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Undergrad > NEUR 3001 Unit 3 > Flashcards

NEUR 3001 Unit 3 Flashcards

1
Q

Process H

A

Homeostatic

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2
Q

Process C

A

Circadian, alerting signal

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3
Q

General ANS structure

A

Autonomic ganglia connect to the spinal cord and brain stem and mediate simple reflexes

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4
Q

Three ANS divisions

A
  1. Sympathetic
  2. Parasympathetic
  3. Enteric
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5
Q

Difference in organization of pre-ganglionic neurons in ANS branches

A

Parasympathetic: Craniosacral

Sympathetic: Thoracolumbar

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6
Q

Differences in peripheral locations of their ganglia in ANS branches

A

Parasympathetic: close to target organs

Sympathetic: further from target organs in sympathetic trunk

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7
Q

Differences in post-ganglionic neurotransmitters in ANS branches

A

Parasympathetic: acetylcholine

Sympathetic: norepinephrine

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8
Q

Superior cervical ganglion

A

Sympathetic neurons that control the redirection of blood to muscles

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9
Q

Loewi experiments

A

Stimulation of the vagus nerve (parasympathetic nervous system) which results in the lowering of the heart rate

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10
Q

Acetylcholine release in a chemical synapse

A
  • Acetyl CoA and choline are substrates for an enzyme to form CoA and acetylcholine
  • Acetylcholine is released into the cleft via a synaptic vesicle
  • Acetylcholine can bind to cholinergic receptors on the post-synaptic membrane
  • Acetylcholinesterase breaks acetylcholine into acetate and choline
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11
Q

Nicotinic receptor activation speed

A

Fast post-synaptic potential

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12
Q

Muscarinic receptor activation speed

A

Slow post-synaptic potential

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13
Q

Pre-synaptic α2 receptors

A

Act on the pre-synaptic membrane to provide negative feedback to inhibit further NE release

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14
Q

Co-release of neurotransmitters in the ANS

A

Pre-synaptic terminal can co-release 2+ NT types onto the same post-synaptic cell

Example: acetylcholine and VIP

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15
Q

Three principles of neurotransmission in ANS

A
  1. Activation of multiple receptors
  2. Pre-synaptic and post-synaptic effects
  3. Co-release of different neurotransmitters
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16
Q

Vagus nerve

A

Cranial nerve X

Regulates heart rate, GI motility, pancreatic endocrine & exocrine secretion, hepatic glucose production

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17
Q

Inflammatory reflex

A

Pathogens activate TLR4 → cytokines release from macrophages and other immune cells are detected by sensory arm of vagus → activation of efferent vagus regulates immune activation and suppresses pro-inflammatory cytokines release

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18
Q

Baroreceptor reflex

A

Decrease in carotid & aortic baroreceptor firing → glossopharyngeal & vagus nerves → increase in sympathetic activation → increase in HR, arterial constriction, venue dilation, & increase in ventricular contractility

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19
Q

Transient receptor potential (TRP) channels

A

Act as cellular sensors to perceive and respond to a variety of environmental stimuli (temperature, taste, pain)

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20
Q

TPRC5

A

Activated by membrane stretching

Expressed in baroreceptor neurons (remember the diagram with the antibody blocking the TPRC5 neurons and expressed in neurons)

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21
Q

Micro-pipette technique

A
  • Suction of the cell membrane
  • Pulse of cell membrane to rupture the membrane patch
  • Future whole cell recording
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22
Q

T5E3 antibody

A

Used to image the presence of TPRC5 channels — blocks these channels

After blocking, there is less negative current where is no pressure and less positive current when there is pressure — may indicate the level of pressure with no current indicating small amount of pressure

Similar results where seen with knockout

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23
Q

TPRC5 knockout

A

Knockout has lower negative current under no pressure and lower positive current under pressure

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24
Q

TPRC5 knockout and mean arterial pressure

A

Higher mean arterial pressure with greater level of variation

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25
Q

TPRC5 knockout and heart rate

A

Higher heart rate with greater level of variation

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26
Q

Enteric nervous system

A

Arrangement of neurons and supporting cells throughout the GI tract from the esophagus to the anus

