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Psyc 275 - Brain and Behaviour > final exam > Flashcards

final exam Flashcards

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1
Q

zygote

A

fertilization to 2 weeks

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2
Q

embryo

A

2 to 8 weeks

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3
Q

fetus

A

9 weeks to birth

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4
Q

cell specification

  • what are the earliest cells of the developing nervous system?
A

the earliest cells of the developing nervous system are totipotent

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5
Q

cell specification

  • what is totipotent?
A

totipotent: they can develop into any type of cell in the body

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6
Q

cell specification

  • what is embryonic stem cells (neural plate)
A

embryonic stem cells (neural plate)

  • virtually limitless capacity for self-renewal
  • can develop into different types of mature cells
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7
Q

cell specification

  • what is multipotent
A

around the time that the neural plate forms, cells become more specified (i.e., multipotent)
- these cells can now only become nervous system cells

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8
Q

phases of development

  • how many phases? and what are they?
A

ovum + sperm = zygote

developing neurons accomplish becoming human in five phases

1) Induction of the neural plate
2) Neural proliferation
3) Migration and aggregation
4) Axon growth and synapse formation
5) Neuron death and synapse rearrangement

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9
Q

induction of the neural tube

  • when does the nervous system start to develop?
  • what are the 3 layers on the embryo?
  • what is a neural plate
  • development of the neural plate is induced by??
A

3 weeks after conception the nervous system starts to develop

  • 3 layers in the embryo: ectoderm (outer), mesoderm (middle), endoderm (inner)
  • Neural plate - ectodermal tissue on the dorsal surface of the developing embryo
  • Development of the neural plate is induced by chemical signals from the mesoderm layer (“organizer”)
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10
Q

cns vs pns

A

Cells that migrate to eventually form the CNS originate in the neural tube

Cells that eventually form the PNS originate from the neural crest
- The neural crest forms from cells that break off from the neural tube

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11
Q

2) neural

  • neural plate folds to form ___ to form the ___?
  • what is inside it?
  • proliferation is chemically guided by ___ & ___ ?
  • neural rube is lined with ___?
  • where does neural stem cells first form??
A

Neural plate folds to form the neural groove, which then fuses to form the neural tube

Inside will be the cerebral ventricles and neural tube

Proliferation is chemically guided by the organizer areas – the roof plate and the floor plate

The neural tube is lined with neural stem cells

Neural stem cells first form the ventricular zone

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12
Q

prenatal brain development

  • what are the three swelling at the anterior end? what will it become
A

neural tube cells proliferate in species-specific ways: three swellings at the anterior end in humans will become the forebrain, midbrain, and hindbrain

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13
Q

4) migration

A

once cells have been created through cell division in the ventricular zone of the neural tube, they migrate

migrating cells are immature, lacking axons and dendrites

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14
Q

migration

A

Once cells are created in the ventricular zone they must migrate to the proper location

For each region of the neural tube subtypes of neurons are created at specific time points and then migrate to predetermined locations

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15
Q

migration and aggregation

  • what is radial migration vs tangential migration?
A

radial migration: moving out

tangential migration: moving in

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16
Q

migration

there are two ways in which cells migrate:

A

1) somal translocation: an extension grows from the cell and the cell body moves into position along with it
- migration can be radial or tangential

2) glial-mediated migration - a temporary network of radial glial cells develops in the neural tube
- cells can migrate into position by moving along radial glial cells
- radial migration only

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17
Q

3) migration and aggregation

A
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18
Q

4) migration & aggregation

- what is the inside-out pattern?

  • why is migration complex?
A

Cellular migration occurs in organized waves from deeper to more superficial layers of the cortex
- Inside out pattern

Migration is complex:
- Many neurons engage in long tangential migrations to reach their final destinations

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19
Q

4) aggregation

  • what is aggregation?
  • aggregation and migration are aided by ?????
A

aggregation: the process by which neurons align themselves with other developing neurons

Aggregation and migration are aided by cell-adhesion molecules (CAMs)

  • Located on the surfaces of neurons
  • Allows the cells to adhere to one another
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20
Q

aggregation pt 2

  • what are gap junctions?
A

Gap junctions pass cytoplasm between cells

  • Prevalent in brain development
  • May play a role in aggregation and other processes
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21
Q

4) axon growth & synapse formation
- what forms once neurons have migrated to the correct locations and gave aggregated?

A

once neurons have migrated to the correct locations and have aggregated, axons and dendrites form

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22
Q

axon growth & synapse formation

  • what is tropic molecules?
A

Each growing axon or dendrite develops a growth cone that are directed by:

  • Cell adhesion molecules (CAMs)
  • Tropic molecules - produced by the target cells being sought by axons
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23
Q

4) axon growth & synapse formation

A

Mechanisms underlying axonal growth are the same across species

A series of chemical signals exist along the way – attracting and repelling

Such guidance molecules are often released by glia

Adjacent growing axons also provide signals

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24
Q

4) axon growth & synapse formation; chemoaffinity hypothesis

A

Chemoaffinity hypothesis - each postsynaptic surface releases a specific chemical label that it uses to attract growing axons to it

Some neurons follow very indirect routes to go from their origin to their destination
- Suggests that a number of different chemicals (guidance molecules) might signal the way for growth cones

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25
Q

axon growthn & synapse formation; chemoaffinity hypothesis

  • pioneer growth cones vs fasciculation?
A

Pioneer growth cones - the first cones to travel along a particular route in the developing nervous system

Fasciculation- the tendency for axons to grow along paths established by pioneer growth cones

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26
Q

4) axon growth & synapse formation
- what is topographical gradient hypothesis?

A

Spatiotopic maps may have developed as a way to minimize the number of neural connections

Point to point mapping of retina to tectum changes as the structures grow
- Chemoaffinity is too simple to explain this phenomenon

  • *Topographical gradient hypothesis** - axons growing from one topographic surface to another are arranged according to the layout of the cell bodies on the original surface
  • This may be accomplished using signaling chemicals
  • E.g. ephrin A (medial-lateral) and ephrin B (dorsal-ventral)
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27
Q

synapse formation

  • what is synaptogenesis? and what does it require?
A

Once axons have reached their target they must form an appropriate pattern of synapses (Require coordination between two different neurons)

in order for a synapse to occur, both presynaptic and postsynaptic cell must agree upon (they need to have some acceptance of one another for that synapse to function)

Synaptogenesis - the formation of new synapses, requires glial cells (astrocytes)

-> basically the creation of synapse but in order for those synapses to maintain themselves, they both need to function (requires coordination)

  • Retinal ganglion cells (in a culture) form 7x more synapses in the presence of astrocytes
  • Synapses quickly deteriorate when astrocytes are removed
  • Astrocytes: nutritional role?
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28
Q

synapse fomation

A

what causes synaptogenesis? what promotes those neurons to agree to synapse with one another

  • Cholesterol provided by astrocytes
  • presence of astrocytes seems to be one of those promoters

Neurons will synapse with any other neuron – promiscuous

  • they just want to synapse on everything / with any neuron
  • during prenatal development, there’s way more synapse happening
  • once you’re born you have 150% more synaptic connections that you need

