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Neuro 1 Midterm > Physiology > Flashcards

Physiology Flashcards

1
Q

50-70% of CSF is made by the:

A

choroid plexus (within 3rd and 4th ventricles)

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2
Q

two-stage process of CSF formation:

A
  1. passive filtration of serum/plasma into ventricle

2. HCO3, Cl-, K+ concentrations controlled by channels on epithelial cells … aquaporins also exist

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3
Q

why would CSF production exacerbate increased intracranial pressure?

A

CSF is continually made, so it would increase intracranial pressure, making it worse

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4
Q

what ions are the same concentration between CSF and plasma? (3)

A

Na+
Cl-
HCO3

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5
Q

what ions/compounds are in greater concentration within CSF than in plasma? (2)

A

Mg2+

CO2

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6
Q

what ions/compounds are in lesser concentration within CSF than in plasma? (4)

A

K+
Ca2+
protein
glucose

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7
Q

Mg2+ blocks ___ channels?

A

Ca2+

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8
Q

pH in the brain can change drastically with changes in CO2 because:

A

we don’t have the protein to buffer it

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9
Q

at what level of CSF do we see no absorption by arachnoid villi? what is normal?

A

< 68 ml CSF

normal = 112 ml

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10
Q

what is the main role of CSF?

A

to protect the brain

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11
Q

capillaries in the brain have two fxns that limit exchange between the blood and the brain:

A
  1. tight jxns between endothelial cells

2. glial endfeet come in close contact with blood vessels

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12
Q

what compounds undergo passive diffusion through the BBB? how and which direction?

A

H2O - via gradient
CO2 - to blood
O2 - to neurons
free steroid hormones cross, but most are protein-bound (can’t cross)

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13
Q

how does glucose get across the BBB?

A

GLUT-1 transporter

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14
Q

is GLUT-1 dependent on insulin?

what forms exist?

A

GLUT-1 is not dependent on insulin
45 kD form - form on astroglia (capillaries to CSF)
55 kD form - form on capillary endothelial cells (blood to capillary)

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15
Q

if children do not possess either the 45kD or 55kD form, what happens?

A

seizures

-membrane depolarizes because glucose is not getting in (no E available to drive ATPase to maintain membrane potential)

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16
Q

role of Na/K/2Cl transporter:

A

move ions from CSF to blood

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17
Q

what ion is the Na/K/2Cl transporter most responsive to?

A

K+ (need it out)

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18
Q

Na/K/2Cl transporter expression is tied to:

A

endothelin (ET) 1 and 3

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19
Q

ET production is tied to signals from _________, which may be tied to [__] in CSF.

A
  • astrocytes

- [K+]

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20
Q

incr [K+] CSF —> astrocytes/astroglia express endothelin 1 and 3 —> incr/decr expression of Na/K/2Cl transporter

A

incr [K+] CSF —> astrocytes/astroglia express endothelin 1 and 3 —> INCREASED expression of Na/K/2Cl transporter

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21
Q

P-glycoprotein is coded by what gene?

A

MDR-1

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22
Q

role of P-glycoprotein:

A

move drugs and compounds from the CSF (have crossed the BBB) back into blood

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23
Q

how does BBB protect chemical composition of CSF from blood-borne agents? (3)

A
  1. tight jxns
  2. end feet of glia
  3. P-glycoprotein
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24
Q

certain places in the brain are exposed to blood (exceptions of BBB). what is different about these places microscopically?

A

the capillaries in these areas do NOT have tight jxns between endothelial cells

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25
Q

brain organs exposed to blood are termed:

they include: (4)

A

circumventricular organs
1. posterior pituitary - release ADH/vasopressin & oxytocin
2. area postrema - at opening of 4th ventricle and spinal cord, vomiting center
3/4. OVLT and subfornical organ - BOTH involved in body water/thirst/blood volume control (angiotensin) … sense osmolarity

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26
Q

receptor for sympathetics (vasoconstriction)

A

alpha-adrenergics

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27
Q

distal blood vessels possess what type of innervation?

A

sensory innervation

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28
Q

what three NTs allows afferents to be sensitive to dilation?