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27
Q

Types of neurons in the ENS

A

Sensory, motor, and interneurons

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28
Q

ENS and other branches of autonomic nervous system

A

Receives input from the parasympathetic and sympathetic branches

Can operate independent of input from either as well

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29
Q

Parkinson’s disease

A

Progressive neurological disorder with some combination of the following symptoms:

  • impaired initiation of voluntary movement
  • increased resistance of passive movement
  • resting tremor
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30
Q

Parkinson’s disease average age onset

A

50 years

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31
Q

Sporadic/idiopathic Parkinson’s disease

A

Occurs in people with no family history of PD and may be linked to metal exposure

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32
Q

Anatomical changes in the substantia nigra in PD

A
  • Loss of dopaminergic cells within the substantia nigra
  • Lewy bodies
  • Diffuse α-synuclein extracellularly and intracellularly
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33
Q

α-synuclein in PD

A

Spreads throughout the brain (early stages mainly concentrated in the substantia nigra)

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34
Q

Leaky gut epithelium

A

Allows for the uptake in the toxins and luminal factors

Protein pathologies can be detected in the ENS, suggesting that the proteins may have originated in the ENS

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35
Q

Vagus nerve and protein pathologies

A

Allow for the retrograde transport of the pathogen from the efferent fibers and the brain

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36
Q

Human findings for Braake hypothesis

A

Exosome transport α synuclein from cell to cell seen in welders exposed to manganese

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37
Q

Braake hypothesis

A

(1) α synuclein infiltrates the cholinergic and monoaminergic brain stem neurons and the olfactory neurons from exposure via retrograde transport by the vagus nerve
(2) Infiltration of similar neurons in the midbrain and basal brain leads to the motor symptoms of PD
(3) As the disease progresses, Lewy bodies will be found later in the limbic and neocortical brain regions

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38
Q

RT-QuIC assay

A

Normally folded prions are the reagents, and they are fluorescently labeled so that they indicate when they are misfolded

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39
Q

Exosomes

A

These are secreted under both physiological and pathophysiological conditions

Will cause modulations of cellular behaviors and delivery of disease-causing entities

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40
Q

Rotenone

A

Toxin that inhibits the electron transport train (no ATP)

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41
Q

Braake hypothesis and rotenone

A

Three groups: control, rotenone, rotenone + vagotomy

Higher level of α synuclein collection in the substantia nigra for rotenone group and reduced for rotenone & vagotomy

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42
Q

Motor learning task and sleep

A

Improvement after a session of sleep — doesn’t alter based on the number of re-tests

Indicates that sleep is necessary for learning

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43
Q

“Sleep is for forgetting” framework

A
  • Targeted erasure of synapses that’s unique to sleep
  • Necessary for efficient learning
  • Deficits in this process may underlie various kinds of intellectual disabilities & mental health problems
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44
Q

Restorative hypothesis

A

Sleep allows for the reduction of the metabolic rate for brain and increasing the amount of metabolites removed from the brain

“Restoring the balance”

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45
Q

Number of hours sleeping

A

Increased metabolism and smaller size

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46
Q

Growth hormone and sleep

A

Increased release of growth hormone during sleep

More is released at night and is more effective

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47
Q

Mitosis and sleep

A

Increased number of mitosis events at night → supports the restorative hypothesis

