells near olfactory epithelium
  • two major vomeronasal receptors: V1R and V2R (both families of G protein-coupled receptors)
  • very sensitive
  • send their info to accessory olfactory bulb which projects to medial amygdala which projects to hypothalamus
230
Q

What 2 parts of the eye focus light?

A

Lens and cornea

231
Q

What is refraction

A

Bending of light rays when they enter the cornea

232
Q

What do ciliary muscles do

A

Adjust the shape of the lens for focus using accommodation (contraction of muscles causes lens to focus in on close or far images to make them sharper on the retina)

233
Q

Describe pupil and retina

A

Pupil size controls that amount of light that can enter the eye and it’s found on the iris (colourful part of eye)

234
Q

What does the drug belladonna do to your eyes

A

Used during eye exams to block acetylcholine transmission in the parasympathetic synapses of the iris which relaxes the sphincter muscles and allows the pupil to open up

235
Q

What do the extra ocular muscles do?

A

They are attached to the eyeball from the orbit (bony socket of eye) and control it’s position and movements; 3 pairs

236
Q

Where do the first stages of visual processing occur? Describe this part of the eye

A

Retina
-receptive surface inside back of eye
-has cells in distinct layers:
1- photoreceptors (2 types are rods and cones which provide colour vision by wavelength)
2- bipolar cells (controlled by neurotransmitter molecules released by photoreceptors; also synapse with photoreceptors)
3- ganglion cells (connect to bipolar cells; their axons form the optic nerve that carries info to brain)
-horizontal/amachrine cells help connect cell layers

237
Q

Most parts of the eye only generate graded local potentials; which part generates action potentials?

A

Ganglion cells because of their electrical activity; transmit info to brain and process it as well

238
Q

What are the two functional systems that process light?

A

1- scotopic system: uses rods and works in dim light, no colour differentiation
2- photopic system: uses cones and works in bright light, shows differential sensitivity to wavelengths=colour vision, less convergence between ganglion cells receiving info

239
Q

Describe hyperpolarization of photoreceptors

A

1- light CHANGES the retinas shape which DEFORMS the rhodopsin (photopigment in rods that responds to light) to ACTIVATE 500 molecules of protein transducin. This activation causes a GTP molecule to replace a GDP molecule bound to transducin
2- activated transducins activate phosphodieterase (PDE) molecules
3- each PDE molecule HYDROLYZES more than 2000 molecules of cGMP which REDUCES it’s concentration
4- REDUCTION of cGMP leads to CLOSURE of Na+ channels and HYPERPOLARIZATION of the receptor. 1 photon of light can block enter of 1 million+ Na+ molecules

240
Q

What are the two parts of the rod and cone photopigments in the eye?

A

1- retinal

2- opsin

241
Q

What are the two receptors of the photopic and scotopic systems?

A

Photopic- cones

Scotopic- rods

242
Q

What’s the difference of receptors per eye of scotopic and photopic systems?

A

Photopic- 4 million

Scotopic- 100 million

243
Q

Difference in photopigments in photopic and scotopic systems?

A

Photopic- three classes of come opsins; base of colour vision
Scotopic- rodopsin

244
Q

Difference in sensitivity of photopic and scotopic systems

A

Photopic- low, needs pretty strong stimulation, used for DAY VISION
Scotopic- high, can be activated by fun light intensity, used for NIGHT VISION

245
Q

Location in retina for photopic and scotopic systems

A

Photopic- concentrated around fovea, also scattered throughout retina
Scotopic- outside fovea

246
Q

Receptive field size/visual acuity difference in scotopic and photopic systems

A

Photopic- small in fovea, so acuity is high; larger outside fovea
Scotopic- larger = less acuity

247
Q

Difference in temporal responses of photopic and scotopic systems

A

Photopic- fast

Scotopic- slow as fuuuuck jk

248
Q

Three major characteristics of the visual system

A

1- SENSITIVITY (weak stimuli are amplified to make better physiological effects
2- INTEGRATION of stimulus over time (makes vision slow but increases it’s sensitivity)
3- ADAPTATION to wide range of light

249
Q

How do our eyes adjust to different intensities of light? 2 ways

A

1- adjusting pupil size (constricted pupil for less light, controlled by specialized retinal ganglion cells that possess their own photopigments, project to superior colliculus to control pupil diameter)
2- range fractionation=handling of diff intensities of light by diff specific receptors

250
Q

2 main factors of adaptation of photoreceptors

A

1- varying concentration of calcium (ca2+) ions and their storage/release is controlled by photoreceptors (which controls sensitivity to light)
2- slow recombination of retinal and opsin after photoreceptor pigment is split by light

251
Q

In what part of the eye is acuity strongest?