A

Substance P
Neurokinin A
CGRP

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29
Q

sensory fibers render blood vessels of the brain extremely sensitive to torsion or manipulation. why is this important when there’s a decrease in CSF?

A

decreased CSF volume —> incr heaviness of brain —> incr brain motion —> torsion of blood vessels —> pain (sensory afferents)

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30
Q

cerebral blood flow is under _____ control

A

local

-O2 consumption dictates where in the brain blood goes

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31
Q

increase intracranial pressure —>
__ venous outflow —>
__ arterial flow

A

increase intracranial pressure —>
decrease venous outflow —>
decrease arterial flow

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32
Q

activation of alpha-adrenergics allows blood vessels to extend the range that blood flow in the brain is held constant. why is this a good thing? think capillaries and BBB…

A

high BP —> vasoconstrict brain vasculature to protect BBB (also protects capillaries in brain from damage)

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33
Q

where is ACh located? (3)

A

centrally

  • pons
  • midbrain
  • striatum
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34
Q

pontine and midbrain group needs ACh to produce _________

A

consciousness

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35
Q

ACh is stored in vesicles and is moved in by _____

A

VAChT

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36
Q

what enzyme is bound to the post-synaptic cell membrane and breaks ACh down?

A

aceylcholinesterase

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37
Q

the neuronal ACh muscarinic receptor is which subtype? by what mechanism does it produce action?

A

M1 (neuronal type)

incr IP3/DAG —> incr Ca2+

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38
Q

where is GABA located? (3)

A
  • cerebellum
  • cortex
  • retina
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39
Q

what is the functional role of GABA?

A
  • major inhibitory NT in higher CNS
  • critical for producing consciousness/awareness
  • control of voluntary motion
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40
Q

from what compound is GABA derived?

what enzyme catalyzes the reaction to form GABA?

A
  • glutamate

- glutamate decarboxylase

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41
Q

what is the effect when GABA binds to GABA(A) receptor?

A
  • Cl- conductance –> hyperpolarization

- has a benzodiazepine site (potentiates the hyperpolarization from the Cl-)

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42
Q

what is the effect when GABA binds to GABA(B) receptor?

  • effect on K+
  • effect on adenylyl cyclase (AC)
A
  • K+ efflux (hyperpolarization) (prevents Na+ channels from opening)
  • decr AC –> decr IP3/DAG –> decr Ca2+ influx (hyperpolarization)
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43
Q

TQ: inhibitory NT in brain (cortex, cerebellum). think…

BUT if location is spinal cord or brainstem think…

A
  • GABA

- glycine

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44
Q

where is glycine located?

A

spinal cord
brainstem
forebrain (less than GABA)

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45
Q

glycine receptors are blocked by:

A

strychnine

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46
Q

where do opioids act? (3)

A

basal ganglia
hypothalamus
parabrachial and raphe nuclei

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47
Q

functions of opioids (2)

A

modification of nociceptive (painful) inputs

modification of mood/affect (neuro 2)

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48
Q

TQ: opioids are base on four precursor molecules (just know these are opioids and they’ll act like opioids)

A
  • proenkephalin
  • pro-opiomelanocortinin (POMC)
  • prodymorphin
  • orphanin FQ (nociceptin)
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49
Q

effect of opioids binding to mu receptors: (5)

A
  • analgesia
  • respiratory depression
  • EUphoria
  • sedation
  • constipation
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50
Q

effect of opioids binding to kappa receptors: (4)

A
  • analgesia
  • DYSphoria
  • diuresis
  • miosis
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51
Q

effect of opioids binding to delta receptors: (1)

A

analgesia

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52
Q

mu opioid receptors (increase/decrease) K+ efflux (hyperpolarization)

A

INCREASE K+ efflux

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53
Q

kappa & delta opioid receptors (increase/decrease) Ca2+ in the cell

A

DECREASE cellular Ca2+

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54
Q

where are endocannabinoids distributed within CNS? (3)