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48
Q

Ultradian

A

Biological cycle with a frequency of less than 24 hours

Example: REM sleep

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49
Q

REM sleep

A

Sleep cycle that resembles awake activity with more vivid dreams

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50
Q

REM sleep duration

A

Increases as sleep goes on

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51
Q

Physiological changes during sleep

A

Reductions in eye movements, head movements, & heart rate

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52
Q

Clearance of Aβ

A

Increased clearance of Aβ in sleep and under anesthesia but reduced in awake

Shown with radioactively tagged Aβ

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53
Q

CSF influx

A

Increased CSF influx compared to the awake state

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54
Q

Neuromodulation in sleep

A

Reduction in cholinergic, adrenergic, serotonergic, orexin in NREM sleep

Increased cholinergic activity in REM sleep

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55
Q

Chemical system promoting sleep

A

Buildup of adenosine

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56
Q

Melanin-concentrating hormone and sleep

A

MCH neurons are concentrated in areas that regulate sleep

Antagonist of MCHR1 reduces sleep

Infusion of MCH increases SWS and REM sleep

MCH-expressing neurons are more active during REM sleep

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57
Q

MCH and memory

A

Conditioned fear was used to establish memory

Greater memory seen in mice with MCH ablation

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58
Q

Sleep distribution and aging

A

Reduction in total sleep time

Relative decrease in ratio of REM sleep to NREM sleep

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59
Q

Mimosa plant and circadian rhythm

A

Exhibit a rhythm of opening and closing of leaves

Even when in darkness, still follow a circadian rhythm — not based on light then

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60
Q

Zeitgeber

A

Any environmental cue that can be used by an organism to align its endogenous rhythm with the external day-night cycle

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61
Q

Establishment of circadian rhythms in plants

A

Photoreceptor proteins → central oscillator → oscillatory rhythms in plants

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62
Q

Hirschsprung disease

A

Disruption of digestion primarily found in newborns

Can be fatal

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63
Q

Gut-brain axis

A

Bidirectional communication between the CNS and ENS, linking the emotional and cognitive centers of the brain with peripheral intestinal functions

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64
Q

Clock gene mutations (same gene, different locations)

A

Arrhythmic, short-period, or long-period irregularities

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65
Q

Negative feedback loop for circadian rhythms in flies

A

TIM and PER are transcribed from tim and per genes

They will dimerize and translocate to the nucleus

They will inhibit the CLK and CYC promoters that drive tim and per transcription

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66
Q

Positive elements in flies

A

CLK and CYC

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67
Q

Negative elements in flies

A

TIM and PER

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68
Q

Positive elements in mammals

A

BMAL1 and CLOCK

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69
Q

Negative elements in mammals

A

PER and CRY

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70
Q

Feedback loop in light

A

Light drives feedback loops in mammals and flies

CRY mediates this in flies

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71
Q

Clock gene-mediated circadian rhythms in nocturnal rodents

A

During “sleeping hours” → less PER2 protein, allowing BMAL1 induction of Per2 transcription

During “waking hours” → reduction in Per2 mRNA due transcription and reduction of BMAL1 activity

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72
Q

Neurotransmitters in SCN

A
  • AVP
  • GABA
  • VIP
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73
Q

Intrinsic circadian rhythmicity

A

Found in diverse classes of SCN neurons (can be AVP, VIP, or neither)

Within a class, can be rhythmic or arrhythmic

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74
Q

SCN neurons and circadian rhythms

A

Small proportion are in sync with rhythm

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75
Q

Core (ventrolateral) in SCN

A

Photo-receptive

Neurotransmitter: VIP

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76
Q

Shell (dorsomedial) in SCN

A

Not photo-receptive

Neurotransmitter: AVP and GABA (connections between core and shell)

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77
Q

VL mechanism for photo-reception

A

Innervated by the optic chiasm

Neurotransmitters: Glu and PACAP

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78
Q

SCN target processes (6)

A
  • Sleep
  • Wake
  • Appetite
  • Neuroendocrine
  • Local brain clocks
  • Autonomic
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79
Q

Adrenaline reverse effect

A

Can bind to β adrenoceptors

Can overpower sympathetic neurotransmission and cause relaxation

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80
Q

Bayliss and Starling findings

A

Motor of intestines occurs even after the complete division of the mesenteric nerves

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81
Q

Vasopressin and SCN

A

Release follows a 24-hr cycle

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82
Q

Feedback system in plant circadian rhythms

A

Feedback auto-regulatory loop

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83
Q

Nickname for SCN

A

Master clock

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84
Q

Temperature and circadian rhythms

A

Increased temperature during awake hours, decreased temperature during asleep hours

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85
Q

SCN physiological changes (6)

A
  • Blood pressure
  • Blood glucose and triglycerides
  • Xenobiotic clearance
  • Cognition
  • Mood
  • Brain homeostasis
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86
Q