A

Fovea (central region that has a dense concentration of cones)

252
Q

Where is the human blind spot?

A

On the optical disk bc no photoreceptors

253
Q

Why is our visual acuity weaker in our peripheral vision?

A

Cones and rods are larger and blood vessels block them so the stimulus is not as intense

254
Q

Describe distribution of rods and cones

A

Cones in fovea and rods in periphery of the retina

255
Q

What’s the name of the process in which neurons in a region are interconnected by axons or interneurons that inhibit their neighbouring neurons?

A

Lateral inhibition

256
Q

Describe how visual info is sent to the brain

A

Ganglion cells in each eye PRODUCE action potentials that are CONDUCTED along their axons to SEND visual info to brain
These axons make up the optic nerve (cranial nerve ll) that brings info to brain on each side, specifically the visual cortex in the occipital lobe at the back of the brain

257
Q

Describe how the retinal image is projected

A

It’s inverted and reversed right to left compared with the visual field

258
Q

What forms the optic nerves?

A

Axons of retinal ganglion cells

259
Q

Describe what the optic chiasm is and what happens there

A

Optic nerves cross the midline here; axons from the TEMPORAL halves = same optic tract on same side and axons from NASAL halves = cross to optic halves on opposite sides

260
Q

Where do axons in optic tract terminate?

A

Lateral geniculate nucleus or a little bit further in the superior colliculus

261
Q

After axons terminate in the lateral geniculate, what do they do?

A

They carry info to the striate cortex via optic radiations

262
Q

Where is most of the primary visual cortex found?

A

On the medial surface of the brain

263
Q

The biggest proportion of the primary visual cortex is made up of what region?

A

The foveal region

264
Q

What is the extrastriate cortex?

A

Visual cortex outside of the primary (striate) visual cortex

265
Q

What is a region of blindness caused by injury to the visual pathway or brain called?

A

Scotoma

266
Q

Describe how photoreceptors excite some retinal neurons and inhibit others

A
  • at resting potential, both rod and come photoreceptors release neurotransmitter glutamate
  • light hyperpolarizes photo receptors which makes them release LESS glutamate.. But the response depends on which type of glutamate receptor the bipolar cell has
  • ON CENTER bipolar cells = receives less glutamate
  • OFF CENTER bipolar cells = receives more glutamate = depolarization
267
Q

Bipolar cells release glutamate, which does what to ganglion cells?

A

Depolarizes them

268
Q

Describe the lateral geniculate nucleus and its layers

A
  • LGN of the thalamus is where most ganglion cells synapse in mammals
  • has six main layers
  • four main dorsal layers = parvocellular aka small cells
  • two main ventral layers = magnocellular aka large cells
  • 1 4 6 receive info from eye on opposite side of body and 2 3 5 receive info from eye on same side of body
269
Q

What are the two categories of cortical cells (based on types of stimuli that’s needed to cause max responses)

A

Simple cortical cells- respond best to edge or bar that has specific width/orientation/location on visual field; receives info from row of LGN cells
Complex cortical cells- elongated receptive fields and show latitude for location aka have more range; receives info from row of simple cortical cells

270
Q

Describe the spatial frequency filter model (vision)

A
  • concept of pattern analysis based on lines and edges

- applies Fourier analysis or linear systems theory rather than analyzing visual patterns

271
Q

What happens in vision when low frequencies or high frequencies are filtered out

A

You can see the pic either way but…
No high freq= no small details or sharp contrasts
No low freq= no large uniform areas or transitions

272
Q

What are the two jobs of the primary visual cortex (V1)

A
  • perceiving objects and events

- forming mental images

273
Q

What are the four dimensions of visual stimulus that the primary visual cortex has representations for?

A

1- location in visual field (with larger more detailed mapping of center of vision compared to periphery)
2- ocular dominance
3- orientation
4- colour

274
Q

How is area V1 organized?