A
  • hippocampus - memory formation
  • basal ganglia - affect/motor
  • spinal cord - nociception
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55
Q
  • found in axons and pre-synaptic terminals of EAA and GABA synapses
  • G(i) protein-coupled receptor (inhibits AC)
  • decreases NT release
  • binds either anandamide or 2-arachidonylglycerol well
A

CB-1 receptor

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56
Q
  • found in brain (microglia, NOT neurons)
  • immune system and gut
  • anti-inflammatory
  • in brain, causes macrophages to remove beta-amyloid
A

CB-2 receptor

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57
Q
  • excitatory NT
  • derived from a-ketoglutarate
  • metabolic pool and NT pool are strictly separated
A

glutamate

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58
Q
  • excitatory NT
  • derived from oxaloacetate
  • NT in visual cortex and pyramidal cells
  • often found with glutamate
A

aspartate

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59
Q

activation of NMDA receptor causes: (1)

A

Ca2+ influx

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60
Q

name NMDA’s modulatory sites (3) and the function of each

A
  • glycine binding site - serves as co-agonist to NT, but CANNOT open channel on its own
  • Mg2+ binding site - block channel
  • PCP binding site - block channel downstream from Mg2+
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61
Q

activation of NMDA receptor leads to a slow ____

A

EPSP

  • long latency (time to remove Mg2+)
  • longer duration (Ca2+ influx slower)
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62
Q

activation of non-NMDA receptor causes:

A

Na+ influx (very little amount of Ca2+, too)

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63
Q

2 subtypes of non-NMDA receptor:

A
  1. AMPA: Na+ entry, but has benzodiazepine binding site, which inhibits the response to NT (decreases Na+ entry)
  2. kainate: Na+ entry (with very small amount of Ca2+)
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64
Q

non-NMDA receptors are co-localized at the same synapse with NMDA receptors. why?

A

the entry of Na+ through non-NMDA leads to a depolarization of the cell membrane, which helps to remove PCP from blocking the NMDA channel and allow the influx of Ca2+

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65
Q

T/F: metabotropic receptors are located on BOTH pre- and post-synaptic neurons

A

TRUE

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66
Q

metabotropic receptors on the pre-synaptic membrane function to: (1)

A

control NT release

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67
Q

receptor that’s assoc with:

  • primary afferents
  • premotor (upper mn)

you think…

A

non-NMDA receptors

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68
Q

receptor that’s assoc with:

  • long-term changes in synaptic strength
  • learning
  • memory

you think…

A

NMDA receptors

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69
Q

receptor that’s assoc with:

  • learning
  • memory
  • motor systems
A

metabotropic receptors

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70
Q

how do neurons and glia get rid of EAA?

A

via high affinity uptake systems…

Na+ dependent 2ndary active transport

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71
Q

what is the specific role of glia in EAA uptake?

A

glia convert glutamate to glutamine and release into ECF

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72
Q

what is the specific role of neurons in EAA uptake?

A

neurons take up glutamine and convert it back to glutamate

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73
Q

activation of NMDA causes influx of Ca2+ —>
Ca2+ binds calcineurin —>
…what happens to NOS?

A

activation of nitric oxide synthase (NOS), which converts arginine to citrulline (NO is a by-product of the reaction)

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74
Q

what happens to a cell’s Na/K/ATPase if the cell is deprived of oxygen?

A

Na/K/ATPase stops
ATP within neurons = 0
–> membrane depolarization

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75
Q

during anoxia, high levels of EAA are released. since EAA re-uptake is Na+ dependent, EAA is not being taken up. how does this affect NMDA?

A

NMDA will be activated by high levels of EAA

–> Ca2+ influx

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76
Q

increased [Ca2+] in the neuron initiates: (4)

A
  • activation of phospholipase A2
  • activation of calcineurin (phosphatase)
  • activation of mu-calpain (protease)
  • activation of apoptotic pathway
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77
Q

activation of phospholipase A2 leads to:

A

release of arachidonate from membrane –>

physical damage to membrane

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78
Q

what intracellular receptor (in ER) does arachidonate also act on? what is the result?