Inappropriate connections that don’t function will die off

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29
Q

5) neuron death and synaptic rearrangement

A

neuron death is a normal part of the development

  • we want cells to go through cell death
  • this is a good thing because it allows other cells to create better/cleaner connections

more neurons than are required (i.e., 50%) are produced

  • we also have too many neurons as well because we’re born with 50% more neurons
  • after we’re born we have to get rid of abt 50% of neurons and 150% of our neural connections (synapse)

Many “waves” of neuron death occur during development

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30
Q

5) neuron death and synaptic rearrangement; two mechanisms of cell death

A
  1. apoptosis (active): cells commit suicide, genetically programmed
    • this is within genetic programming
  2. necrosis (passive): die from malnutrition
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31
Q

5) neuron death & synaptic rearrangement

A

Apoptosis is safer, DNA and other structures are cleaved apart and packaged into membranes (majority of neuron death through development is from apoptosis)

  • Attracts scavenger microglia = phagocytosis
  • Problems with apoptosis can lead to cancers or neurodegenerative diseases

Problems: Neurons that die usually have formed improper connections (cell that should have died, don’t die which leads to a tumor) -> when cells are supposed to die and they don’t they create a mass (creating tumor)

what if cell is pre programmed to die too son: you

Membranes contain molecules to attract microglia

Dark side – if apoptosis is blocked – cause cancer; if over-active – neurodegenerative disease (alzheimers, MS)

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32
Q

life-preserving chemicals

A

Neurons that fail to establish correct connections are particularly likely to die

Space left after apoptosis is filled by sprouting axon terminals of surviving neurons

Ultimately leads to increased selectivity of transmission

Cells programmed for early death – complete function and die

Cells fail to obtain life-preserving chemicals that are supplied by targets – neurotrophins – nerve growth factor

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33
Q

neuron death

A

More neurons are produced than needed by the adult brain

  • neuron cell death happens in waves at different parts of the brain and different time
  • this is a sign that the brain is mature / reac
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34
Q

postnatal neural development

A

postnatal growth is a consequence of:

  • •Synaptogenesis
  • Myelination – sensory areas and then motor areas. Myelination of prefrontal cortex continues into adolescence
  • Increased dendritic branches

Overproduction of synapses may underlie the greater plasticity of the young brain

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35
Q

Postnatal neural development

A

•The human brain quadruples in size between birth and adulthood (Not due to additional neurons)

Brain keeps growing until we are 2 years – NOT due to more neurons

We have all the neurons we need by 7 months – 150% more synapses

  • Exception - olfactory bulb and hippocampus
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36
Q

postnatal neural development

A

•Synaptogenesis occurs at different rates in different regions (Visual cortex vs. frontal cortex)

150% more synapses by age 2 than adult

Diff for diff brain areas – e.g. V1 prunes by age 3 – frontal cortex by puberty

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37
Q

postnatal neural development

A

•Myelination follows the pattern of functional development

  • Sensory regions, then motor regions, then higher-level areas

Sensory within first few months

Prefrontal cortex by early adulthood

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38
Q

postnatal neural development

A

•Dendritic branching progresses from deeper to more superficial layers of cortex

Occurs even in adulthood

Happens in seconds

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39
Q

development of prefrontal cortex

A

the human prefrontal cortex has been linked to:

  1. Working memory - maintaining relevant information to keep it accessible for short periods of time
  2. Planning and sequencing actions
  3. Inhibiting contextually inappropriate responses
  4. Following rules for social behaviour
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40
Q

perseveration and working memory

A

•Around 7-12 months of age, children tend to make a large number of perseveration errors

  • Inability to suppress the previous response when the task demands change

Involves holding information in working memory about where to toy was placed AND being able to supress that response if toy placed in a different location.

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41
Q

perseveration and working memory

A

•The Wisconsin card sorting test is typically used to assess frontal lobe function/dysfunction

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42
Q

effect of early experience

critical and sensitive period

A

Critical period - when it is absolutely essential for an experience to occur during a particular interval

Sensitive period - when the experience has a great effect on development at a certain interval, but can still have effects outside of the interval

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43
Q

deprivation vs enrichment

A

•Rats raised in the dark had fewer synapses in visual cortex

  • Had problems with depth and pattern vision as adults

•Rats raised in “enriching” environments solved mazes faster than rats raised in non-enriched environments (Hebb, 1947)

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44
Q

deprivation vs enrichment

A

•Antonini & Stryker (1993) – found that a few days of monocular deprivation produced a massive decrease in axonal branching from the sensory layer in V1

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45
Q

rewiring sensory systems

A
  • Roe (1990) - altered the course of developing retinal ganglion cell projections to the MGN
  • Neurons in auditory cortex acquired a retinotopic map!
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45
Q

rewiring sensory systems knudsen and brainerd (1991)

A

•Knudsen and Brainerd (1991) - raised barn owls with prisms that shifted their vision in one direction (e.g., 20° to the right)

oAuditory spatial maps were realigned to match the visual map

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46
Q

rewiring sensory systems - munte et al (2002)

A

•Munte et al. (2002) - early music training enlarges the size of auditory cortex that responds to complex musical tones

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47
Q

neuroplasticity in adults

neurogenesis?

A
  • Neurogenesis – the growth of new neurons
  • Nottebohm et al. (1983) found brain structures involved in singing increased before each mating season

–

  • Most researchers believed that neurons could not be regenerated in adulthood
  • In the 1990’s researchers observed two important findings
  1. New neurons are continually added to the olfactory bulbs in rats
  2. New hippocampal neurons are continually added in primates
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48
Q

experience guides in neuroplasticty

A
  • Tinnitus (ringing in the ears) – produces major reorganization of primary auditory cortex
  • Adult musicians who play instruments fingered by left hand have an enlarged representation of the hand in S1

Skill training leads to reorganization of motor cortex

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49
Q

disorders of development

A
  • Much of what we know about normal development has emerged from studying cases where development is abnormal
  • Autism is a complex developmental disorder that appears before age 3
  • A reduced ability to interpret the emotions of others
  • Reduced capacity for social interaction and communication
  • Preoccupation with a single object or activity
  • Autism is a spectrum disorder

o80% are male

o50% have mental retardation

o35% have seizures

oOlder parents (mothers over 30, fathers over 40)?

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50
Q

the autism spectrum

A

•Early indicators of autism:

•

1.Delayed language development

•no meaningful phrases by 24 months

2.Delayed development of social interaction

•no happy expressions by 9 months, no communicative gestures by 12 months

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51
Q

the autism spectrum

A

•Autism is one of the most prevalent childhood neurological disorders

o1990’s < 1 in 1000 births

oRecent estimates are 1 in 88!

oBroadening diagnostic criteria?

oIncreased public awareness?