Phase shift from zeitgebers

A

Induced molecular changes in the SCN

Seen with jet lag — shift activity from one time to another

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87
Q

Neuropathology and circadian rhythms

A

Neuropathology → abnormal NT release → sleep/circadian disruption → co-morbid pathologies, abnormal light-dark exposure, disrupted social behavior, stress axis activation

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88
Q

Autoregulatory system

A

Modify inputs and outputs to meet certain set point as determined by an error signal which controls negative feedback and positive feedforward

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89
Q

Four components of autoregulatory system

A
  1. Input subsystem
  2. Regulated compartment with sensor
  3. Output subsystem
  4. Error signal
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90
Q

Baroreceptor reflex (def. 2)

A

Example of autoregulatory system

Baroreceptor firing modulates vasoconstriction and vasodilation to control blood pressure with comparison to a setpoint via descending vasomotor activity (hypothalamus)

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91
Q

6 vital functions regulated by the hypothalamus

A
  1. BP and electrolyte composition
  2. Energy metabolism
  3. Reproductive behavior
  4. Body temperature
  5. Defensive behavior
  6. Sleep-wake cycle
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92
Q

3 sensory signals for fluid balance

A
  1. ANG II (signaling in response to low blood volume)
  2. Osmolality/osmolarity
  3. Baroreceptors in circulatory system
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93
Q

ANG II control system

A

SFO in hypothalamus detects ANG II and releases ANG II onto MePO, PVN, OVLT, and LHA

PVN will drive drinking behaviors

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94
Q

Baroreceptor control on PVN

A

Baroreceptors inhibit the MePO, which will inhibit the PVN

It will prevent further drinking behaviors

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95
Q

Optogenetics

A

Infects specific cells with a virus to cause the placement of an opsin channel on the membrane

The opsin channel will open with light, causing either excitation or inhibition

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96
Q

Two possible opsins

A
  1. Channelrhodopsin — opens sodium channel (excitation)

2. Halorhodopsin — opens chloride channel (inhibition)

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97
Q

Six steps of optogenetics

A
  1. Piece together the genetic construct (promoter to drive expression and gene-encoding opsin)
  2. Insert construct into virus
  3. Inject virus into animal brain
  4. Insert optrode (fiber-optic cable plus electrode)
  5. Shine light to open channels
  6. Observe behavioral changes
98
Q

Excitation of glutamatergic SFO neurons

A

Drive fluid intake

99
Q

Inhibition of glutamatergic SFO neurons

A

Suppress fluid intake

100
Q

Excitation of GABAergic SFO neurons

A

Suppress fluid intake

101
Q

Osmolality sensors in the hypothalamus

A

SFO and OVLT

Lack blood-brain barrier → well-positioned for osmoreceptors

102
Q

Hyperosmotic

A

Greater than reference solution

103
Q

Hypoosmotic

A

Less than reference solution

104
Q

Vasopressin

A

Hormone that increases blood pressure and increases reabsorption of water in the kidney

105
Q

4 theoretical mechanisms for osmoreceptors sensing cell volume changes

A
  1. Direct stretch
  2. Tethering to cytoskeleton
  3. Changes in membrane curvature
  4. Interactions with integrins (upstream of cytoskeleton changes)
106
Q

Integrins

A

Join the cytoskeleton on the side of the cell to the extracellular matrix

Heterodimers of alpha and beta subunits

107
Q

Water restriction

A

Activation of glutamatergic SFO neurons (will de-activate within 1 minute of drinking)

108
Q

Oral vs. gut infusion water

A

Oral infusion causes immediate decrease in calcium signaling in SFO, while gut infusion causes a delayed decrease

Must be something involved in perception of water intake prior to osmolarity

109
Q

Gulping

A

Motor activity of the pharynx and esophagus signals via the vagus to inhibit the drive to drink — anticipatory modulation

110
Q

Temperature of water

A

Reduces the activity of SFO glutamatergic neurons as temperature decreases

111
Q

Long-term feedforward satiation signal

A

Osmolality

112
Q

Pre-absorptive inputs (3)

A
  1. Water
  2. Fluid taste/temperature/texture
  3. Stomach distension
113
Q

Post-absorptive inputs (3)

