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Lectures Flashcards

1
Q

Types of receptors

A

1) Ionotropic
excitatory - Glutamate - AMPA + KA –> Na+
NMDA –> Na+ + Ca2+
Acetylcholine - nicotinic –> Na+
inhibitory - GABA - GABAA –> Cl-
Glycine - Glycine R –> Cl-
2) Metabotropic
excitatory - Glutamate - mGluR 1-8
Acetylcholine - muscarinic (M1- M5)
inhibitory - GABA - GABAB –> prevents Ca2+ entry

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2
Q

Summation

A

1) Temporal - 1 neuron, high frequency, <15ms

2) Spatial - multiple neurons, low frequency

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3
Q

Refractory period

A

1) Absolute - Na+ channels inactive –> nothing can overcome
2) Relative - K+ channels open –> very strong repolarisation needed

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4
Q

Cotransmission

A

Vesicles containing a neuropeptide Y, substance P and VIP are co-released with the typical NTs for:
complex effects
longer lasting
prevents blockage of main NT by still carrying functions

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5
Q

Types of fibres

A

1) Proprioception, Vibration, fine touch - heavily myelinated, fast conducting, large diameter
A alpha - proprioception from muscle spindles
A beta - touch (slightly slower)
2) Pain, Temp, crude touch - unmyelinated, slower, smaller diameter
A delta - pain and temperature
C fibres - Pain, temp, itch

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6
Q

Types of neurons

A

1) Pseudounipolar - 1st order - somatosensory pathway
2) Multipolar - Reflex arc - motor neurons
3) Bipolar - Special senses

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7
Q

Dorsal Column

A

Touch and proprioception
2 major tracts -
fasciculus gracilis - medial dorsal column - lower limb (after C6)
fasciculus cuneatus - lateral dorsal column - upper limb (before C6)

1) 1st order neuron ascends in dorsal column and ipsilaterally
synapses with 2nd order neuron at either nuceli gracilis or cuneatus (lower or upper limb)
2) 2nd order neuron decussate in the low medulla
3) 2nd order neuron synapses with 3rd order neuron at the thalamus and projects into somatosensory cortex (post central gyrus)

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8
Q

Spinothalmic pathway

A

Pain and Temperature
2 major tracts -
Anterior - crude touch and pressure
lateral - pain and temperature

1) 1st order synapses with 2nd order neuron immediately at the dorsal root ganglion
2) 2nd order neuron ascends in either anterior or lateral fasciculi of the spinal cord an decussate 2/3 of the way there and continues to ascend on the contralateral side.
3) 2nd order neuron synapses with 3rd order neuron at the thalamus and projects into somatosensory cortex

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9
Q

Posterior Dorsal Spinocerebellar Tract

A

Direct – no decussation
2 neuron pathway –> fine movement to individual muscles

1st order neuron ascends to the upper lumbar segment/ CLARKE’S COLUMN in the IPSILATERAL POSTERIOR SPINOCEREBELLAR TRACT to the cerbellum via the INFERIOR CEREBELLAR PEDUNCLE.

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10
Q

Anterior Ventral Spinocerebellar Tract

A

Double cross - Ipsilateral also
2 neuron pathway –> movement of limb as a whole

1st order neuron ascends to the upper lumbar segment where they synapse with 2nd order neurons.
2nd order neurons then ascend in the CONTRALATERAL ANTERIOR SPINOCEREBELLAR TRACT to the cerbellum via the SUPERIOR CEREBELLAR PEDUNCLE where it decussates again to terminate on the Ipsilateral side.

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11
Q

Acuity

A

This is the ability to discriminate between 2 points.

1) Density of receptors inc - inc acuity
2) size of receptors dec - inc acuity
3) connection with other second order neurons more connections = more signals
4) lateral inhibition - capacity of an excited neuron to inhibit the other. Axon collaterals activate inhibitory interneurons which then inhibit surrounding neurons = 1 clear signal

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12
Q

Adaptation and types of receptors

A

Adaptation that is the reduction of receptor (generator) potential overtime despite continued presence of a stimulus. Hence a reduction in the frequency of AP.

1) tonic receptors - slow increase in frequency overtime –> continuous
muscle stretch
merkel’s disc
ruffini
2) phasic receptors - rapidly adapt with the fast decrease in frequency
meissner corpuscle
pacinian corpuscle
olfactory
3) phasic-tonic - rapidly decrease but has long-lasting tonic response after

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13
Q

Supporting Cells of NS

A

Glial cells provide structural support and Myelin

1) astrocytes - structural support and blood brain barrier
2) oligodendrocytes - form myelin in the CNS
3) Schwann cells - form myelin in the PNS
4) ependymal cells - cells that line the ventricles and produce CSF
5) microglial - macrophages of the CNS

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14
Q

Fibres within the brain

A

1) Association fibres - same hemisphere
2) commissural fibres - crosses hemisphere
3) projection fibres - cortex to sub cortical structures

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15
Q

Reflex arcs

A

Three components - none involved in the Brain.