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52
Q

the autism spectrum

A

•Autism is a heterogeneous disorder

  • Some individuals with autism are severely impaired in some skills, but excel rapidly at others

•Autistic savants - are individual with autism who display incredible abilities in certain areas

oArtists / Musicians / Mathematical abilities

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52
Q

neural correlates of autism

A
  • Because the disorder is so heterogeneous it is hard to pin down any underlying neural abnormalities
  • One characteristic of autism that has received considerable attention is their lack of social interaction
  • Look less at faces and disinterested in making eye contact
  • Abnormal FFA activity in individuals with autism
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53
Q

william’s syndrome

A
  • Occurs in 1 in 7500 births
  • Is a neurodevelopmental disorder characterized by:
  • Near normal language abilities
  • Normal or superior musical abilities
  • Very emotionally expressive and socially interactive (hypersociability
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54
Q

william’s syndrome

A

•Is a neurodevelopmental disorder characterized by:

oMental retardation (IQ below 60)

oSevere visuospatial problems

  • Spatial memory / Drawing

oGenetic basis

  • Abnormalities on chromosome 7

oCortical thinning

  • Parietal-occipital junction / Orbital-frontal cortex

oCortical thickening

  • Primary and secondary auditory corticles
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55
Q

causes of brain damage:

A

•Many potential sources of brain injury:

  1. Tumors
  2. Cerebrovascular disorders
  3. Closed head injuries
  4. CNS infections
  5. Neurotoxins
    6) Genetic influences
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56
Q

1) tumors

A

•A tumor or neoplasm- a mass of cells that grows independently of the rest of the body

oApproximately 20% of tumors in the CNS are meningiomas

oMeningiomas are encapsulated

oExert pressure on surrounding tissue (mass occupying)

oMost are benign (i.e., non-cancerous

Grow between meninges that protect the brain

Exception rather than rule

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57
Q

1) tumors; infiltrating tumors

A

•Most brain tumors are infiltrating tumors

oNot encapsulated and grow diffusely throughout the brain

oMost are malignant (i.e., cancerous)

o10% of tumors are metastatic; originate in another part of the body and are transferred via the bloodstream

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58
Q

2) cerebrovascular disorders

A

•Strokes- a sudden interruption in blood supply to the brain that results in brain damage

oLeading cause of brain damage and adult neurological disability

oSymptoms depend on brain region affected

oCommon outcomes: memory loss, aphasia, paralysis, vision loss

oSigns of stroke onset: weakness, trouble speaking, vision problems, headache, dizziness

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59
Q

strokes: infarct vs penumbra

A

Dead brain tissue resulting from a stroke is called an infarct

“At risk” tissue surrounding the infarct is called the penumbra

Most interventions aim to minimize the penumbra

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60
Q

2) cerebrovascular disorders; two major types

A

1) cerebral ischemia: is a disruption of blood supply caused by a blockage in a blood vessel
2) cerebral hemorrhage: •when a blood vessel ruptures and blood seeps into surrounding tissue causing damage

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61
Q

strokes: cerebral hemorrhage

A
  • Cerebral hemorrhage- when a blood vessel ruptures and blood seeps into surrounding tissue causing damage
  • Aneurysm- a balloon like swelling in an artery
  • Caused by defective elasticity in an artery
  • Can be congenital- arteriovenuousmalformation(AVM)

oCerebral angiogram

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62
Q

stroke: cerebral ischemia

A

•Cerebral ischemia- is a disruption of blood supply caused by a blockage in a blood vessel

oThrombosis- plug formed in a vessel (blood clot, fat, tumor cells, air bubble, oil, etc.)

•Tissue plasminogen activator (tPA)

oEmbolism- a plug that forms in a larger vessel that travels to a smaller vessel

  • Transient ischemic attack (TIA)

arteriosclerosis- narrowing of blood vessels because of fat deposits

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63
Q

ischemia and brain damage

A
  • Ischemia-induced brain damage:
  • takes time
  • does not occur equally in all parts of the brain
  • mechanisms of damage vary with the brain structure affected
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64
Q

stroke and the brain’s blood supply

A
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65
Q

3) closed head injuries

A

1) closed head injuries: injuries (CHI)- are any blow to the head that does not penetrate the skull leading to brain injury

2) Contusion- any CHI that involves damage to brain’s circulatory system

oBrain slams against the inside of the skull causing damage

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66
Q

hematoma

A
  • Build-up of clotted blood (bruise) in brain tissue following a contusion
  • Causes pressure on underlying brain tissue
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67
Q

concussion

A

•A general term for cognitive disturbances following a closed head injury where there is no evidence of a contusion or other brain damage

oLoss of consciousness

oEffects of multiple concussions

- “Punch-drunk syndrome”

—

Damage from concussion can usually be seen only on autopsies of brains from cadavers.

•The brain of John Grimsley and the boxer show large amounts of abnormal tau protein in the amygdala

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68
Q

4) bacterial brain infections

A
  • When bacteria infect the brain they commonly lead to the formation of cerebral abscesses / i.e., pockets of puss in the brain
  • Meningitis is caused by bacterial infection (25% of adult cases are fatal)
  • Syphilis bacteria also leads to severe brain damage / STD passed through genital sores, can be dormant for years

General paresis – the syndrome of insanity/dementia that results from syphilitic infections of the brain

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69
Q

viral brain infections

A

•Rabies virus- transmitted via a bite from an infected animal (e.g., bats, cats, raccoons, dogs, mice)

oHas an affinity for the nervous system

oVirus attacks the brain about 1 month after the bite

oExtreme aggressiveness

oUsually fatal if not treated

•Mumps & Herpes virus can also attack the brain

oHerpes encephalitis

Attacks all tissue, including brain

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70
Q

5) neurotoxins

A

•The nervous system can be damaged through the intake of a variety of chemicals

oLead (“crackpot”)

oMercury (“mad hatter”)

oPesticides and farming chemicals?

•

•Toxic psychosis- chronic insanity produced by a neurotoxin (Tardive dyskinesia (TD) )

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71
Q

neuropsychological dieseases

  1. Epilepsy
  2. Multiple sclerosis
  3. Alzheimer’s Disease
  4. Parkinson’s Disease
A
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72
Q

1) epilepsy

A

the characteristic feature of epilepsy is seizures (spontaneous / reoccurring)

•People with epilepsy (1% of population) have chronic seizures caused by underlying brain abnormalities

oMany different subtypes depending on nature of seizures

  1. Partial seizures- involve only part of the brain
  2. Generalized seizures- involve the entire brain (Epileptic auras- psychological changes that occur prior to a seizure)
  • Many different causes - i.e., brain damage,toxins, viruses, tumors, genetics
  • Many cases are due to improper inhibitory synapses
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73
Q

epilepsy and eeg

A

note: Not all seizures are due to epilepsy (Neurotoxins and Febrile seizures)

•Epilepsy diagnosis relies heavily on EEG recordings

  • Sudden onset of high amplitude EEG waves
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74
Q

epilepsy; partial and generalized

A

Partial – does not involve the entire brain

Generalized – involves the entire brain

— note

(Partial) Not usually associated with a loss of consciousness

Patient remains alert and can remember the experience

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75
Q

epilepsy: simple partial seizures and complex partial seizures (part of partial seizures)

A

1) Simple partial seizures – symptoms are primarily sensory or motor or

Short lasting (less than a few minutes)

Symptoms depend on where in the brain the seizure originates from

2) Complex partial seizures – patients engage in compulsive, repetitive, simple behaviours (automatisms) and more complex behaviours can appear perfectly normal

Usually restricted to the temporal lobes

During an episode the patient engages in compulsive repetitive behaviours

E.g., repetitive mouth movements, buttoning and unbuttoning a shirt, walking, driving

Patient appears conscious but memory loss for the event is common

About 50% of adults cases of epilepsy are complex partial

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76
Q

epilepsy; petit mal and grand mal (part of generalized seizures)

A

1) Petit Mal - no convulsion. The primary symptom is the petit mal abscense (disruption of consciousness, cessation of ongoing behaviour, vacant look, fluttering eyelids)

Petit mal seizure- “little trouble” - No convulsions

Petit mal absence- disruption of consciousness, cessation of behaviour, vacant look, “day dreaming”

More common in children

2) Grand Mal - Loss of consciousness, loss of equilibrium, violent tonic-clonic convulsion. Tongue-biting, urination, and cyanosis are also common.