A
  1. Plasma volume/blood pressure
  2. Plasma osmolarity
  3. Plasma sodium
114
Q

Hormonal signals (2)

A
  1. Atrial natriuetic peptide

2. Angiotensin II

115
Q

G_q DREADDs

A

Excitatory

116
Q

G_i DREADDs

A

Inhibitory

117
Q

Prandial thirst

A

Thirst during or relating to the consumption of food

118
Q

Relative occurrence of prandial thirst

A

Develops before the ingested food has altered the blood tonicity

119
Q

Prandial thirst proportion of fluid intake

A

75%

120
Q

Theoretical causes of prandial thirst (4)

A
  1. Facilitation of chewing and swallowing
  2. Improving sensory stimulation and taste
  3. Reduction of sensations by irritants
  4. Anticipation of physiological deprivation
121
Q

Normal drinking behavior

A

Anticipatory in nature → brain predicts impending changes in fluid balance and adjusts behavior pre-emptively

122
Q

SFO and prandial thirst

A

Optogenetic inhibition of SFO glutamatergic neurons blocks prandial thirst

123
Q

Key regulator of energy balance

A

Leptin

124
Q

Site of leptin release

A

Release from the fat cells

125
Q

Leptin signaling

A

Inhibits AgRP neurons (hunger) and excites α-MSH neurons (satiety)

126
Q

Hunger neurons

A

AgRP neurons

127
Q

Satiety neurons

A

α-MSH neurons

128
Q

Additional signaling beyond arcuate neurons

A

Occur within lateral hypothalamus and paraventricular neurons

129
Q

Activation of AgRP neurons

A

Increases anabolic signals (promote energy storage)

130
Q

Activation of α-MSH neurons

A

Increases catabolic signals (promote use of energy)

131
Q

MC4R receptor location

A

Located on satiety neurons

132
Q

MC4R receptor agonist

A

α-MSH

133
Q

MC4R receptor antagonist

A

AgRP

134
Q

Ghrelin origin

A

Released from the stomach

135
Q

Ghrelin target

A

Drives activation of AgRP neurons

136
Q

Ghrelin action

A

Rapid and powerful but short-term signal to stimulate hunger

137
Q

Most common monogenic forms of human obesity

A

MC4R mutations

138
Q

Warm food theory

A

The gut has less work to do to acquire the energy and there is a system in place to let it know

139
Q

Warm food mechanism

A

Activation of TRPV1 receptors → activate α-MSH neurons → increase satiety

140
Q

Additional rapid-acting satiety signals (3)

A
  1. Potentiates VGLUT2 by increasing the expression of AMPA receptors
  2. Combined activation of VGLUT2 & α-MSH neurons required for satiety mechanism to work properly
  3. VGLUT2 are hormone-activated (oxytocin) — faster than α-MSH neurons alone
141
Q

Neurocircuitry controlling reward

A

Begins in the pedunculopontine & lateral dorsal regimental areas, which drives dopaminergic release from VTA

VTA activates the medial PFC and nucleus accumbens

Inhibition includes the medial PFC, nucleus accumbens, and ventral pallidum (GABA)

142
Q

Nucleus accumbens neurons

A

Dopamine release occurs for pleasurable stimuli from VTA — closer in synaptic spine

Glutamate release is from medial PFC — further in dendritic spine

143
Q

Pursuit of reward

A

Strengthened by increases in dopaminergic synaptic transmission

144
Q

Reward prediction and dopaminergic neurons

A

Unexpected reward: increase in DA firing

Predicted reward that occurs: increase in DA firing when anticipating

Predicted reward that doesn’t occur: decrease in DA firing during normal occurrence of reward

145
Q

Optogenetic activation of VTA dopamine neurons

A

Cause “addiction-like” behavior

146
Q

VTA activation in response to a painful stimulus

A

Reduced VTA activation

147
Q

cFos

A

Protein marker for neuronal activity

148
Q

cFos and optogenetic stimulation of VTA

A

Shows increased activity within the frontal cortex → marked by cFos

149
Q

Frontal cortex and addiction

A

D2 receptors receive modulation from the frontal cortex enabling goal-directed decision-making