A

Organized into ocular dominance columns (region of the cortex where one eye or the other provides more synaptic input) and these are arranged into ocular dominance slabs about .5 mm wide where neurons of all layers respond preferentially to one eye
-orientation columns too

275
Q

What are the three dimensions of colour perception?

A

1- brightness
2- hue
3- saturation (rich/full to dull)

276
Q

Trichromatic vs opponent-process hypothesis

A 
Trichromatic= hypothesis of colour perception saying that there are 3 diff types of cones, each excited by a different region of the spectrum and each have separate pathway to brain 
Opponent-process= theory that colour vision depends on systems that produce opposite responses to light of diff wavelengths
277
Q

Under ordinary conditions, how many sets of cones are activated when responding to visual stimuli?

A

At least two kinds of cones to ensure acuity and good perception of form

278
Q

What are the three names for cones based on their peak areas of wavelength sensitivity

A

Short (very low amount of these), medium, long

279
Q

Describe the photopigments of human genes

A

We have two on the X chromosome: 1 for medium and one for long wavelength cones
*short wavelength cones are found on the autosome

280
Q

Describe how some retinal ganglion cells and parvocellular LGN cells show spectral opponency

A

When two regions of the spectrum have opposite effects on the rate at which the neuron fires action potentials
1: +L/-M
2: +M/-L
3: +(L/+M)/-S
4: +S/-(L+M)
These are the second stage of colour perception but cannot be called colour cells for two reasons:
1: they send info to many higher circuits to determine form depth movement hue etc
2: their peak wavelength sensitivities do not correspond exactly to the wavelengths that we see as the principal hues
- = darkness
+ = brightness

281
Q

What’s the third stage of the colour vision system?

A

Spectral opponent cortical cells

282
Q

What’s the forth stage of the colour vision system?

A

Visual cortical region V4 that is rich in colour-sensitive cells that respond best if background colour is different than object colour; used for distinguishing object and background and also for spatial frequency

283
Q

What area of the brain works in the perception of visual motion?

A

Cortical area V5

284
Q

Optic ataxia

A

Damage to posterior parietal cortex that causes people to have difficulty reached for and grasping objects but not identifying them

285
Q

Describe the two main cortical processing streams

A

Ventral processing stream= identifying objects (what); includes regions of occipitotemporal, inferior temporal, inferior frontal areas
Dorsal stream= appreciating location of objects and guiding movement towards objects (where)

286
Q

Describe what happens when we see someone doing an action

A

Mirror neurons that represent the action are activated by the observer’s premotor cortex

287
Q

Describe myopia and it’s possible causes

A

Nearsightedness bc of eye too long so eye is forced to focus objects in front of the retina instead of in the retina so distant objects appear blurred

They think it’s caused by indoor lighting (environmental factors)

288
Q

Describe amblyopia

A

Acuity is poor in one eye despite the eye and retina being normal
Caused by the two eyes not being aligned properly in early years of life, so the primary visual cortex tends to suppress info from one eye, making it functionally blind

289
Q

Define emotion

A

Subjective mental state accompanied by distinctive behaviours and involuntary physiological changes

290
Q

Diff between sympathetic and parasympathetic nervous systems

A 
Sympathetic= fight or flight system that prepares body for action; arises from thoracic and lumbar spinal cord
Parasympathetic= prepares body to relax and recuperate; arises from cranial nerves and sacral spinal cord
291
Q

Describe the two theories of emotions causing bodily changes or vice versA

A

James-Lange theory= emotions we experience are caused by bodily changes (failed bc no distinctive autonomic pattern for each emotion)

Cannon-bard theory= cerebral cortex analyzes stimuli and simultaneously activates emotion and bodily response to go with it

292
Q

Cognitive attribution model of emotion

A

Theory that our emotions result from a cognitive analysis of the context around us and bodily changes just accentuate these emotions (don’t specify emotions)

293
Q

How many basic emotions are there (supposedly) and what are they (in pairs)

A

Eight: joy/sadness, affection/disgust, anger/fear, expectation/surprise

294
Q

What emotions are commonly non universal?

A

Disgust and surprise

295
Q

According to Fridlund, what’s the major role of facial expression?