1) afferent sensory neuron - carries AP to spinal cord at the dorsal root.
2) interneuron (area of integration) - received AP from afferent neurons and elicits excitatory or inhibitory effects and activates AP in motor neurons
3) Motor neuron - leaves from ventral horn to effector organ skeletal muscle (somatic) or smooth/cardiac (ANS)

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16
Q

what brain area is rich in enkephalin synapses

A

periaqueductal grey

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17
Q

Why does some motion eg spinning lead to dizziness?

A

movement of the otoliths (crystals) to the semi-circular canal

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18
Q

Function of palatine tonsil

A

produces lymph which drains into the jugulodigastric group of lymph nodes

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19
Q

what part of the neuron does the following

  1. receives signal
  2. transmits signal
A
  1. dendrite

2. axon

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20
Q

what is stimulus duration based on?

A

duration of AP

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21
Q

is the stimulus duration based on the continual presence of stimulus

A

NO

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22
Q

what structure does a reflex integrate with directly?

A

Spine

**NOT the brain

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23
Q

Give an example of a monosynaptic reflex

A

stretch reflex

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24
Q

describe the structure of B type fibres

A

myelinated, small diameter fibres of ANS

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25
Q

where is melatonin produced

A

pineal gland

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26
Q

function of melatonin

A

induces sleep

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27
Q

what hormone is secreted during NREM or slow wave sleep

A

Growth hormone

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28
Q

what ion contributes to excitotoxicity within neuronal cells?

A

Calcium

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29
Q

Sweat glands are stimulated by the _________ NS.

A

Cholinergic Sympathetic

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30
Q

What produces CSF? What percentage does it produce?

A

choroid plexus (70%), other brain capillaries

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31
Q

Absorption in the subarachnoid space is done by ________.

A

Bulk transport

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32
Q

What is the value of normal ICP?

A

10mmHg

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33
Q

An increase in _______ leads to an increase in ICP.

A

volume

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34
Q

What does the 1A sensory afferents synapse on?

A

alpha motor neuron

**NO INTERNEURON

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35
Q

What do muscle spindles regulate?

A

length/rate of change of length

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36
Q

What does golgi tendon organs regulate?

A

tension/rate of change of tension

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37
Q

What is the relationship of length and tension of muscles?

A

they are inversely proportional

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38
Q

Where are the muscle spindles found?

A

They are found in the extrafusal fibres which wraps around the intrafusal fibres.

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39
Q

How is muscle length and tension balanced?

A

Muscle spindles –> 1A –> CNS –> alpha motor neurons –> extrafusal fibres –> length
Golgi tendon –> 1B –> CNS –> gamma motor neurons –> intrafusal fibres –> tension

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40
Q

What is the relationship between firing of sensory receptors and 1) stretch, 2) tone?

A

as firing increases, stretch increases, tone decreases

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41
Q

What happens to the length and tone of the muscle after the initial stretch.

A

stretch –> muscle contracts –> length dec, tone inc

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42
Q

What regulates tone?

A

stretch reflex

**tone is not a characteristic of the muscle itself

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43
Q

Describe the mechanism by which golgi tendon organ works.

A

detects tension

inhibits alpha motor neuron

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44
Q

Describe the sequence of occurrences of the knee jerk.

A

tapping patellar ligament –> brief stretch of the muscle –> stretch of muscle spindles –> firing of 1A sensory afferent fibres increases –> alpha motor neuron activity in quads increases –> contraction of quads –> knee extends and leg kicks forward.

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45
Q

What are polysynaptic reflexes?

A

These reflexes involve 1 or more interneurons.

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46
Q

When does reciprocal innervation occur? Explain the mechanism.

A

When a muscle (protagonist) contracts, interneurons release inhibitory NTs (such as GABA, Glycine) causing the antagonist muscle to relax.

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47
Q

What is the antagonist of the knee-jerk reflex?

A

semitendinosus

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48
Q

Explain the withdrawal reflex.

A

it is a polysnaptic reflex.
sensory neurons –> interneuron –> stimulates biceps (flexor) to contract ; inhibits contraction of the extensor triceps (antagonist)

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49
Q

Explain the responses of the flexors and extensors during the crossed extensor reflex.