Reduction in D2 receptor availability and glucose metabolism

150
Q

Long-term addiction

A

Reduction in D2R availability in the nucleus accumbens

Reduced orbitofrontal cortex activity

151
Q

Key effect of addictive drugs

A

Increased release of dopamine from the VTA

152
Q

Three mechanisms for increasing VTA DA release

A
  1. Interference with dopamine reuptake
  2. Indirect disinhibition of dopamine neurons
  3. Direct activation of dopamine neurons
153
Q

Top-down inhibition of drug and food-seeking

A

Depends heavily on the pre-frontal cortex

154
Q

Macroscopic changes in brain anatomy due to cocaine addiction

A

Loss of frontal cortex gray matter

155
Q

Function of frontal cortex

A

Adaptive action-consequence decision making

156
Q

Method for measuring action-consequence decision making

A

Contingency degradation test

157
Q

Contingency degradation tasks

A

Operant conditioning trains the association between an action and consequence

In contingency degradation task, the action-consequence relationship is degraded by providing the reward independent of the action

A probe test measures if the organism has adjusted its understanding of the action-consequence relationship

158
Q

Mechanism for updating action-consequence relationships

A

Frontal-cortex-activity-dependent structural remodeling

Shown with inhibitory DREADDs within the frontal cortex during degradation change → exhibit a response pattern indicating no change value for acting the degraded nose-poke

159
Q

Drug use and age

A

The younger the person is at the onset of illicit drug use → the lower their odds of seeking treatment throughout their lifespan

Impaired action-consequence decision-making abilities due to frontal cortex dysfunction

160
Q

Frontal gray matter during adolescence

A

Peaks in volume at 11 yo for females and 13 yo for males

Declines steadily with age

161
Q

Dendritic spines in frontal cortex during adolescence

A

Declines in spine concentration as adolescence progresses

162
Q

Cocaine exposure and frontal cortex

A

Adolescent cocaine exposure causes dendritic spine loss in the frontal cortex

163
Q

Neurocircuitry controlling drug addiction

A

Non-addicted brain: healthy frontal cortex regulates the action of the nucleus accumbens and VTA. Actions are goal-directed.

Addicted brain: hypoactive frontal cortex can’t regulate the NA and VTA. Actions are driven by “habits.”

164
Q

Dendritic spines and integrins

A

Binding of integrins to ECM proteins supports intracellular signaling pathways that promote dendritic spine stability

165
Q

Arg

A

Inhibition of a protein (ROCK2) to stabilize the cytoskeleton

166
Q

Fasudil

A

Inhibits the ROCK2 protein

Is used to treat stroke

167
Q

Knockdown of β1 integrin

A

Accelerates operative response for cocaine and energizes cue-induced reinstatement of cocaine seeking

168
Q

Adolescent onset loss of Itgb1 within oPFC

A

Accelerates acquisition of stable cocaine self-administration and energizes cocaine-seeking

169
Q

Depression

A

A mental health disorder characterized by persistently depressed mood or loss of interest in activities, causing significant impairment in daily life

170
Q

Depression prevalence

A

17%

171
Q

Factors increasing risk for depression (4)

A
  • Experiencing stressful events in your life
  • Difficult childhood
  • Certain personality traits
  • Family history of depression
172
Q

Hypoactive brain centers in depressive patients

A

Frontal and temporal (hippocampus) areas

173
Q

Hyperactive brain centers in depressive patients

A

Amygdala

174
Q

VFT frontal cortex activation

A

Improvement in depressive symptoms

175
Q

Shift in signaling pathways under stress

A

Normally pre-frontal cortex regulates striatum, hypothalamus, amygdala, and brainstem emotional reflexes

Under stress conditions, loss of prefrontal regulation, causing the amygdala to take control

176
Q

HPA axis

A

CRH (hypothalamus) → ACTH (anterior pituitary) → cortisol (adrenal cortex)

Negative feedback of cortisol on anterior pituitary and hypothalamus

177
Q

Cushing’s syndrome

A

Increased release of cortisol

Co-morbid with depression

178
Q

Early life stress

A

Reduced birth weight and gestational time

Alterations in development and behavioral disorders (including depression)