Grand mal seizure- “big trouble”/ loss of consciousness / violent tonic-clonic convulsions

Cyanosis- turning blue from excessive extraction of oxygen from the blood

Hypoxia can occur resulting in further brain damage

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77
Q

2) multiple sclerosis (MS)

A
  • A progressive disease that destroys myelin in the CNS
  • Typically onsets in early adulthood
  • Starts with microscopic damage, later leads to axon degeneration
  • MS is an autoimmune disorder
  • Periods of remission for up to 2 years

Causes a variety of symptoms:

oVisual disturbances / Muscular weakness / Ataxia (loss of motor coordination) / Cognitive deficits

78
Q

epidemiology of MS

A

Genetic factors in MS

oHigher concordance rate in monozygotic (25%) vs. dizygotic (5%) twins

o3 x higher rate of MS in females compared to males

oMuch higher rates in Caucasians (0.15%) than other ethnic groups

Environmental factors in MS

oHigher rates in populations living in colder climates (distance from equator), vitamin D

oRisk of developing MS changes with migration between climates

oSmokers are at greater risk for developing MS

notes:

Highest rates in Canada are here in Alberta

Also those exposed to the Epstein-Barr virus – common cause of Mono.

79
Q

3) alzheimer’s disease (AD)

A
  • The most common cause of adult dementia
  • Terminal progressive neurodegenerative disease

o_Early stages_- decline in memory functions, attention problems, personality changes

o_Intermediate stages_- confusion, irritability, anxiety, deterioration of speech

o_Advanced stages_- lose control over bodily functions

–

Can occur in 40s-50’s

10% of people over age 65

35% incidence in people over age 85

80
Q

alzheimer’s disease; neurofribrillary tangles and amyloid plaques

A

•Neurofibrillary tangles- are tangles of protein in the neural cytoplasm

oDestroys microtubules / Tau protein

–

•Amyloid plaques- clumps of scar tissue made up from dying neurons and beta amyloid protein

81
Q

alzheimer’s disease

A
  • Alzheimer’s disease destroys association cortex
  • Distribution of plaques and tangles in AD
82
Q

treatments for alzheimer’s disease

A

•Finding an effective treatment rests on finding the primary symptom

oPlaques or tangles?

oPrevention is key!

•Treatments for Alzheimer’s Disease

oAll 3 genes implicated in early onset AD influence amyloid production

oAmyloid vaccine?

oAcetylcholine?

Deep brain stimulation?

AD has a major genetic component - People who have AD in their family have a 50% chance of getting the disease in their 80’s

Genetic component of AD is complex

  • 3 specific genes in early onset AD (age 40)
  • Over 20 chromosomes implicated in late onset AD
  • Suggests AD is due to epigenetic mechanisms
83
Q

basal ganglia and PD

A
  • Comprised of 3 nuclei: caudate, putamen, globus pallidus
  • Receives input from most areas of cortex
  • Plays a critical role in modulating the force of movements
  • Also plays an important role in motor learning
84
Q

parkinson’s disease

A
  • Results from death of dopamine (D) secreting cells in the substantia nigra
  • Absence of D results in not enough inhibition of the GPi in the direct pathway and too much excitation of the GPi in the indirect pathway
  • Characterized by:

oMuscular rigidity / Hypokinesia (loss of movement) /Resting tremor /Cognitive impairments

Deep brain stimulation inhibits STN (subthalamic nucleus)

STN = subthalamic nucleus

85
Q

animal models

A
  • Animals models offer the unique opportunity to understand the ultimate causes of neurological diseases
  • Animals models help with the development of treatments
  • Not perfect!
86
Q

kindling model of epilepsy

A
  • A series of periodic brain stimulations eventually elicits convulsions: the kindling phenomenon
  • Neural changes are permanent
  • Produced by stimulation distributed over time
  • Convulsions are similar to those seen in some forms of human epilepsy – but they only occur spontaneously if kindled for a very long time
  • Kindling phenomenon is comparable to the development of epilepsy (epileptogenesis) seen following a head injury
87
Q

transgenic mouse model of AD

A
  • Only humans and a few related primates develop amyloid plaques
  • Transgenic – genes of another species have been introduced
  • Genes accelerating human amyloid synthesis introduced in mice

oPlaque distribution comparable to that in AD

oUnlike humans, no neurofibrillary tangles

88
Q

E.g. The MPTP model of Parkinson’s Disease

A
  • In 1982 small group of drug users each reported to a local emergency room with sudden onset of Parkinson’s symptoms (Awakening the frozen addicts)
  • Each had used a new type of synthetic heroin
  • Later analysis revealed that the heroin contained a neurotoxin- MPTP was selectively toxic to dopamine
89
Q

MPTP model of Parkinson’s Disease

A
  • When MPTP is administered to monkeys it creates Parkinson’s Disease like symptoms
  • Leads to major cell loss in the substantia nigra
  • Research using the MPTP model discovered that Deprenylblocks the effects of MPTP
90
Q

neuroplastic responses to damage

A

•A common way to study neural degeneration is to cut the axons of neurons (axotomy) and observe the effects

two types of degeneration occur:

1) anterograde degeneration
2) retgrograde degeneration

91
Q

anterograde degeneration

A

1.Anterograde degeneration- is the degeneration of the distal segment, i.e., between the cut portion and the terminals

–Occurs quickly over a few hours

92
Q

retrograde degeneration

A

2.Retrograde degeneration- degeneration of the segment between the cut portion and the cell body

  • Occurs slowly over a few days
  • Decrease in cell body size suggests cell will die
  • Increase in cell body size suggests cell will attempt to replace the cut segment
93
Q

transneuronal degeneration

A

•Transneuronal degeneration - Sometimes damage spreads from damaged neurons to neurons within the network

oAnterograde – spreads from damaged neuron to the neuron it synapses with

oRetrograde – spreads from damaged neuron to the neuron that synapses on it

94
Q

neural regeneration

A
  • Does not proceed successfully in mammals and other higher vertebrates – capacity for accurate axonal growth is lost in maturity
  • Regeneration is virtually nonexistent in the CNS of adult mammals and unlikely, but possible, in the PNS
95
Q

neural regeneration in PNS

A
  • PNS neurons can regenerate starting 2-3 days after injury
  • Recovery depends on the nature of the injury
  • Schwann cells clear debris and promote regeneration
  • Produce neurotrophic factors and cell-adhesion molecules