A

+ flexor 1, - extensor 1
- flexor 2, + extensor 2

**spinal reflexes are not limited to one side of the body such as the crossed reflex

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50
Q

What are the classifications of pain and nociceptors? Are they adaptive or maladaptive?

A

Actue - adaptive
Subacute - adaptive
Chronic - maladaptive

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51
Q

Describe the characteristics of acute pain.

A

transient
few seconds
associated with detection of potentially tissue damaging stimuli.

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52
Q

Describe the characteristics of subacute pain.

A

associated with tissue damage and immune cell infiltration

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53
Q

Describe the characteristics of chronic pain.

A

exceeds possibility to resolve damage

may become pathological

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54
Q

What does it mean if a pain is said to be adaptive?

A

there is a protective mechanism present to prevent further damage

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55
Q

What are nociceptors?

A

pain receptors that respond to a mechanical or chemical stimuli or both.

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56
Q

What is the term given to describe a nociceptor that responds to both types of stimuli?

A

polymodal

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57
Q

what type of fibres are involved in the pain pathway?

A

Adelta and C

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58
Q

Describe the pain associated with A delta fibres.

A

highly localised first pain

afferent pathway for reflex - low threshold

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59
Q

Describe the pain associated with C fibres.

A

polymodal, poorly localised, second pain, much slower

high threshold

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60
Q

Where does the somatic pain pathway pass?

A

goes along lateral spinothalmic tract (corticospinal)

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61
Q

What does the salience model of drug taking imply?

A

Users want the drug more when reward the cues are present

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62
Q

The opening of a what channel is common to both graded potentials and action potentials?

A

Sodium channels

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63
Q

What nociceptive stimuli is released by the immune system?

A

Inflammatory chemicals such as histamine

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64
Q

Falx cerebri

A

separates hemispheres of the cerebrum

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65
Q

separates hemispheres of the cerebrum

A

Falx cerebri

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66
Q

tentorium cerebeli

A

separates cerebrum and cerebellum

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67
Q

separates cerebrum and cerebellum

A

tentorium cerebeli

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68
Q

what produces aqueous humour?

A

cilliary between cornea and lens of eye and retinal cells in the vitreous part of the eye.

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69
Q

What cells have the longest source of electrical signals of output to the optic nerve?

A

ganglion cells

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70
Q

What cells contribute to visual signal transduction?

A

horizontal

amacrine

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71
Q

What nucleus regulates the circadian rhythm? where is it located?

A

Suprachiasmatic nucleus in hypothalamus

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72
Q

What is the significance of a vitamin A deficiency?

A

nightblindness

inability ot regenerate rhodopsin

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73
Q

What vitamin is important in the regeneration of rhodopsin?

A

Vitamin A

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74
Q

What characteristic of light do neurons in the visual cortex respond to?

A

orientation

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75
Q

what structure within the eye is over-represented in visual processing?

A

fovea

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76
Q

What part of the brain re-inverts an image?

A

cortex

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77
Q

what is the sensory component of the occulomotor nerve?

A

optic nerve

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78
Q

eustation tube function

A

connects nasal cavity to middle ear

equalizes pressure and drains fluid from the throat

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79
Q

what is the result of a positive rinne/ weber test?

A

BC

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80
Q

what part of the inner ear controls balance?

A

vestibular

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81
Q

what part of the inner ear controls hearing?

A

cochlear

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82
Q

What comprises the continuous fluid system in the ear?

A

scala vestibuli

scala tympani

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83
Q

separation of scala vestibuli and scala tympani

A

helico trema directly

scala media indirectly

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84
Q

tectorial membrane

A

in the organ of corti
stiff membrane
involved in mechanotransduction of sound by shearing of cilia of hair cells

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85
Q

Damage to what structure within the ear causes a cochlear implant to not work?

A

cochlear nerve fibres

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86
Q

hair cells in cochlear apparatus

A

cilia

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87
Q

hair cells in vestibular apparatus

A

stereocilia

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88
Q

where is perilymph found

A

scala vestibuli

scala tympani

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89
Q

where is endolymph found

A

scala media

semicircular canals

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90
Q

rate of use of heat from metabolic oxidation of food

A

80kcal/hr

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91
Q

thermoneutral zone

A

range range where temperature control is maintained by vasomotor responses only

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92
Q

vasomotor responses

A

constriction and dilation of peripheral vessels

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93
Q

cranial nerve pain pathway

A
  • 1st order neuron travels via trigeminal nerve to brainstem
  • synapses with 2nd order neuron
  • decussates and ascends into thalamus
  • synapse with 3rd order neuron
  • to cortex
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94
Q

ascending nociceptive pathway

A

excitatory
glutamate - AMPA, NMDA, KA
Substance P - Neurokinin 1

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95
Q

Descending nociceptive pathway

A

inhibitory
GABA - GABAa, GABAb
opioids - afferent pain fibres (3 receptors)
endocannabinoids

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96
Q

What substance allows for the transmission of signals from periphery to brain?