A

It’s para linguistic (an accessory to verbal communication that provides emphasis and direction in conversation)

296
Q

What are the two categories of facial muscles

A

1- superficial facial muscles= attach only to facial skin and on contraction they change the shape of the mouth/eyes/nose
2- deep facial muscles= attach to bone and enable movements like chewing and large movements of the face

297
Q

Human facial muscles are inner aged into which two cranial nerves

A

1- facial nerve (Vlll)= innervates the superficial muscles of the facial expression
2- motor branch of the trigeminal nerve (V)= innervates muscles that move the jaw

298
Q

Facial feedback hypothesis

A

Hypothesis that our emotional experience is affected by the sensory feedback we receive during specific facial expressions like smiling

299
Q

Describe Bell’s palsy

A

Disorder usually caused by a viral infection where the facial nerve on one side stops conducting action potentials =paralysis of one side of face

300
Q

What are the three distinct facial expressions in nonhuman primates (according to redican)

A

1- grimace (like our fear or surprise)
2- tense mouth (like our anger)
3- play face (like our laugh)

301
Q

What is the scientific name for the tendency of people to have the same emotional reaction to an event throughout the lifetime?

A

Individual response stereotypy

302
Q

Describe brain self-stimulation

A
  • Process where animals will work to provide electrical stimulation to particular parts of their brain, assumably bc feels good (ex: septum=feelings of pleasure and warmth)
  • will work for subcortical sites but cerebral cortical stimulation doesn’t have that pleasurable of a response
  • most effective sites are concentrated in hypothalamus and extend into brainstem especially the medial forebrain bundle and nucleus accumbens
303
Q

What caused decorticate rage in dogs? What conclusions can be drawn from this?

A

Removing dogs cortex made them have random bursts of rage without direction; this means that emotional behaviours like this must be organized at subcortical level, with cerebral cortex being the part to stop the emotional response (Papez)

304
Q

Papez circuit

A

Interconnected regions of brain that include the mammillary bodies of the hypothalamus, the anterior thalamus, the cingulate cortex, hippocampus and fornix
Later became the limbic system (with amygdala added)

305
Q

Describe Kluver-Bucy syndrome and the monkey experiment that helped discover it

A

When large portions of the temporal lobe were removed in monkeys, they became very tame, ate everything, and were hypersexual
The syndrome itself is brought on by bilateral amygdala damage, that is characterized by dramatic emotion changes like no fear or anxiety

306
Q

What is fear conditioning?

A

A type of classical conditioning where a neutral stimulus is paired with shock or another unpleasant experience, causing the patient to eventually act fearful in response to the previously neutral stimulus

307
Q

The amygdala is a key structure in what emotion? Describe it’s high and low roads

A

Fear; located at anterior medial portion of the temporal lobe
Low road=direct projection from thalamus to amygdala which bypasses conscious processing for a quick reaction to fear stimulus
High road=goes thru sensory cortex and integrated into higher level conscious processes such as memory

308
Q

Describe the pathway of fear info (4 steps ending in 3 emotional responses)

A

1- info about stimulus from several parts of brain (including sensory cortex) reach lateral portion of amygdala
2- neurons in amygdala encode association between stimuli and aversive events like electrical shock
3- lateral amygdala triggers network within amygdala that then activates central nucleus
4- central nucleus transmits info to various brainstem venters to evoke three diff aspects of emotional responses
1: pathways through central grey= emotional behaviours
2: pathways through lateral hypothalamus= autonomic responses
3: pathways through bed nucleus of stria terminalis= hormonal responses

309
Q

What type of drug could maybe be used to treat phobias one day?

A

Cannabinoid drug bc cannabinoid receptors help unlearn learned fears

310
Q

What happens with blood flow when humans are shown visual stimuli related to fear/pain?

A

Blood flow to the amygdala increases

311
Q

Describe patients with amygdala damage

A
  • have trouble recognizing fear in facial expressions
  • don’t startle or find scary things scary
  • breathing air with high concentration of carbon dioxide bc brain has another way of letting these patients know that they need oxygen
312
Q

What’s the difference in emotional symptoms after left or right hemisphere damage?

A

Left: depression and language deficit
Right: (or temporal cortex) very cheerful

313
Q

Difference in processing emotional stimuli between the left and right hemispheres

A

Right: (left visual field) faster reaction times and more accurate identification of emotional states

314
Q

What hemisphere is dominant for facial expression of emotion?