Regeneration depends on the environment – not necessarily the neurons (CNS vs PNS)

96
Q

neural regeneration in PNS

  • why can’t this happen in the CNS?
A
  • Oligodendroglia (myelinate CNS neurons) do not clear debris, or guide and stimulate regeneration
  • Instead, they release factors that actively block regeneration!
97
Q

collateral sprouting

A
  • Collateral sprouting- axon branches can sprout from nodes of Ranvier to connect to adjacent neurons
  • more accurate in invertebrates than vertebrates

When they lose a limb, the regenerating axons produce a growth factor that promotes regeneration of the limb

98
Q

neural reorganization

A

Pons and colleagues (1991)- mapped S1 in monkeys whose contralateral arm sensory neurons had been cut 10 years prior

oFound that the cortical face representation had expanded into the former hand region

99
Q

neural reorganization

~ sanes, suner, and Donoghue (1990)

A
  • Sanes, Suner, and Donoghue (1990)
  • Transected motor neurons that controlled the muscles of rat whiskers
  • A few weeks later, the area of the motor cortex that had previous elicited movement of the whickers now activated other muscles of the face
100
Q

reorganization in humans

A

•Brain-imaging studies indicate there is continuous competition for cortical space by functional circuits

oe.g. Auditory and somatosensory input may be processed in formerly visual areas in blinded individuals

101
Q

mechanisms of neural reorganization

A

•Two mechanisms might explain the reorganization of neural circuits:

1) Strengthening of existing connections through the release from inhibition

  • Recovery often happens very quickly
  • Change is never greater than 2mm of cortex

2) Establishment of new connections via collateral sprouting

•Long term recovery can be too dramatic to be explained by small changes in existing circuits

note: These two mechanisms may work together

Other possibilities: dendritic branching, neural degeneration, and adult neurogenesis

102
Q

recovery of function

A

•Hard to study because of other compensatory changes, for example:

oCerebral edema (brain swelling) decreases a week or two after damage

olearning of new cognitive or behavioural strategies

oCognitive reserve (education and intelligence) can also play a role in helping patients accomplish tasks in alternate ways

–

Most likely the case when: lesions are small and patient is young

Kapur (1997) – examined doctors and neuroscientists with brain damage who had great recovery – not due to recovered brain function but strategy

Might also be why educated people are less susceptible to age-related brain deterioration

103
Q

adult neurogenesis

A
  • There is a lot of interest in finding out whether adult neurogenesis could contribute to recovery
  • Stem cells tend to migrate short distances following brain damage
  • E.g., increase in neurogenesis in dentate gyrus following ischemia damage

No evidence that stem cells migrate from their sites of generation

104
Q

age and recovery

A

•Younger people recover better over the long run!

105
Q

treatments for brain damage

A

1) reducing braind damage by blocking neurodegeneration
2) promoting regeneration
3) neuro-transplantation

105
Q

1) blocking neyridegeneration

A
  • Various neurochemicals can block or limit neurodegeneration
  • Neuroprotective molecules tend to also promote regeneration

–

Estrogen – may be why brain disorders are more common in men

  • Seen to protect the brain in brain damage (found mostly in women)

This is stopping cell suicide (usually happens in stroke)

Can we produce nerve growth factors?

-Maybe iy can create an environment that is more regenerative

106
Q

1) blocking neurodegeneration

A

•Researchers induced cerebral ischemia in groups of rats

oControl group - damage to the hippocampus and poor performance in the Morris water maze

oExperimental group - treated with a virus that was engineered to release an apoptosis inhibitor protein

oRats in the experimental group had less hippocampal damage and performed better in the Morris water maze task

–

107
Q

2) promoting regeneration

A
  • CNS regeneration does not normally occur in mammals
  • But can be induced in lab animals
  • Cheng et al. (1996) severed the spinal cord of rats making them paraplegic

oTransplanted sections of myelinated peripheral nerves into the spinal cord

oSpinal cord regenerated through the myelin sheaths of the implanted Schwann cells

oRats regained movement of legs

108
Q

3) neuro-transplantation

A

•Fetal tissue transplants have been used to treat Parkinson’s Disease in some animals and humans

oTreatment was successful

oLimited success with humans

PD – lack domapine-releasing cells

Could stem cells implanted do that job?

It was first on the list but now last

  • Reseracrhechs worked mainly on Parkinsons
  • They believed that if they can take stem cells, they could become anything and then they transplant it to the substantial nigra
  • It was working (regaining some function) and about 3 weeks or so it stopped working
  • They stopped the research because they didn’t take they have enough research abt the environment
109
Q

3) nuero-transplantation

A

•Neural stem cells have been used to repair spinal cord injuries in rats (McDonald et al. 1999)

  • Injected embryonic stem cells migrate to the area of injury and develop into new nerve cells
  • Paraplegic rats regained ability to support weight with legs and walk

•More research is needed to maximize the survival and growth of neurons

oNeurons need to mature and make proper connections to enhance recovery

oMethods for keeping new neurons healthy still need to be developed

110
Q

rehabiliative training

A

•Facilitated walking as an approach to treating spinal injury (90% of trained walkers – only 50% using conventional rehab)

epidural stimulation -

111
Q

benefits of enrichment

A
  • Rodents raised in enriched environments are resistant to induced neurological conditions (epilepsy, models of Alzheimer’s, Huntington’s, etc.)
  • Physical activity promotes adult neurogenesis in rodent hippocampus

Wheel-running increases neurogenesis in hippocampus of rats

Also reduced growth of amyloid plaques in models of AD

112
Q

learning and memory (ch 11)

A

Learning and memory are two sides of the same coin

Learning – how the experience changes the brain

Memory – how these changes are stored and reactivated

If we couldn’t learn or remember, we would be frozen in the present

113
Q

amnesia

A
  • Amnesia- loss of memory, usually as a result of brain injury
  • Anterograde amnesia is typically accompanied by some degree of retrograde amnesia
114
Q

anterograde amnesia: patient H.M.

A

HM (1926-2008) had severe epilepsy and drugs could not prevent his seizures

  • At age 27, Dr. Scoville performed a bilateral temporal lobe resection to treat his epilepsy (1953)
  • Following the surgery his seizures were dramatically reduced
  • He had some retrograde amnesia for events shortly before the surgery

oCould remember his childhood and everything about 2 years prior to the surgery

  • He had a normal IQ and a normal short-term memory post-surgery
  • However, H.M. presented with a profound anterograde amnesia
  • He could not remember people he met since his surgery
  • He could read the same jokes and stories over and over again
115
Q

the learning process

A

Short-term memory-immediate memory, limited capacity

Long-term memory-memory for past events, unlimited capacity

Consolidation- the process of converting short-term memories into long-term memories

116
Q

conclusions based on H.M + spared abilities in H.M.