A

substance P

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97
Q

action of opiates

A

inhibit NT release from 1st order neurons and hyperpolarise the 2nd order neurons

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98
Q

types of endogenous opioid receptors

A

Mu and beta endorphins – increases K+ conductance on postsynaptic neuron
delta and enkephalins
kappa and dynorphins

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99
Q

action of endogenous opioid receptors

A

inhibits substance P and glutamate release by stopping ca2+ release and inhibit their effects on postsynaptic neurons, hyperpolarising them
Mu and beta endorphins – increases K+ conductance on postsynaptic neuron

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100
Q

where are endogenous opioid receptors found?

A

pre-synaptic except Mu

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101
Q

action of endocannabinoids

A

GABA released - binds to GABA receptor on post-synaptic neuron
releases 2-AG and Anandamides into synaptic cleft
bind to GPCR cannabinoid receptors (CB1, CB2)
analgesic effects

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102
Q

inhibition of adenylyl cyclase leads to ….

A

decrease cAMP
blocks Ca2+ channels
increase K+ channels

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103
Q

k+ is mediated by what endogenous opioid receptor

A

Mu

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104
Q

Gate theory

A

lg diameter fibres (Aalpha and Abeta) synapse with interneurons
block transmission of c fibres

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105
Q

what is the ‘gate’ in gate theory

A

interneurons

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106
Q

when is the gate open

A

no stimuli

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107
Q

the large fibre _____ the gate
the small _______ it
no fibre _____ it

A

closes
opens
closes

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108
Q

Allodynia

A

feeling of pain when not normally stimulated

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109
Q

hyperalgesia

A

enhanced sensation of pain at normal threshold

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110
Q

enhanced states of pain

A

protective measures of sensitisation

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111
Q

protective measures of sensitisation

types

A

enhanced states of pain
peripheral
central

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112
Q

peripheral sensitisation

A

release of substance p –> increase in sensitivity in surrounding cells

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113
Q

release of substance p –> increase in sensitivity in surrounding cells

A

peripheral sensitisation

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114
Q

central sensitisation

A

increase NMDA receptors on dendrites of second order neurons

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115
Q

increased NMDA receptors on dendrites of second order neurons

A

central sensitisation

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116
Q

pathological pain

A

chronic pain

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117
Q

neuropathic pain

A

neural lesions

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118
Q

symptoms of neural lesions

A

positive - increased chronic pain

negative - sensory loss/ numbness

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119
Q

dysfunctional pain

A

non-neural lesion

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120
Q

symptoms of non-neural lesion

A

positive - increased chronic pain

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121
Q

types of neuropathic pain

A 
central:
strokes
cord injury 
MS
PD

peripheral:
Nerve fibres
diabetic neuropathy

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122
Q

diabetic neuropathy

A

peripheral neuropathic pain

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123
Q

strokes

A

central neuropathic pain

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124
Q

corticobulbar pathway

A

conveys info from cortex to cranial nerve motor nucleus

UMN axons –> genu –> decussate just before synapsing with LMN

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125
Q

cell body of UMN

A

pre central gyrus

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126
Q

cell body of LMN in corticobulbar pathway

A

motor nucleus of trigeminal nerve

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127
Q

corticospinal pathway

A

conveys info from cortex to ventral horn cells of spinal cord
UMN axons –> posterior limb –> through midbrain, pons, pyramids
85% decussates at pyramids –> lateral corticospinal tract –> descends spinal cord and synapses with LMN
15% does not decussate –> anterior corticospinal tract –> descend and decussate near termination (LMN)

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128
Q

cell body of LMN in corticospinal pathway

A

ventral horn

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129
Q

decussation in lateral corticospinal tract

A

85%

at pyramids

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130
Q

decussation in anterior corticospinal tract

A

15%

near termination

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131
Q

What pathway passes through the genu?

A

corticobulbar pathway

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132
Q

What pathway passes through the posterior limb of the internal capsule?