A

ryanodine receptor

-more Ca2+ is then released inside cell (ER & mito)

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79
Q

release of Ca2+ from intracellular store in the ER leads to: (3)

A
  • TQ: unfolded protein response - stops making protein
  • activation of eIF2(alpha)-kinase
  • impaired mito function
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80
Q

activation of mu-calpain (protease) leads to: (2)

A

proteolysis:

  • spectrin - structural damage
  • eIF4G - interferes with protein synthesis
81
Q

activation of calcineurin leads to: (2)

A
  • a phosphatase

- TQ: activation of NOS –> increased NO synthesis

82
Q

the disruption of mitochondrial and ER fxn (increases/decreases) free cytosolic Ca2+

A

increases

83
Q

as mito membranes are disrupted, cytochrome C and caspase 9 are released, leading to: (2)

A
  • activation of caspase 3

- proteolysis/apoptosis

84
Q

when O2 re-perfuses neurons, they’re no longer normal. if mito can’t use it (they’re impaired), what does the O2 become?

A

free radicals

85
Q

kinases take ATP (from mito) and make: (2)

A

ADP and PO4

86
Q

phosphorylation by eIF2(alpha) kinase leads to: (2)

A
  • decreased protein synthesis

- activation of caspase 3 (increased apoptotic signaling)

87
Q

in high quantity, NO causes:

A

edema - by damaging capillary endothelial cells

88
Q

prevention of the reperfusion injury cycle includes: (pre/post)-treatments focusing on what receptor?

A

pre-treatments focusing on NMDA receptors

89
Q

consciousness has 2 parts:

A
  1. arousal

2. awareness

90
Q

coma:

A

neither awake nor aware

91
Q

persistive vegetative state:

A
  • physiologically identifiable sleep/wake cycles appear

- no evidence of awareness

92
Q

minimally conscious state:

A
  • sleep/wake cycles
  • reproducible evidence of awareness - ability to respond to simple demands
  • limited/absent communication
93
Q

disruptions of consciousness result from smaller lesions in the: (3)

A

brainstem, midbrain, or hypothalamus

94
Q

EAA: (2)

A
  1. reticular activating system

2. parabrachial nucleus

95
Q
  • occupies “mid-ventral portion” of medulla and midbrain
  • loose collection of neurons and fiber tracts
  • ALL ascending sensory tracts send info here (as do: trigeminal, auditory, visual)
  • process enough to excite cortex to pay attention
A

EAA: Reticular Activating System (RAS)

96
Q

2 output pathways from RAS:

A
  1. Dorsal pathway

2. Ventral pathway

97
Q

TQ: what is the Dorsal pathway?

A

via non-specific nuclei of thalamus, including the intralaminar nucleus of the thalamus

98
Q

what is the Ventral pathway?

A

via basal forebrain and hypothalamus

99
Q
  • located in pons, crucial for arousal/activation
  • sensory inputs similar to those seen in RAS
  • difference: the outputs are likely exclusively via Ventral pathway (TQ) with extensive, diffuse innervation of entire cortex
A

EAA: Parabrachial Nucleus

100
Q

EAA role in arousal:

A

baseline excitation that is crucial to cortical activity

101
Q
  • similar to RAS - receive so much input that all modality-specific info is lost
  • outputs are via the dorsal and neutral pathways used by RAS
  • major NT = ACh
A

Cholinergic: Pedunculopontine tegmental and laterodorsal nuclei (PPT/LDT)

102
Q

cholinergic role in arousal:

A

baseline excitation that is crucial to cortical activity (same as EAA)

103
Q

would damage to PPT/LDT cause coma?

A

No, but it would produce cognitive deficits with slowing of cortical processes

104
Q
  • outputs: both ascending and descending
  • ascending: dorsal and ventral with RAS
  • ascending fibers from this group of cells become the dorsal noradrenergic bundle
A

Noradrenergic: Locus coereuleus

105
Q

functions of the Locus coereuleus: (3)

A
  • startle and alerting responses on EEG
  • sleep-wake
  • behavioral vigilance
106
Q
  • inputs: multiple, difficult to decide which ones relate to arousal system
  • outputs: for arousal, both Dorsal and Ventral pathways are used
A

Serotonergic: Raphe nuclei

107
Q

function of the Raphe nuclei: (3)

A
  • quiet awareness
  • mood and affect (non-RAS activity)
  • modulation of pain (non-RAS activity)
108
Q

functions of the dopaminergic (Ventral Tegmental Area (+ Substantial Nigra)): (3)

A
  • cognitive functions
  • motor activity
  • emotion
109
Q

the Dorsal pathway synapses in the non-specific nuclei of the thalamus (e.g. intralaminar). from there, what NT is used?