A
  1. The hippocampus is not the location of long-term memories
  2. The hippocampus is not the location of short-term memories
  3. The hippocampus is involved in converting short-term memories into long-term memories (consolidation)

–

•Following his surgery HM had normal short-term memory

oDigit span

•HM also demonstrated other remarkable spared abilities

oMotor learning (mirror drawing, rotary pursuit)

oPerceptual learning (incomplete pictures test)

oPavlovian (classical) conditioning

117
Q

spared motor learning

A

The picture is viewed through a mirror so the image is reversed

After a few trials people get better at copying the picture

When tested after a delay people typically show retention

HM showed retention over several days- but never remembered doing the task!

118
Q

intact perceptual learning

A

HM’s ability to recognize broken line drawings improved over subsequent testing sessions

HM insisted that he had never seen the pictures before

119
Q

intact pavlovian conditioning

A

•H.M. was able to acquire a classically conditioned eye-blink response

oHe still showed retention 2 years later

120
Q

multiple memory systems

why can H.M still learn sensormotor tasks?

A

Why two parallel memory systems???

Implicit is simple, doesn’t involved consciousness

Explicit allows for flexibility in using that learned knowledge in a different context

121
Q

semantic vs episodic memory

A

•Two different types of explicit memories:

oSemantic memory- are explicit memories of factual information

oEpisodic memory- are explicit memories for specific events (i.e., episodes)

  • Many amnesics (other than HM) can acquire new semantic memories but fail at tests of episodic memory
  • Temporal lobe amnesia seems to be a specific disorder of episodic memory
122
Q

the case of K.C - man who can’t time travel

A
  • Damage to medial temporal lobes via a motorcycle accident
  • General intelligence and language normal
  • Semantic memory intact
  • Severe amnesia for personal experiences (autobiographical memory)
  • Cannot imagine himself in the past or future – “time travel”

–

Knows facts of early life – birth date, where he lived, summer cottage was located, names of schools attended, etc

Difficult to spot these episodic deficits because we don’t have knowledge of one’s personal past

122
Q

the hippocampus and amnesia

A
  • Patient R.B. (52 year old male) suffered a heart attack and subsequent anoxia (loss of oxygen = stroke)
  • Although he was revived he suffered permanent anterograde amnesia
  • Autopsy revealed selective damage to the CA1 field of the hippocampus
123
Q

amnesia in alzheimer’s disease

A

•AD causes widespread degeneration of association cortex including the medial temporal lobe

oAnterograde + retrograde amnesia

oShort term + implicit memory also affected

•There is also degeneration of the basal forebrain which generates acetylcholine

oAChE inhibitors

124
Q

posttraumatic amnesia

A
  • Concussions often result in a loss of consciousness
  • Many individuals will experience amnesia for events immediately preceding and following the concussion
125
Q

memory consolidation

A
  • Concussions disrupt consolidation (storage) of recent memories
  • Hebb’s theory – memories are stored in the short term by neural activity
  • Interference with this activity prevents memory consolidation

Examples:

oBlows to the head (i.e., concussion)

oECS (electroconvulsive shock)

126
Q

models of memory consolidation

A
  • Electroconvulsive Shock (ECS) – an intense, brief, diffuse, seizure inducing current that is administered to the brain through large electrodes
  • Shock disrupts consolidation
  • The length of the retrograde amnesia could give an estimate to how long consolidation takes
127
Q

animal models of consolidation

A
  • Thirsty rats learned where the water bottle was in a box cage
  • Then 10 secs, 1 min., 10 mins., 1 hr., 3 hrs. later the rat would receive ECS

Consolidation took between 10mins and 1 hour

128
Q

animal models of amnesia

A
  • HM’s case study was the first to indicate that the hippocampus was critical for forming new memories
  • Researchers attempted to create an animal model of amnesia to better understand the underlying anatomy
  • Early attempts at creating an animal model were unsuccessful

oResearchers were overly focused on the hippocampus (What about the amygdala + rhinal cortex?)

oHad difficulty demonstrating memory deficits in animals with hippocampal lesions (Using the wrong memory tests?)

Animals mostly tested for explicit memory

129
Q

monkey model of amnesia mid 1970s

A

Delay non-match to sample (DNMS) task

130
Q

delayed non-match-to-sample task

A
  • “Normal” monkeys perform the DNMS task correctly on 90% of trials
  • Monkeys with medial temporal lesions perform worse as the delay interval increases
131
Q

hippocampus or rhinal cortex?

A

Is it really damage to the hippocampus that causes amnesia?

Much of the input to the hippocampus from the cortex must go through the rhinal cortex!

–

R.B. had damage to CA1 subfield – ischemia-induced hyperactivity damaged regions outside the hippocampus

132
Q

hippocampus and rhinal cortex

A

Subsequent studies in rats found that damage to the rhinal cortex led to amnesia NOT the hippocampus

R.B. had damage to CA1 subfield – ischemia-induced hyperactivity damaged regions outside the hippocampus

133
Q

so what does the hippocampus do?

A
  • Subsequent studies have shown that the hippocampus plays a critical role in spatial memory
  • Rats with hippocampal lesions perform poorly on both the Morris water maze, as well as the radial arm maze
134
Q

hippocampal place cells

A

•Specific cells in the hippocampus respond only when the animal is in a particular location in space

oReflects where the animal thinks it is in space

oThis map is created in the hippocampus through learning

  • Found mostly in the dorsal (posterior) hippocampus in pyramidal cells in the CA1 field
  • Rhinal cortex has “grid neurons”
135
Q

the hippocampus and navigation

A
  • Black-capped chickadees show an increase in the size of the hippocampus during late fall
  • London taxi drivers were found to have larger posterior hippocampal volumes (Maguire et al., 2000)
136
Q

where are memories stored?

A
  • Each memory is stored diffusely throughout the brain structures that were involved in its formation.
  • Some structures have particular roles in storage of memories.

oHippocampus: spatial location

oPerirhinal cortex: object recognition

oMediodorsal nucleus: Korsakoff’s symptoms

oBasal forebrain: Alzheimer’s symptoms

137
Q

where are memories stored?

A

5 other memory areas:

  1. Medial-temporal cortex
  2. Amygdala- fear conditioning; strengthening of emotional memories
  3. Prefrontal cortex- temporal sequences of episodic memory; working memory
  4. Cerebellum - classical conditioning; habit formation
  5. Striatum - classical conditioning; habit formation
138
Q

how are memories stored ?

donald hebb

A

•Hebb’s rule - if a synapse becomes active repeatedly at the same time that the post-synaptic neuron fires the synapse will be strengthened

Efficiency in synaptic transmission was the basis for long-term memory

139
Q

classical conditioning

A
140
Q

how are memories stored?

A

Neurons within the hippocampus appears to follow Hebb’s rule!