A

corticospinal pathway

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133
Q

decussation in corticospinal pathway

A

just before synapsing with LMN

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134
Q

Extrapyramidal pathways

A

rubrospinal
tectospinal
vestibulospinal

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135
Q

rubrospinal pathway

A

cerebellum –> cortex

tone of flexor muscles of limbs

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136
Q

tectospinal pathway

A

superior colliculi

reflex movement to audio and visual stimuli

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137
Q

vestibulospinal pathway

A

vestibular nuclei in pons and medulla

tone of extensor muscles

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138
Q

tectum

A

posterior to aqueduct in midbrain

superior and inferior colliculi

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139
Q

superior colliculi

A

visual reflex

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140
Q

inferior colliculi

A

auditory reflex

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141
Q

tegmentum

A

all of brainstem anterior to aqueduct

homeostatic and reflexive pathways

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142
Q

consciousness

A

state of self awareness

ability to respond to stimuli

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143
Q

sleep

A

changed consciousness, can be aroused by stimulation

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144
Q

coma

A

profound unconsciousness
inability to respond and sense external stimuli
loss of the sleep-wake cycle

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145
Q

vegetative state

A

unconsciousness
when coma progresses
sleep-wake cycle
no response to external stimuli other than pain

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146
Q

brain dead

A

lack of brain activity and cranial nerve reflexes

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147
Q

state of self awareness

ability to respond to stimuli

A

consciousness

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148
Q

changed consciousness, can be aroused by stimulation

A

sleep

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149
Q

profound unconsciousness
inability to respond and sense external stimuli
loss of the sleep-wake cycle

A

coma

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150
Q

unconsciousness
when coma progresses
sleep-wake cycle
no response to external stimuli other than pain

A

vegetative state

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151
Q

lack of brain activity and cranial nerve reflexes

A

brain dead

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152
Q

stages of sleep

A 
awake with eyes open 
awake with eyes closed
NREM 1
NREM 2
NREM 3
NREM 4
REM
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153
Q

rhythm when awake with eyes open

A

beta

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154
Q

rhythm when awake with eyes closed

A

alpha

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155
Q

NREM 1

A

light sleep
slow eye movement
theta waves of high amplitude and low frequency

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156
Q

NREM 2

A 
no eye movement 
slow brain waves
bursts of rapid waves
low frequency 
k complexes 
spindles
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157
Q

NREM 3

A

extremely slow

delta waves interrupted by small and faster waves

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158
Q

NREM 4

A

exclusively delta waves

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159
Q

REM

A

EEG - fast and low amplitude
EOG - very rapid eye movements
EMG - flaccid/ hypotonic (little to no wave)

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160
Q

light sleep
slow eye movement
theta waves of high amplitude and low frequency

A

NREM 1

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161
Q 
no eye movement 
slow brain waves
bursts of rapid waves
low frequency 
k complexes 
spindles
A

NREM 2

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162
Q

extremely slow eye movement

delta waves interrupted by small and faster waves

A

NREM 3

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163
Q

exclusively delta waves

A

NREM 4

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164
Q

EEG - fast and low amplitude
EOG - very rapid eye movements
EMG - flaccid/ hypotonic (little to no wave)

A

REM

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165
Q

theta waves

A

NREM 1

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166
Q

k complexes

spindles

A

NREM 2

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167
Q

delta waves interrupted by small and faster waves

A

NREM 3

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168
Q

exclusively delta waves

A

NREM 4

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169
Q

slow eye movement

A

NREM 1

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170
Q

no eye movement

A

NREM 2

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171
Q

extremely slow eye movement

A

NREM 3

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172
Q

no response to external stimuli other than pain

A

vegetative state

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173
Q

inability to respond and sense external stimuli

A

coma

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174
Q

brain wave of: NREM 1

A

theta waves

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175
Q

brain wave of: NREM 2

A

k complexes

spindles

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176
Q

brain wave of: NREM 3

A

delta waves interrupted by small and faster waves

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177
Q

brain wave of: NREM 4

A

exclusively delta waves

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178
Q

brain wave of: REM

A

EEG - fast and low amplitude
EOG - very rapid eye movements
EMG - flaccid/ hypotonic (little to no wave)

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179
Q

How long does it take to complete 1 alternating cycle of the sleep cycle?

A

90 minutes

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180
Q

As sleep progresses, NREM sleep becomes ___A____ while REM sleep becomes ___B___.

A

A - less deep

B - longer

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181
Q

In what order does the stages of NREM disappear?

A

1 and 4

3

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182
Q

How many alternating cycles are typically undergone in one night?

A

5-6

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183
Q

what trend is observed in the sleeping patterns of infants

A

many short naps which eventually increase in length and decrease in number

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184
Q

what trend is observed in the sleeping patterns of adults

A

duration of sleep and length of REM becomes shorter

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185
Q

What age group is known to have many short naps which eventually increase in length and decrease in number

A

infants

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186
Q

What controls the sleep cycle?