A

EAA

110
Q

the neurons that leave the thalamus with EAA input interact with __________ neurons that release ____

A

the neurons that leave the thalamus with EAA input interact with intracranial neurons that release GABA (creates oscillations seen on EEG)

111
Q

function of RAS/Parabrachial EAA system:

A

increases general excitability of cortical neurons

112
Q

function of the cholinergic system:

A

adds to the general excitation by the EAA system

113
Q

function of the noradrenergic and serotonergic systems:

A

move us from being awake to being more generally aware of incoming information

114
Q

Function of the dopaminergic system:

A

Adds to awareness

115
Q

During sleep, what happens to thalamocortical neurons?

A

Hyperpolarized and show occasional bursts

116
Q

Why would hyperpolarization of neurons be beneficial during sleep?

A

Hyperpolarization cuts cortex off from excitatory influence during the deepest levels of sleep

117
Q

Where are odorant receptors (OR) located?

A

On the cilia that protrude into the mucus layer

118
Q

What kind of receptors are ORs?

A

G protein-coupled Rs

Gs protein - but specific to olfaction - creates cAMP

119
Q

Once Gs(olf) protein is stimulated, cAMP leaves to bind and open a:

A

Cyclic nucleotide-gated ion channel, which brings in Na+ and Ca++ …. get depolarization and an action potential

120
Q

What happens if an odorant persists for more than a few minutes? (at the receptor level)

A
  • Sensitivity of the cyclic nucleotide-gated channel to the cAMP is reduced
  • Decreased Na+ and Ca++ entry
  • Reduced probability of an AP in axon
121
Q

Each olfactory neuron expresses the same OR on ALL of its cilia. What is the impact of that?

A

Way to increase sensitivity of smelling

122
Q

Different ORs are localized to (same/different) parts of the olfactory epith - but not equally between these areas.

A

Different
-Each zone (area) in the olfactory epith has a different receptor type that predominates, even though many different receptor types are present in each zone

123
Q

What’s the advantage to the distributed localization of the ORs?

A

Even if I damage one part of the olfactory epith, I still have the ability to detect/sense that odorant in a different “zone.”

124
Q

How do we detect a characteristic odor (in terms of different combos of ORs)?

A

Each odorant activates different combos of ORs to produce its characteristic odor (different sets of activated ORs)

125
Q

Perceived smell is changed by odorant _________.

A

Concentration
-At higher concentrations, the odorant starts to bind to receptors with a lower affinity for the odorants in addition to the receptors with a high affinity.

126
Q

What’s one consequence of having different ORs localized to different parts of the olfactory epith and that perceived smell changes with odorant concentration?

A

If you’re sick or your olfactory epith gets damaged, perceived smell (and taste) will change b/c the concentration or area of receptors available isn’t normal (not using the same set of ORs anymore, e.g., pt undergoing chemo or has a cold)

127
Q

Activation of trace amine-associated receptors (TAARs) produces:

A

Physiologic/endocrine responses to pheromones - not really leading to conscious awareness of an odor
(many of the chemicals that activate TAARs are found in greatest concentration in urine from the male species)

128
Q

The axons of the olfactory neurons pass through the _________ _____.

A

Cribriform plate

129
Q

After passing through the [short] cricbriform plate, the neurons will hit the ________ ____

A

Olfactory bulb

130
Q

The olfactory bulb consists of 5 layers:

A
  1. Olfactory nerve layer
  2. Glomerular layer
  3. External plexiform layer
  4. Mitral cell layer
  5. Granule cell layer
131
Q

The first synapse occurs in what layer of the olfactory bulb?

A

Glomerular layer (Layer 2)

132
Q

Cell bodies of Tufted cells are located in what layer of the olfactory bulb?