141
Q

the hippocampus

A
142
Q

long term potentiation

A

LTD-long term depression can also occur following low frequency stimulation (<10Hz)

•Two key properties link LTP to learning:

(1) Can last a long time
(2) Only occurs in BOTH sending and receiving neurons are firing – called co-occurance

143
Q

associative LTP

A

When a strong stimulus is paired with a weak one, their connection becomes strengthened

144
Q

synaptic strengheting

A
  • Rapid stimulation causes the EPSPs to summate which depolarizes the postsynaptic membrane
  • LTP requires 2 events:
  1. Activation of pre- synaptic neuron
  2. Depolarization of the postsynaptic neuron
145
Q

N-Methyl-D-Aspartate (NMDA)

A
  • Found mostly in the CA1 subfield
  • Controls a calcium ion channel which is normally blocked by a magnesium (MG2+) ion
  • If postsynaptic membrane is depolarized the MG2+ ion is ejected, and Ca2+ enters
  • Glutamate must also be present
146
Q

NMDA receptors

A
  • NMDA receptors are active ONLY when glutamate is present and when the postsynaptic membrane is depolarized
  • NMDA receptors are both NT and voltage dependent
  • Blockage of NMDA receptors with AP5 prevents LTP
  • AP5 does not interfere with LTP that has already been established
147
Q
A
148
Q

associative LTP

A

Allows neural networks to learn associations

149
Q

synaptic plasticty

A
  • The strengthening of synapses relates to an increase in postsynaptic AMPA receptors
  • AMPA receptors are glutamate receptors that control Na+ channels
  • The creation of new AMPA receptors increases the postsynaptic response to glutamate

–

Maintanence of LTP - memory

150
Q

AMPA Receotirs

A
  • After Ca2+ enters the postsynaptic dendrites it activates CaM-KII, a protein kinase
  • CaM-KII then delivers AMPA receptors to the membrane via vesicles
151
Q

perforated synapses

A

Dendritic spine splits active zone

Each active zone grows

152
Q

presynaptic changes

A

•Presynaptic changes can also occur following LTP

oe.g., Increase release of glutamate release

  • Presynaptic changes may be related to the activation of nitric oxide (NO)
  • NO can act as a presynaptic messenger
153
Q

putting it all together…

A

Glutamate released and binds to NMDA receptor

Calcium enters and activates CaMKII which causes insertion of AMP receptors

LTP also causes perforated synapses or new ones

Calcium activates NO which diffuses out and back into terminal button to increase glutatmate release

154
Q

why do we sleep??

A

•All mammals and birds sleep (need REM)

•

•We spend about 1/3 of our life sleeping

•

  • Sleep deprivation can disrupt cognitive functions and has a profound effect on mood (irritability)
  • One good nights sleep can make up for days of deprivation

Boy who went 264 hours without sleep – Guinness Record

oAfter this ordeal he slept for 15 hours 1st night, 10 hrssecond and 9 hrs 3rd

oOnly 7% of stage 1 and 2 made up, but 68% of stage 4 and 53% of REM were made up

155
Q

why do we sleep?

recuperation theories

A

•Recuperation theories

oSleep is needed to restore homeostasis

oWakefulness causes a deviation from homeostasis

156
Q

why do we sleep when we do?

adaptation theories

A

•Adaptation theories

oSleep is the result of an internal timing mechanism

oSleep evolved to protect us from the dangers of the night

157
Q

how much sleep do we need?

A
158
Q

Electroencephalogram (EEG)

A

•Attach electrodes to scalp to measure brain waves while sleeping

159
Q

EEG stages of sleep

A

Sleep spindles – we get it every few minutes / mask outside noises

K complexes –

160
Q

wakefulness

A
  • Two basic patters: alpha and beta
  • Alpha consist of regular, medium frequency (8-12 Hz) waves
  • Usually occurs when eyes are closed and in a relaxed state
  • Beta waves are irregular and lower amplitude (13-30 Hz)
  • Shows asynchrony due to multiple neural circuits at work
161
Q

stage 1 sleep

A
  • Theta Waves (3.5-7.5 Hz)
  • Usually transition between sleep and wakefulness
  • EOG show rolling eye movements
  • Stage lasts for about 10 minutes
  • If awoken, people will often claim that they were “thinking”
162
Q

stage 2 sleep

A
  • Mixed frequencies with occasional bursts of 12-14 cps
  • Sleep spindles may be the mechanism that decreases the brains sensitivity to sensory input - Found throughout stages 1-4.
  • Older people have fewer sleep spindles - more awakenings
  • K complexes only found during stage 2 - Can be triggered by noises
163
Q

slow wave (deep) sleep

A
  • Stages 3 and 4 - High amplitude Delta waves (>3.5 Hz)
  • Deepest stage of sleep - if woken, will be groggy and confused
164
Q

rapid eye-movement (REM)

A
  • Paradoxical sleep because brain is awake but body is asleep
  • If awoken during REM, person will be alert and attentive
  • They will invariably report that they were dreaming
  • Complete muscle atonia - prevents us from acting out our dreams
  • Erections in males, increased vaginal blood flow in females - not related to content of dreams.

–

165
Q

a typical night’s sleep

A
  • 90 min cycle
  • 4-5 periods of REM sleep
  • Each period is about 30 min long
  • Refractory period following REM

–

Deep sleep (3 & 4) – ure body is at rest

During ren sleep ur body is sleeping but ur brain is active

166
Q

effects of sleep deprivation

A

•It is difficult, if not impossible, to separate the effects of stressors used to prevent sleep from the effects of lost sleep

167
Q

sleep deprivation in humans

A

•3-4 hours of deprivation in one night

oIncreased sleepiness

oDisturbances displayed on written tests of mood

oPoor performance on tests of vigilance

•

•2-3 days of continuous deprivation

oExperience microsleeps, naps of 2-3 seconds

oUpdating plans and strategies

oInnovative, lateral, insightful thinking

oReference memory

168
Q

sleep deprivation increases sleep efficiency

A
  • After sleep deprivation, most of lost stage 4 is regained and SWS is increased
  • Short sleepers get as much SWS as long sleepers
  • Naps without SWS do not decrease the night’s sleep
  • Gradual reductions in sleep time lead to decreases in stages 1 and 2
  • Little sleepiness produced with repeated REM awakenings, unlike SWS

–

Short sleepers and long sleepers get the same quality of sleeo

20-30 mins (ure not tajing that sleep wave or rem sleeo so ull still be able to sleep at night)

169
Q

rem-sleep deprivation

A

•Two consistent effects

oProceed more rapidly into REM as REM deprivation increases

oREM rebound – more time spent in REM when deprivation is over

•REM rebound suggests that REM sleep serves a special function

–

We can wake u up during rem sleep -> eeg or

They experience more rem sleep if the day before if they get woken up during their REM stage

Our brain needs it (don’t rlly know what that function is yet)

170
Q

functions of REM sleep

A

•Promotes learning

oDevelopmental evidence

  • REM duration peaks at most active stage of development
  • 70% of newborn’s sleep is REM
  • 6mths - 30%, 8yrs - 22% and adulthood - 15%
  • Could be determined by the fact that REM is necessary for development OR REM increases with learning
171
Q

purpose of REM

A

•Processing of explicit memories?