A

RAS reticular formation

SCN (suprachiasmatic)

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187
Q

RAS reticular formation

A

controls sleep cycle
involves cholinergic neurons (Ach) and monoaminergic (monoamines)
During NREM both pathways slow down
During REM cholinergic neurons fire, monoaminergic stops

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188
Q

The pathways in the RAS reticular formation involve what type of neurons?

A

cholinergic neurons (Ach) and monoaminergic (monoamines)

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189
Q

What events occur during NREM of RAS reticular formation?

A

both pathways slow down

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190
Q

What events occur during REM of RAS reticular formation?

A

cholinergic neurons fire, monoaminergic stops

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191
Q

The response below is generated by the RAS reticular formation. Identify what stage of sleep has this response.
cholinergic neurons fire, monoaminergic stops

A

REM

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192
Q

The response below is generated by the RAS reticular formation. Identify what stage of sleep has this response.
both pathways slow down

A

NREM

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193
Q

SCN (suprachiasmatic)

A

controls sleep cycle

input from retina links light to day-night cycle

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194
Q

What gland makes melatonin?

A

pineal gland

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195
Q

function of melatonin

A

induce sleep

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196
Q

In a standard sleep schedule, at what point is the sleep schedule is growth hormone release?

A

NREM/ slow wave sleep

10pm - 2am

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197
Q

Where is CSF made?

A

tufts of capillaries that invaginate ventricles called the choroid plexus

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198
Q

What part of the brain is CSF transported to after production?

A

subarachnoid space (cisterns)

199
Q

what mechanisms are used to transport CSF to the subarachnoid space?

A

passive and active transport

200
Q

function of CSF

A

supports and protects the brain

201
Q

structure of choroid plexus

A

2 cell thick layer

endothelial cells of capillary and ependymal cells (tight junction)

202
Q

describe the movement of hydrophilic molecules across the blood CSF barrier.

A

do not freely move

rely on transport proteins (glucose - GLUT1)

203
Q

describe the movement of hydrophobic molecules across the blood CSF barrier.

A

freely moves across both layers

204
Q

What type of molecules do not freely move through the blood CSF barrier and rely on transport proteins.

A

hydrophilic molecules

205
Q

What type of molecules freely moves across both layers of the blood CSF barrier.

A

hydrophobic molecules

206
Q

compare the composition of blood and CSF

A 
CSF has:
more Na+Cl-
less glucose 
little to no proteins 
less K+
207
Q

Between blood and CSF which has:

more Na+Cl-

A

CSF

208
Q

Between blood and CSF which has:

less glucose

A

CSF

209
Q

Between blood and CSF which has:

little to no proteins

A

CSF

210
Q

Between blood and CSF which has:

less K+

A

CSF

211
Q

Between blood and CSF which has:

less Na+Cl-

A

Blood

212
Q

Between blood and CSF which has:

more glucose

A

blood

213
Q

Between blood and CSF which has:

more K+

A

blood

214
Q

What forms the blood-CSF barrier?

A

choroid plexus
capillaries
transporters

215
Q

Compare the BBB and the CSF-blood barrier.

A

functionally the same]
structurally different - BBB is only one cell think composed of flattened endothelial cells of capillaries connected by tight junctions and astrocytes.

216
Q

describe the structure of the BBB

A

only one cell think composed of flattened endothelial cells of capillaries connected by tight junctions and astrocytes.

217
Q

What type of cells are found in the CSF-blood barrier but not the BBB?

A

ependymal cells

218
Q

One structural similarity of the CSF-blood barrier and the BBB

A

presence of tight junctions

219
Q

What type of cell is found in the BBB but not in the CSF-blood carrier?

A

astrocytes

220
Q

What is the function of astrocytes in the BBB?

A

give structural support

221
Q

function of the BBB

A

maintains constant environment for neurons in CNS

222
Q

Clinical significance of BBB when taking medications.

A

avoids CNS side effects as the drug must be able to cross the BBB

223
Q

How do the presence of tumours disrupt the functioning of the BBB when taking medications?

A

They have no barriers and hence allows for the free entry of substances

224
Q

Is the cranium compressible?

A

NOPE

225
Q

How does a rise in ICP affect blood vessels?

A

compresses them

226
Q

How does a rise in ICP affect cerebral blood flow?

A

decreases –> ischemia

227
Q

What is cushing’s reflex?