179
Q

Stress hypothesis of depression

A

Stress increases glucocorticoids which activate GRs to decrease BDNF, CREB, and TrkB activity

Decreases monoaminergic NTs & growth factors

180
Q

Glucocorticoids and spine stability

A

Frontal cortex has reduced spine concentration with increasing GC levels

181
Q

Anhedonia

A

Inability to feel pleasure from typically rewarding events

182
Q

Measuring anhedonia

A

Sucrose consumption test — rodent has a choice between water or sucrose solution

183
Q

Elevated GC experiment in rats (depression)

A

Decrease in dendritic spines in the frontal cortex & decreased sucrose consumption

184
Q

Genetic manipulations with GC elevations

A

Over-administration of glucocorticoids in mice with heterozygosity of cytoskeletal supporting genes leads to significantly reduced sucrose consumption and reduced dendritic spine concentration

185
Q

Heterozygosity

A

Expect 50% reduction in protein

186
Q

Subthreshold

A

Dosing that doesn’t cause behavioral deficits in healthy animals

187
Q

Serotonin hypothesis of depression

A

Proposes hat diminished activity of serotonin pathways plays a causal role in the pathophysiology of depression

Amine-depleting drugs, like reserpine, cause depression-like behaviors

Drugs that potentiate the effects of serotonin at the synapse alleviate depression

188
Q

Mechanisms of anti-depressant drugs (4)

A
  • Stimulation of autoreceptor agonist
  • Stimulation of receptors as partial agonist
  • Inhibition of MAO
  • Inhibition of reuptake
189
Q

SSRI effect onset

A

6 weeks

190
Q

Ketamine effects on synaptic function

A

Ketamine at low doses selectively binds to GABAergic neurons (instead of glutamatergic neurons)

Causes disinhibition of excitatory glutamatergic neurons in frontal cortex → glutamate burst

191
Q

Ketamine effect onset

A

Within hours

192
Q

Autism prevalence

A

1 in 54 children in the US

More males than females

193
Q

DSM criteria for autism spectrum disorder

A
  • Difficulty with communication and interaction with other people
  • Restricted interests and repetitive behaviors
  • Symptoms that hurt the person’s ability to function properly in school, work, and other areas of life
194
Q

Sally Anne test

A

Sally put her ball into the basket and leaves & Anne moves the ball to her box — where will Sally look for her ball?

Answer for children on spectrum → box
Answer for children not on spectrum → basket

195
Q

ASD neuroanatomy (4)

A
  • Frontal cortex
  • Fusiform gurus
  • Superior temporal sulcus
  • Amygdala
196
Q

Frontal cortex & ASD

A

Social deficits

197
Q

Fusiform gyrus & ASD

A

Face processing

198
Q

Superior temporal sulcus & ASD

A

Perception of living organisms moving

Have a role in the perception of intention of actions

199
Q

Amygdala & ASD

A

Emotional processing

Stops developing at about 8 yo in ASD boys (18 yo typically)

200
Q

Frontal and parietal attentional brain systems

A

Facilitate orientation to social stimuli appear to exert less top-down control in autism

201
Q

Autism risk factors (4)

A
  • Having a sibling with ASD
  • Having older parents
  • Very low birth weight
  • Having certain genetic conditions (e.g. Down syndrome or fragile X syndrome)
202
Q

Neuroligins

A

Involved in tethering the post-synaptic terminal to the pre-synaptic terminal

203
Q

Neuroligin knock-in and social interest

A

Equal interest in empty and stranger compartments of the apparatus

Assesses relative interest in socialization

204
Q

Neuroligin knock-in and somatosensory cortex

A

No change in EPSCs but increased number of IPSCs

Enhance inhibitory response to GABA

205
Q

Neuroligin knock-out and inhibitory feedback

A

Doesn’t affect inhibitory input

206
Q

GI tract and serotonin

A

90% 5-HT made in gut

Intrinsic primary afferent neurons

207
Q

Hyper-serotonemia

A

Due to enhanced serotonin transporter activity

208
Q

Double heterozygous of serotonin transporter and integrin genes

A

Integrin and serotonin transporter het increase V_max significantly more than control or each single mutation