oInconsistent findings

oAntidepressant REM-blocking drugs do not interfere with memory

•Default theory: it is difficult to remain in NREM sleep (essentially, rem sleep is not rlly needed)

oNycamp and others (1998) awoke sleepers in REM for 15 minutes. Result: no sleepiness or REM rebound the next day

oREM-blocking drugs cause periods of wakefulness

172
Q

sleep and dreaming

A
  • Many REM dreams are emotional, illogical, and prone to sudden shifts in plot
  • Non-REM dreams are shorter, more thought-like, repetitive, concern daily stresses
  • Dreams are usually associated with negative emotions and events

Dreaming is our other state of consciousness (our internal)

It is hard to study – experiments are subjective

Rem dreams are different (lucid / more emotional ) than non rem sleep (story-like / they make sense / not emotional or exciting so you don’t rlly remember it)

75% of dreams are negative – sex dreams arw also low (9%)

173
Q

rem sleep and dreaming

A

•80% of awakenings from REM yield reports of story-like dreams

Common beliefs:

  • External stimuli may be incorporated into dreams
  • Dreams run on real time
  • Everyone dreams
  • Penile erections are not a result of erotic dreams
  • Sleepwalking and talking are less likely to occur while dreaming
174
Q

mental activty during sleep

A
  • Even people who claim NEVER to dream will describe dreams if awoken during REM
  • Prone to forgetting
  • High CBF in visual association areas - low in V1 and frontal areas
  • Dreams are high in visual content but poorly organized in time and rarely make sense

–

During rem sleep – the whole frontal lobe is inactive -> frontal lobe is not available to make any sense of any them ->

175
Q

lucid dreaming

A
  • Knowing you are dreaming while you’re asleep
  • Most of us have experienced one lucid dream
  • Usually very colourful and associated with anxiety
  • Opens the door to controlling our dreams!

a skill you can apparantly develop

176
Q

circadian rhythm

A

•Biological clock (24 hour cycle)

177
Q

zeitgeber

A

oLight = zeitgeber (timegiver) that entrains 24.18 hour clock to 24 hour cycle

oEven a brief burst of light will reset our circadian rhythms

oIf given soon after dusk then our clock is set back a few hours

oIf given at after dawn, then our clock it set forward a few hours

oWe use technology to be able to go to bed later and wake up later

This is what keeos up awake – signals that keep our circadian rhythm alive

Eating / physical activity / Light

178
Q

free-running circadian sleep-wake cycles

A

•Remove zeitgebers – still see circadian sleep-wake cycles?

oFree-running periods vary, but are usually constant within a subject

oMost are longer than 24 hours ~ 25

•What happens on days when you don’t need to get up?

179
Q

shift work and jet lag

A
  • Both will desynchronize circadian rhythms
  • Physical activity can be a zeitgeber
  • Solution is to get internal clock synchronized with external environment as quickly as possible
180
Q

superchiasmatic nucleus (SCN)

A
  • If you lesion this hypothalamic nucleus you disrupt circadian rhythms - will sleep in bouts during the day
  • Same amount of sleep, but won’t be synchronized
  • Some direct connections from visual pathways - retinohypothalamic pathway

–

It gets information from our eyes -> visual info from certaoins cells in the retina

Tehse cells are timekeepers (active for 12 hrs not active for 12 hrs)

If we take it away, we’ll still sleep but not for 24 hrs (no rhythm in ur sleep cycle)

How does it do that?? -> Melanopsin

181
Q

melanopsin

A

oPhotochemical in ganglion cells that transmit information from the retina to the rest of the brain

oInvolved in papillary response as well

–

It’s the change in light overtime activates this cell

182
Q

circadian rhythm / pineal gland

A

Pineal gland – essentially releases melatonin (our sleepy hormone)

  • Distributed to our body when we’re supposed to be sleepy / melatonin will be sleepy
  • It helps our circadian rhythm stay in circadian rhythm
183
Q

melatonin

A
  • Synthesized from serotonin in the pineal gland
  • Melatonin levels follow circadian rhythms controlled by the SCN
  • Pineal gland triggers seasonal reproductive changes in fish, birds, reptiles, and amphibians – human function is unclear
  • Melatonin is not a sleep aid, but may be used to shift circadian rhythms

–

Keeps rhythm intact

If your circadian rhytm is fine then you shouldn’t rlly take it

184
Q

brain areas involved in sleep; two areas of the hypothalamus

A

Two areas of the hypothalamus:

  • Economo found that the posterior hypothalamus and the anterior hypothalamus were related to excessive sleep or inability to sleep, respectively

Findings were in patients that had encephalitis lethargica

–

Hypothalamus -> for motivation behaviors / sleeping behavior / 4fs

The anterior hypo is most important for sleeping (if you damage it you will be asleep forever)

Post is good for wakefulness (if u damage it ppl will be awake forever?)

185
Q

four evidence that the reticular activating system is involved in sleep

A
186
Q

reticular REM-sleep nuclei

A
  • Similarities between REM and wakefulness suggest that the same brain area might be involved in both
  • REM sleep is controlled by nuclei in the caudal reticular formation, each controlling a different aspect of REM
187
Q

insomnia

A
  • Affects 25% of population at some time
  • Must be defined in relation to a person’s sleep needs
  • Paradoxically insomnia often caused by sleep medications because of tolerance - withdrawal cycle called drug dependency insomnia
  • People who report insomnia normally fall asleep within 30 minutes and get 6 hrs of sleep in a night
188
Q

insomnia; ways to get a good night’s sleep

A
  1. Don’t do anything stressful and relax before bedtime
  2. Sleep and wake-up at regular times
  3. Sleep in a cool room
  4. Avoid caffeine, taking naps longer than 20 mins, or watching t.v. or surfing the web before bed
  5. Sleep only when tired
  6. Get out of bed if you can’t sleep and go back when you’re tired
189
Q

sleep apnea

A
  • Stop breathing (briefly)
  • Carbon dioxide in the blood stimulates chemoreceptors that causes the person to wake up gasping for air
  • Occurs in most people, especially those who snore
  • Obstruction of airway that can be surgically corrected
190
Q

narcolepsy

A
  • REM phenomena sneaking into waking hours
  • Sleep attack - overwhelming urge to sleep mostly during monotonous boring tasks.
  • Sleep generally lasts 2-5 minutes
  • Wake up feeling refreshed
  • Narcoleptic patients generally skip slow wave sleep and go directly to REM from waking
191
Q

sleep paralysis

A
  • Inability to move just before the onset of sleep or when waking in the morning
  • Can snap out of it if poked or called by name
  • REM can also occur, such that the person dreams while lying awake - hypnagogic hallucinations
192
Q

REM sleep behaviour disorder

A
  • Opposite of cataplexy (paralysis)
  • Failure to exhibit paralysis during REM sleep
  • People act out their dreams
  • Could be a neurodegenerative disorder – usually associated with Parkinson’s Disease and MS
  • Could also be caused by brain damage to neural circuits in brainstem
193
Q

pavor nocturnus

A
  • Night terrors
  • Most intense acceleration of heart rate in all of human experience - more rapid than 100 meter Olympic sprinters
  • STAGE 4 not REM
  • Crushed, suffocated, screaming, trembling – but do not remember
  • Usually harmless

Psyc 275 - Brain and Behaviour (4 decks)

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