A

a pathophysiological reflex triggered when there is a severe decreases in cerebral perfusion.

228
Q

describe cushing’s reflex.

A

a pathophysiological reflex triggered when there is a severe decreases in cerebral perfusion. –> hypercapnia and hypoxia –> activates medullary vasomotor centre –> increases peripheral vasoconstriction –> blood redirected to brain –> increase in arterial Bp (increase in firing of baroreceptors) –> reflex bradycardia (cardio inhibitory centre)

229
Q

end result of cushing’s reflex.

A

reflex bradycardia

230
Q

there is an increase in firing of what type of receptors as arterial Bp incresases?

A

baroreceptors

231
Q

what does a decrease in cerebral perfusion lead to in cushing’s reflex?

A

hypercapnia and hypoxia

232
Q

hypercapnia and hypoxia activates what centre of the brain?

A

medullary vasomotor centre

233
Q

what does the activation of the medullary vasomotor centre result in?

A

increases peripheral vasoconstriction

234
Q

what there is an increase in peripheral vasoconstriction, what happen to the blood during cushing’s reflex?

A

redirected to brain

235
Q

the blood redirected to brain in cushing’s reflex results in what?

A

increase in arterial Bp

236
Q

“brain’s shortcut for emotion” pathways

A

slow - proper interpretation

fast - thalamus –> amygdala - autonomic arousal and hormonal responses

237
Q

what emotional pathway allows for proper interpretation

A

slow

238
Q

what emotional pathway allows for autonomic arousal and hormonal responses

A

fast

239
Q

what structures are involved un the fast emotional pathway?

A

thalamus –> amygdala

240
Q

what are the functions of the hypothalamus

A 
modulation of ANS activity
modulates the circadian rhythm 
controls homeostasis
controls emotional behaviour 
*hunger centre
241
Q

where is the hunger centre of the brain located?

A

lateral hypothalamus

242
Q

what does a damage in the hunger centre lead to?

A

lack of appetite

243
Q

what results from a lesion of the anterior hypothalamus

A

disruption in circadian rhythm

244
Q

hippocampal formation

A

structures involved in learning, memory and recognition of novelty

245
Q

amygdaloid complex

A

modulates endocrine activity, sexuality, reproduction, autonomic responses and emotion.
facilitates perceptual and memory functions in those regions

246
Q

what part of the brain is involved in learning, memory and recognition of novelty

A

hippocampal formation

247
Q

what part of the brain modulates endocrine activity, sexuality, reproduction, autonomic responses and emotion.

A

amygdaloid complex

248
Q

what part of the brain facilitates perceptual and memory functions in those regions

A

amygdaloid complex

249
Q

What key structures regulate emotions

A

orbital prefrontal cortex and ventromedial prefrontal cortex
dorsolateral prefrontal cortex
amygdala
anterior cingulate cortex

250
Q

what parts of the PFC are involved in regulation of emotional responses?

A

orbital prefrontal cortex and ventromedial prefrontal cortex

dorsolateral prefrontal cortex

251
Q

function of PFC

A

tasks that need attention
inhibitory control
decision making

252
Q

what is the result of the destruction in any key emotional regulatory structure?

A

increase propensity for impulsive aggression and violence

253
Q

Kluver-Bucy Syndrome

A

after bilateral destruction of the anterior temporal lobes, including the amygdaloid complex
symptoms: triad of docility (absence of fear), hyperorality and hyper-sexuality

254
Q

the triad of docility (absence of fear), hyperorality and hyper-sexuality is associated with what illness?

A

Kluver-Bucy Syndrome

255
Q

what is the name given the illness cause by the bilateral destruction of the anterior temporal lobes, including the amygdaloid complex

A

Kluver-Bucy Syndrome

256
Q

is the amygdaloid complex destroyed in Kluver-Bucy Syndrome?

A

YUP

257
Q

damage to amygdala

A

decrease conditioned fear response

decreased ability to recognise meaningful facial and vocal expressions of anger in others

258
Q

damage to hippocampus

A

inability to make and store long term memories

259
Q

death of neuronal hippocampal cells are present in what illness?

A

Alzheimers

260
Q

What physical changes do the hippocampus and amygdala undergo in schizophrenia

A

decrease in size

261
Q

A decrease conditioned fear response is a typical symptom of damage to what structure of the brain?

A

amygdala

262
Q

A decreased ability to recognise meaningful facial and vocal expressions of anger in others is a typical symptom of damage to what structure of the brain?

A

amygdala

263
Q

The inability to make and store long term memories is a typical symptom of damage to what structure of the brain?