A

External plexiform layer (Layer 3)

-Tufted cells are one of the relay neurons to the rest of the brain

133
Q

Mitral cells (located in the Mitral cell layer), like Tufted cells, function to:

A

Relay olfactory information to the rest of the brain

134
Q

Granule cell (located in Granule cell layer, projections don’t go anywhere else) functions to:

A

Modify signal inside the olfactory bulb

135
Q

Within the olfactory bulb, we find glomeruli, where the axon terminals from olfactory neurons synapse (EAA) on the dendritic trees of the post-synaptic neurons. What are 3 kinds of post-synaptic neurons?

A
  1. Mitral cells (Mitral cells Layer 4)
  2. Tufted cells (External Plexiform Layer 3)
  3. Periglomerular cells (axons will remain in the olfactory bulb - Layer 2)
136
Q

There is tremendous convergence of the olfactory neurons onto the ______ and _____ cells.

A

Mitral and Tufted

-Convergence helps to intensify the signal for detection

137
Q

Mitral and Tufted cells join the olfactory tract in order to:

A

Relay information to the brain

138
Q

The Periglomerular cells release ____ at their synaptic contacts with other glomeruli and inhibit the activity from those glomeruli. Why?

A

GABA

  • Since these glomeruli are likely related odorants, the odorant producing the strongest stimulation will suppress the input from other glomeruli that weren’t as strongly activated
  • Improves the signal specificity in the brain
139
Q

Granular cells (Layer 5), like Periglomerular cells, also release GABA at their synaptic contacts, but they synapse with _____ and _____ cells.

A

Mitral and Tufted

140
Q

After leaving the olfactory bulb, the first synapse is in the:

A

Anterior olfactory nucleus

  • Relay information to the contralateral side
  • Axons also continue on to the ipsilateral side
141
Q

The olfactory cortex is composed of several parts: (4)

A
  • Piriform cortex
  • Anterior cortical amygdaloid nucleus
  • Periamygdaloid cortex
  • Lateral entorhinal cortex
142
Q

What is the primary olfactory cortex?

A

Piriform cortex

143
Q

The olfactory cortex as a whole is responsible for:

A

-Identifying the odorant
-Arriving at an experience of ‘smell’
(not the only processing that must occur)

144
Q

TQ: What is the role of the Entorhinal cortex?

A

Relays information to the hippocampus

-Crucial in memory formation

145
Q

Memory formation and recall is facilitated by:

A

Olfactory input

146
Q

TQ: The Piriform cortex projects to the lateral hypothalamus, which is important in the control of ______.

A

Appetite

duh - olfactory inputs can influence appetite

147
Q

TQ: The Piriform cortex also projects to the medial orbitofrontal cortex (via the thalamus) to provide more advanced processing that is used to:

A

Identify the flavor of foods, among other things

148
Q

The olfactory cortex also sends input BACK to the olfactory bulb/olfactory epith to:

A

Modify the receptor responses to odorants via Centrifugal fibers
(e.g., if you’re hungry, you’re more sensitive to food smells)

149
Q

What are the 5 taste buds/receptors distributed on the tongue/mouth?

A
  1. Sweet (sugar)
  2. Bitter (citrus peels)
  3. Salty
  4. Sour (vinegar)
  5. Umami (savory - meat)
150
Q

How are sour tastes produced?

A

Hydrogen ion enters the taste bud via H+ channel

151
Q

How are salty tastes produced?

A

Na+ or Ca++ ion enter the taste bud via Na+ or Ca++ channel

152
Q

How are umami (savory) tastes produced?

A

Metabotropic glutamate receptor activated by glutamate

153
Q

How are sweet and bitter flavors produced?

A

Second-messenger systems to depolarize the cell, but they’re not directly related to the metabotropic receptors that detect the umami (savory) sensation

154
Q

Gustatory inputs synapse in the: (3)

A
  1. NTS
  2. Thalamus
  3. Gustatory Cortex (includes anterior insular cortex)
155
Q

From the thalamus, the axons go to the cortex AND to the ______ ________, which has a significant impact on appetite.