209
Q

Co-morbidities of ASD (5)

A
  • Epilepsy
  • Chronic GI disorders
  • Chronic sleep problems
  • Depression
  • Schizophrenia
210
Q

Positive symptoms

A

Additional sensory/motor/affects

Example: hallucinations, delusions, disorganized speech, thought disorder, disorganized behavior

211
Q

Negative symptoms

A

Reduced sensory/emotional/motor

Example: alogia (speech deficits), flat affect, poor attention, avolition (loss of motivation), anhedonia (lack of pleasure), loss of social interests, attentional deficits

212
Q

Schizophrenia neuroanatomy (3)

A
  • Reduced activity in the dorsolateral PFC
  • Exaggerated loss of gray matter
  • Enlarged lateral ventricles
213
Q

Schizophrenia genetic support

A

Increased likelihood for monozygotic twins and in descending order with other family members

214
Q

Schizophrenia gene x environment

A

Early trauma interacts with genes causing developmental delays, behavioral problems, stress vulnerability → leads to lasting epigenetic changes

215
Q

GAD1

A

Associated with increased risk for childhood-onset schizophrenia

Significant decrease in the GAD1 promoter-enhancer interaction frequency & overly repressive histone marking in schizophrenic patients

216
Q

Copy number variation

A

Type of structural variation where you have a stretch of DNA which is duplicated in some people

217
Q

Donezepil

A

Cholinesterase inhibitor improves cognitive performance in AD patients

218
Q

Pharmacotherapy for AD

A

Ach is critical in cortical areas for attention, learning, and memory functions

Significant loss of cholinergic cells within nucleus basalis for AD

Cholinesterase inhibitors — popular choice

219
Q

Visualization of Aβ deposits

A

Radioactively labeled bezothiazole binds to Aβ deposits and can be visualized using PET

220
Q

Mutations in γ-secretase

A

Higher plasma Aβ than controls

221
Q

Early-onset familial AD

A

Mutations in human APP and γ-secretases

Perfect correlation between offspring who inherited the full mutation and AD

222
Q

APP role in vivo

A

Helps direct movement (migration) of neurons during early development

223
Q

Production of amyloid β

A

Cleaved from amyloid precursor protein (APP) through a process involving 3 different secretases

224
Q

Amyloid plaques composition

A

Primarily of Aβ plaque

225
Q

Tau in AD

A

Is hyperphosphorylated causing it to separate from the microtubule and aggregate into tangles

226
Q

Tau

A

Supports the stability of the microtubule

227
Q

Location of plaques

A

Occipital language areas

228
Q

Location of tangles

A

Temporal lobe (memory areas)

229
Q

Diagnosis of AD

A

Confirms the presence of tangles and plaques — can only be post-mortem

230
Q

Tangles

A

Located intracellularly

Affects approximately 1/3 of neurons

231
Q

Plaques

A

Located extracellularly

Disrupt localization of dendrites and dendritic spines

232
Q

Disagreement in AD field

A

Primary contributor to AD deficits — plaques or tangles?

233
Q

Genetic mutations and AD

A

Only seen with plaques — not with tangles

234
Q

Imaging with silver-staining (Golgi) in AD

A

Amyloid plaques and neurofibrillary tangles

235
Q

Neurodegeneration in AD (5)

A
  • Cerebral cortex
  • Entorhinal area
  • Hippocampus
  • Neocortex
  • Nucleus basalis
236
Q

Prevalence of AD

A

1 in 20 people by age 65

6th leading cause of death

237
Q

Prognosis of AD

A

Can live 4-8 years after diagnosis

But can be up to 20 years depending on lifestyle choices

238
Q

Late Alzheimer’s

A

Patients requires around the clock monitoring

Loses awareness of recent experiences as well as of their surroundings

239
Q

Middle Alzheimer’s

A

Requires caretaker

Feels moody or withdrawn, especially in socially or mentally challenging situations

240
Q

Early Alzheimer’s

A

Still functions independently

Experiences increased trouble with planning or organizing

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