Neuro Exam 3

Light information goes from eye to SCN via what path?

retinohypothalamic

How does the 24 hour clock?

1. CLOCK/BMAL1 dimers promote transcription of Period (PER) and Cryptochrome (CRY) genes, and thus more PER and CRY proteins

2. PER/CRY dimers build up, inhibit transcription of their own genes

3. PER and CRY are degraded in a few hours, which lowers inhibition of their transcription, so after ~24 hrs, a new cycle begins

SCN controls more than sleep like

wake, appetite, autonomic NS, neuroendocrine, local brain clocks

brain and body function are

not independent of the time of day

what do lesions of the SCN cause

disruptions of circadian rhythms

SCN lesions DO NOT

abolish other rhythms

SCN regulates pineal gland’s secretion of WHAT

melatonin (regulates sleep)

how does light reset the clock

by supressing melatonin secretion

human average free run

24 hrs and 11 min

N1-3 EEG activity

slow-wave EEG activity

REM (what’s goin on)

rapid eye movementts, breathing and heart rate speed up, muscles relax

how long do cycles last

90-110 min

cycles early in the night have more

deep sleep

cycles later in the night have more

REM sleep

we dream in what type of sleep

both! we dream in REM AND N states

vivid dreams occur in what type of sleep

REM

N dreams (describe)

likely to be brief fragments that are less emotional and less visual than REM sleep dreams

nightmares

frightening dreams that awaken sleeper from REM sleep

night terrors

sudden arousals from N3, marked by fear

as we age how does sleep change

total time asleep declines, and awakenings increase

how does brain wake up

Suprachiasmatic nucleus turns off inhibition of the brainstem reticular activating system, which turns on the cortex via the thalamus

how does brain fall asleep

VLPO nucleus of hypothalamus turns off the brainstem

ascending upper brainstem system

activates cortex

descending pons system

triggers REM, paralyzes body

what do we do in N sleep

recall (replay)

what do we do in REM sleep

consolidate

A 60-90-minute nap containing REM and non-REM sleep improve

learning

when we learn something how does rem sleep change

it increases

replay of learned material is synchronized with

hippocampus

how does memory erasure occur

brain purges unwanted memories during REM sleep

in REM what is in overdrive

hippocampus and limbic system

in REM what is shut down

the frontal cortex

in narcolepsy what happens

they do not go through N before REM

cataplexy

sudden loss of muscle tone

narcoleptic dogs have mutation where

orexin receptor in brainstem

in narcoleptic people there is BLANK attack on BLANK

autoimmune, orexin receptor

what does orexin do

stabilizes the sleep-wake see-saw

sleep paralysis what happens

pontine center triggers muscle relaxation

enuresis

bed wetting

night terror and enuresis occur in

N sleep

Somnambulism

sleep walking

Somnambulism happens when

during deeper N sleep

what happens in sleep apnea

Breathing stops (apnea) – blood oxygen drops rapidly

Chest/diaphragm muscles relax too much or pacemaker respiratory neurons in the brain stem do not signal properly

Accompanied by snoring/gasping

Each apnea arouses the person to breathe, so → daytime sleepiness

REM sleep behavior disorder

Paralysis that normally occurs during REM sleep is incomplete or absent, so the person ‘acts out’ their dreams

which protein linked to alzheimer are cleared from brain during sleep

amyloid

rods have

rhodopsin

cones have

iodopsin

where are the rods

peripheral retina

where do rods function well

in dim light

do rods distinguish color?

no

where do cones work well

bright light

what are the three types of iodopsins

red,blue,green and they each respond to a different wavelength

where are the cones

central retina (fovea)

two types of lateral processing cells

amacrine and horizontal cells

amacrine cells

contact bipolar and ganglion cells

horizontal cells

contact photoreceptors and bipolar cells

what makes ganglion cells special

they can fire action potentials

receptive fields of ganglion cells from rods are

large

receptive fields of ganglion cells from cones are

small

cones visual acuity

high

rods visual acuity

low

how is retinal activated

light strikes rhodopsin

transduction

light closes Na channels, hyperpolarizes, and turns rods off

Leber’s congenital optic degeneration

RPE65 is defective; photoreceptors degenerate (Gene therapy can treat this disease)

lateral inhibition

inhibiting one’s neighbors produces contrast

visual pathways

1. Retina

2. Optic chiasm

3. Lateral geniculate nucleus (thalamus)

4. Visual cortex (occipital lobe)

neurons in retina have two types of receptive fields

TYPE 1- on center and off surround TYPE 2- off center and on surround

fibers from the nasal part of the retina

cross over

fibers from the temporal part of the retina

stay on the same side

information from the right visual field

travels to left part of the brain

information from the left visual field

travels to the right side of the brain

Three stages of vision processing

LGN (thalamus), Visual cortex (v1-v5), secondary visual cortex

3 cell types in LGN

parvocellular, magnocellular, koniocellular

parvocellular

small cells, small receptive fields

Magnocellular

large cells, large receptive fields

Koniocellular

layers with very small cells, between main layers

Primary visual cortex

most of the visual information arrives here first, simple and complex cortical cells,

brain maps of visual space are mostly devoted to

the fovea

simple cortical cell

respond to an edge or bar of a particular width, orientation, and location

complex cortical cells

also respond to a bar of a particular width and orientation, but it may be anywhere in the visual field

Simple cortical neurons receive input from

neurons in lateral geniculate

complex neurons receive input from

simple cortical cells

V1 (primary visual cortex): needed

to form all visual images, also breaks down visual image into components

V2,V4 and the inferior temporal lobe

perceive complex form

v5

specialized for motion perception

what pathway of vision

infero-temporal cortex

where pathway

parietal cortex

ocular dominance column

a region of cortex with greater synaptic input from one eye

V1 (parallel processing)

color ,shape location all at once

v2

fills in gaps, vision is extrapolating from what is actually seen

v4 cells respond to

concentric and radial stimuli, also involved in color perception

motion detection process

retinal periphery (rods) sensitive to motion project to v5

motion blindness

akinetopsia

motion detection brain questions

if an object is moving before asking what it is

final stage of visual processing, responds to complex forms (like even ones we recognize)

inferotemporal cortex

hierarchy of visual processing

from simple edges and borders to complex forms as you move from V1 to IT

three channels from retina to higher visual cortex

M channel, P-IB channel, blob channel

M channel

(magnocellular pathway) analysis of object motion, orientation selective, directional sensitive for movement, no color sensitivity

P-IB channel (parvocellular interblob pathway)

high orientation sensitivity, no color sensitivity, small receptive fields - analysis of object shape

blob channel (parvocellular blob and koniocellular pathway)

no orientation sensitivity, color sensitivity - analysis of object color