A

Lateral hypothalamus

156
Q

Neither the Gustatory cortex nor the Olfactory cortex can provide information regarding:

A

Flavor

157
Q

Perception of Flavor requires: (3)

A
  1. Gustatory input from the Gustatory cortex
  2. Olfactory input from the Olfactory cortex (esp Piriform cortex)
  3. Somatosensory info from the mouth (there’s food in my mouth)
158
Q

TQ: Neurons from the Gustatory cortex, Olfactory cortex, and Somatosensory info send axons to the ______ ______ _______ cortex to produce the sensation of flavor and appreciation of food

A

Lateral posterior orbitofrontal cortex

159
Q

A large part of what we ‘taste’ was really detected in our noses. Therefore, anything that interferes with the sensation of smell will:

A

Alter the tastes/flavors we perceive

e.g., in the common cold, tastes are different due to the damage on olfactory epith

160
Q

Near vision is harder than far vision b/c:

A

It takes more refraction (bending) to make the diverging rays focus on the retina

161
Q

To focus the image on the retina, the eye uses:

A

Refraction

162
Q

Where is the first site (and best) for refraction?

A

Cornea

  • 2/3 of the ability of the eye to bend light
  • Amount of bending is fixed (can’t control it)
163
Q

What part of the eye actually allows us to see near vs. far?

A

Lens

-Allows convergence on the retina (more specifically, the fovea, with all the cones - best for color and acuity)

164
Q

Accommodation requires: (3)

A
  1. Ciliary muscle
  2. Suspensory ligaments
  3. Lens itself
165
Q

Near vision:

  • Ciliary muscle ________, suspensory ligaments are released
  • > Natural elasticity of the lens causes lens to become (more/less) round
  • > (Increased/Decreased) curvature of the lens increases the refractive power of the lens
A

Contracts
More
Increased

166
Q

Far vision:

  • Ciliary muscle _______, suspensory ligament tension is increased
  • > Natural elasticity of the lens causes lens to become (more/less) round
  • > (Increased/Decreased) curvature of the lens (lens flattens) decreases the refractive power of the lens
A

Relaxes
Less
Decreased

167
Q

The near response includes: (3)

A
  1. Contraction of the ciliary muscles
  2. Convergence of the eyes to the point of focus
  3. Constriction of the pupil
168
Q

Multiple cell types in the retina: (5)

A
  • Photoreceptors (rods & cones) (straight to brain)
  • Bipolar cells (straight to brain)
  • Ganglion cells (straight to brain)
  • Horizontal cells (modifier)
  • Amacrine cells (modifier)
169
Q

The vertical pathway of the retina:

A
  • Photoreceptor - provides input
  • Bipolar cell - relay (link) b/t photoR and ganglion cell
  • Ganglion cell - provides output, leaves via optic N
170
Q

The photoRs (rods & cones) have a constant release of:

A

Glutamate

171
Q

When it’s dark, the release of glutamate is (high/low).

A

High

172
Q

When a photon activates the photoR, the release of glutamate (increases/decreases).

A

Decreases

173
Q

Vertical pathway for cones: (3)

A
  1. Photoreceptor struck by a photon

2. Decreases NT release onto Bipolar cell (NT = glutamate)

174
Q

Describe ON-center bipolar cells in terms of photoreceptor activation.

A
  • Activation of a photoreceptor in the center of the bipolar cell’s receptive field causes depolarization and the bipolar cell
  • Activation of a photoreceptor in the surrounding region causes hyperpolarization
175
Q

Describe OFF-center bipolar cells in terms of photoreceptor activation.