A

Right hemisphere

315
Q

What are the three components of stress?

A
  • stressful stimuli
  • stress processing system
  • responses to stress
316
Q

Describe the four stages of stress response

A

1- hypothalamus activates sympathetic nervous system to stimulate other psychological systems
2- one of these is the adrenal medulla (center of adrenal gland) which is activated to release epinephrine and norepinephrine (FAST)
3- anterior pituitary also stimulated to release hormones that drive the outer part of the adrenal cortex to release hormones like cortisol (SLOW)
4- these hormones then prepare the body for action

317
Q

Describe Selye’s adaptation stage and exhaustion stage

A

Adaptation stage= second stage in stress response which includes successful activation of appropriate response systems and re establishes homeostatic balance

Exhaustion stage= stage in stress response where stress is often repeated or prolonged, which increases chances of disease

318
Q

Describe concept of stress immunization

A

Mild stress early in life makes an individual better at handling stress later

319
Q

Describe epigenetic regulation

A

Process which affects the expression of a particular gene or genes without affected the order of nucleotides that makes up the gene

320
Q

Psychosomatic medicine

A

Field of medicine that looks at the impact of psychological factors in disease

321
Q

Health psychology

A

Aka behavioural medicine

Field that studies psychological influences on health-related processes such as how people get sick or remain healthy

322
Q

Psychoneuroimmunology

A

Study of the immune systems interactions with the nervous system and behaviour

323
Q

Describe the immune system

A
  • in blood, there are diff classes of white blood cells (leukocytes)
    • phagocytes (eat and destroy germs)
    • 3 types of lymphocytes to tell them when to attack
      1: B lymphocytes (form bone marrow) produce proteins called antibodies that latch onto foreign bacteria and summon phagocytes/proteins to destroy them
      2: T lymphocytes (T cells from the thymus gland) attack against foreign substances; also special T lymphocytes called helper T cells secrete cytokines (cell signalling proteins that regulate activity of B lymphocytes/phagocytes
      3: these cells form in the thymus gland, bone marrow, spleen and log nodes
324
Q

How does the brain affect the immune system?

A
  • Through autonomic nerve fibers that innervate immune system organs like the spleen and thymus gland
  • fibers=noradrenergic, sympathetic postganglionic axons that affect antibody production and immune cell proliferation
  • brain also carefully monitors immune reactions to make sure they are not too extreme or harmful to the body
325
Q

What are the two systems that interact with the immune system?

A

Nervous and endocrine systems

326
Q

How and why does stress suppress the immune system?

A

How: brain tells adrenal cortex to release steroid hormones like cortisol that directly suppress immune system
Why: to be able to rapidly mobilize energy for temporary suppression of immunity

327
Q

What are the three effects of chronic stress

A

Degeneration of hippocampus and prefrontal cortex

Expansion of amygdala

328
Q

Unipolar depression

A

Depression that alternates with normal emotional states

329
Q

How does the brain change with depression?

A
  • increased blood flow (=greater activity) in prefrontal cortex and amygdala
  • decreased blood flow (=less activity) in parietal, posterior temporal cortex, and anterior cingulate (systems connected with attention)
  • increased blood flow in the amygdala never goes away
  • adrenocorticotropic hormone (ACTH) is released in excessive amounts by the anterior pituitary gland
330
Q

Descendants of people with sever depression have what changes in the brain?

A
  • thinner cortex across parts of the right hemisphere

- possibly smaller hippocampus

331
Q

Describe the different treatments for depression

A
  • electro convulsive shock therapy (ECT)
  • transcranial magnetic stimulation (TMS) = alters cortical electrical activity
  • drugs that affect monoamine transmitters (first antidepressants were inhibitors of MAO which is the enzyme that normally inactivates the monoamines aka norepinephrine, dopamine and seratonin) like tricyclics
  • reserpine CAUSES depression
  • moderns drugs like selective seratonin uptake inhibitors (SSRIs)
332
Q

Serotonin syndrome

A

If serotonin levels in the body get too high, it causes confusion, muscle spasms and fever; risk of taking SSRI’s

333
Q

Vagal nerve stimulation

A

Electrodes surgically wrapped around the vagus nerve and pacemaker provides mild electrical stimulation at intervals (expensive and little proof that it works)

334
Q

Deep brain stimulation (DBS)

A

Mild electrical stimulation of areas of the brain thru a surgically implanted electrode, specifically in the cingulate cortex for depression

335
Q

Cognitive behavioural therapy (CBT)

A

Psychotherapy with the goal of correcting negative thinking and improving interpersonal relationships
(Most effective treatment is this paired with SSRIs)
Looks at cycle antisocial behaviour, negative thoughts and low mood

336
Q

What syndrome is caused by high levels of circulating glucocorticoids like cortisol? What can it say about depression?