A
  • Activation in the center causes hyperpolarization

- Activation in the surrounding region causes depolarization

176
Q

If the photoreceptor activates an ON-center bipolar cell:

  • What receptor is activated?
  • NT release causes (incr/decr) in cation influx
  • In the dark, the ON-center cell is (depol/hyperpol)
A
  • Metabotropic receptor
  • NT causes decrease cation influx
  • Dark = hyperpolarized
177
Q

With light, release of glutamate from the photoreceptor (incr/decr)

  • > cation current (incr/decr)
  • > ON-center bipolar cell is (depol/hyperpol)
A
  • Decreased glutamate release
  • Increased cation influx
  • Light = depolarized
178
Q

If the photoreceptor activates an OFF-center bipolar cell:

  • What receptor is activated?
  • NT release causes (incr/decr) in cation influx
  • In the dark, the OFF-center cell is (depol/hyperpol)
A
  • AMPA receptor (non-NMDA)
  • NT release causes an increase in cation influx
  • Dark = depolarized
179
Q

Ganglion cells are also: (2)

A

ON-center or OFF- center

whatever the connecting bipolar cell is

180
Q

When do we actually see action potentials in the vertical pathway for cones?

A

Ganglion cell axons become the fibers on the optic nerve

NT = glutamate

181
Q

The vertical pathway for rods is composed of:

A
  • Many rods
  • Converge on one ON-center Bipolar cell
  • > synapses on an A11 amacrine cell
  • > synapses on a Cone ON-center Bipolar cell
  • > Activates a Ganglion cells
182
Q

What situation is for Rods?

A

Low-light

-We need many rods to converge on a Bipolar cell to increase our chances of seeing what we need to see

183
Q

Role of ON-center and OFF-center cells:

A
  • Help to increase the ability to detect edges (therefore help to sharpen our vision)
  • ON-center cell tells us where something begins;
  • OFF-center cell tells us where it ends
184
Q

The amacrine and horizontal cells add to the ON- and OFF-center cell roles by providing _______ signals that modify activity of neighboring photoreceptors, bipolar cells or ganglion cells.

A

Inhibitory

185
Q

In what cells to action potentials occur?

A

Ganglion cells

186
Q

The retina from each eye sees:

A

Two different visual fields

187
Q

Reconstructing the visual image:

Functions of the Lateral Geniculate Body (LGN): (4)

A
  • Identify major elements within our visual image
  • Identify motion
  • Control the motions of the eyes
  • Control focusing
188
Q

Reconstructing the visual image:

The Primary Visual Cortex (V1): 6 layers

A
  • Layers 1, 2, and 3 allow networking between V1 and other parts of cortex
  • Layer 4 receives inputs from the LGN (crucial)
  • Layers 5 & 6 send information BACK to the LGN
189
Q

The cortex is composed of columns that start from the surface of the cortex and extend through all 6 layers of V1 cells. Neighboring columns have (related/unrelated) jobs.

A

Neighboring columns have RELATED jobs.

-e.g., If one column detects horizontal edges, a neighboring column detects edges oriented at 30 degrees

190
Q

A lot of columns in V1 receive input from photoreceptors in the:

A

Macula (location of greatest receptor density)

191
Q

Major job of V1:

A

To identify the edges/contours

192
Q

Major job of V2:

A

To identify disparities in the visual images presented by the two eyes (used for depth perception)

193
Q

Another role of V1:

A 
Color detection (basic)
-Accurate color detection depends on the input from all three sets of cones (RGB)
194
Q

Major job of V4:

A

To complete the processing of the color inputs

195
Q

Although we’ve processed the image, we could NOT: (4)

A

-Name the image
-Copy the image
-Aim at the object in the image
-Recognize your husband/wife/mother/father
(We must rely on other areas of cortex to interpret what the primary visual cortex and assoc areas have done so far

196
Q

What is the role of the DORSAL pathway leaving the occipital cortex?

A

The DORSAL pathway relays visual information to the motor cortices (parietal/frontal lobes) and enables us to complete motor acts based on visual input
(e.g., play catch with your friends)

197
Q

What is the role of the VENTRAL pathway leaving the occipital cortex?

A

The VENTRAL pathway relays visual information to areas of the brain (temporal lobe) involved in higher processing of sensory inputs… the integration of visual input with other sensory inputs
(e.g., Naming the object, copying the object)

198
Q

Describe higher processing in the visual lobe.

A
  • Copying and naming/recognizing are separate functions and damage to the temporal lobe can selectively impair one without impairing the other
  • Similar or related objects are all coded for in localized regions
  • Facial recognition

Neuro 1 Midterm (5 decks)

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