A

Cushings disease

  • depression first symptom
  • dysfunction of hypothalamic pituitary adrenal axis could be involved in depression, may as a depression inducing stress reaction
337
Q

What test can assess the hypothalamic pituitary adrenal function?

A

Dexamethasone suppression test can reveal a tendency to release extra cortisol

338
Q

What is dexamethasone and what does it do?

A

Used in dexamethasone suppression test; it usually suppresses the rise in ACTH of normal people in the morning but doesn’t work on people with depression

339
Q

How does sleep change with depression?

A

Less stage 3 SWS and more stage 1 and 2

REM sleep comes faster and is more intense

340
Q

Learned helplessness

A

Animal is exposed to repeated stressful stimulus like an electric shock to which it can’t escape
Linked to decrease in serotonin and dopamine like depression

341
Q

What happens when you remove the olfactory bulb from rodents?

A

Creates a model of depression; irritable, preference for alcohol, high levels of corticosteroids (all reversible with antidepressants)

342
Q

Two types of bipolar disorder

A

Rapid cycling= four or more distinct cycles between depression and mania in a year
Cyclothymia= cycling between dysthymia (poor mood or mild depression) and hypomania (increased energy and positive mood without the weird symptoms of more intense mania)

343
Q

Differences in the brain of people with bipolar disorder

A
  • have three affected genes, one being the gene that encodes brain-derived neurotrophic factor (BDNF)
  • enlarged ventricles that enlarge more with each manic episode
344
Q

What element is said to be a good treatment for bipolar disorder

A

Lithium, as it interacts with circadian clock proteins and boosts BDNF
Increases volume of grey matter and decreases symptoms

345
Q

What are two alternative treatments for bipolar disorder that aren’t drugs?

A

Transcranial magnetic stimulation and CBT

346
Q

What are the major types of anxiety disorders

A
  • phobic disorders= intense irrational fears that lead person to avoid a thing or situation
  • generalized anxiety disorder=constant anxiety for months
  • panic disorder=reoccurring panic attacks
347
Q

Differences in the brain of a person with panic disorder

A

Temporal lobe abnormalities (ex: lower volume) and changes in amygdala and associated circuitry

348
Q

What are the two types of drugs that help anxiety

A

Benzodiazepines; anxiolytics which bind with GABA receptors and enhances their ability for post synaptic inhibition; especially bind to receptors in the cerebral cortex/hippocampus/amygdala
Ultimately regulates the permeability of neuronal membranes to chloride ions (Cl-)

349
Q

What is Buspar (drug) used for and what does it do?

A

Agonist at serotonin 5HT1A receptors that can provide relief from anxiety; buspirone

350
Q

What two qualities can make someone more susceptible to PTSD?

A

Smaller hippocampus and lower rates of adult epigenesis

351
Q

Fear conditioning and what in the brain causes it

A

A form of learning where fear becomes associated with a previously neutral stimulus; caused by NDMA antagonists in the brain delivered to the amygdala that prevent someone from forgetting a traumatic memory and sensitivity to cortisol goes up to increase reaction to stress

352
Q

Describe patients with OCD

A

-increased metabolic rates in orbitofrontal cortex, cingulate cortex and caudate nuclei

353
Q

Name three OCD drugs and what they have in common

A

Fluoxetine (Prozac)
Fluvoxamine (Luvoc)
Clomipramine (Anafranil)
All of them inhibit reuptake of serotonin at serotonergic synapses, which increases the synaptic availability of serotonin

354
Q

What is the co-morbid disease of OCD?

A

Tourette’s syndrome as both involve abnormalities of the basal ganglia

SFU- semester 1 (5 decks)

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