A

hippocampus

264
Q

What happen to the cells of the hippocampus in an illness such as Alzheimers?

A

death of neuronal hippocampal cells

265
Q

The hippocampus and amygdala decrease in size in what illness?

A

schizophrenia

depressive disorder

266
Q

what does anxiety result from?

A

hyper-activation of the amygdala

267
Q

in severe anxiety disorders, what structures are not functioning normally? what happens?

A

decreased threshold for amygdala to detect potential threats
decrease in ventrolateral prefrontal cortex activation (severe)

268
Q

What physical changes occur to structures in the brain in depressive disorders?

A

decrease size of amygdala

decrease size of PFC specifically the orbitofrontal cortex

269
Q

in depressive disorders, what structures are not functioning normally? what happens?

A

increased amygdala activation in response to fear and sad faces
increased activity of PFC (ventral)

270
Q

How do antidepressants work?

A

they decrease the hyperactivation of the amygdala and the ventral PFC

271
Q

what is the maslow heirachy of motivation

A

from bottom –> top
physiological (water and food)
safety (security and protection)
love/belongingness (closeness and affiliation)
esteem (self and others)
self-actualisation (express oneself; growth; actualise potential of one’s self)

272
Q

place the following elements of the maslow heirachy of motivation in order (bottom to top)
esteem (self and others)
love/belongingness (closeness and affiliation)
physiological (water and food)
self-actualisation (express oneself; growth; actualise potential of one’s self)
physiological (water and food)

A

from bottom –> top
physiological (water and food)
safety (security and protection)
love/belongingness (closeness and affiliation)
esteem (self and others)
self-actualisation (express oneself; growth; actualise potential of one’s self)

273
Q

Motivation disorders can be broadly categorised into __A__ categories. what are these categories. give an example of each.

A

A - 2

1) apathy and physiological defects (eg. schizophrenia and mood disorders)
2) addictions (misdirection of motivation) - Eg frug addiction

274
Q

schizophrenia and mood disorders falls into what category of motivation disorder?

A

apathy and physiological defects

275
Q

what is the basic mechanism of integration of motivation in the brain

A

the brain weighs the cost:benefit ratio depending on: physiological state
environment
past history

276
Q

How does the brain interpret repeat experiences?

A

repeat experiences make pathways that links the experience to specific thoughts, memories and behaviours.

277
Q

How does an increase in dopamine affects behavioural patterns?

A

reinforces the behaviour

278
Q

Anterior cingulate cortex (ACC)

A

regulates one’s own behaviour and monitors the behaviour of others
determines when behaviour needs to be modified

279
Q

what part of the brain makes dopaminergic neurons?

A

pars compacta of the substantia nigra

280
Q

what does the pars compacta produce?

A

dopaminergic neurons

281
Q

Nucleus Accumbens

A

evaluates stimuli that produces a wanting or liking response (usually those that release dopamine)
learning from feedback and in reward based decision-making.

282
Q

substantia nigra and the ventral tegmental areas

A

produces dopamine

delivers it to other regions that are involved in motor function and in motivating and rewarding behaviours

283
Q

raphe nuclei

A

seretonin production

deliver to network circuits in the brain including structures related to motivation, reward and threat detection

284
Q

what structure produces serotonin?

A

raphe nuclei

285
Q

what structure delivers dopamine to other regions that are involved in motor function and in motivating and rewarding behaviours

A

substantia nigra and the ventral tegmental areas

286
Q

where is dopamine delivered to?

A

other regions that are involved in motor function and in motivating and rewarding behaviours

287
Q

where is seretonin delivered to?

A

to network circuits in the brain including structures related to motivation, reward and threat detection

288
Q

Serotonin pathways

A

key factor in ‘liking’
combines with other neurochemical to convey euphoria
widest distribution in the brain
major influence on emotional states, sleep cycles, eating and other rewarding behaviours

289
Q

What substance conveys euphoria?

A

Serotonin

290
Q

What substance has the widest distribution in the brain?

A

Serotonin

291
Q

What substance has a major influence on emotional states, sleep cycles, eating and other rewarding behaviours

A

Serotonin

292
Q

what does Serotonin influence?

A

emotional states, sleep cycles, eating and other rewarding behaviours

293
Q

What psychiatric diagnoses involves a dysregulation of serotonin?

A

depression

294
Q

What psychiatric diagnoses are involved with motivational deficits?

A 
depression
schizophrenia
bipolar disorder
PTSD
anxiety disorders
295
Q

How do motivational deficits affect normal functioning?

A

interfere with cognitive abilities
impede functional outcomes
impair subjective wellbeing

296
Q

1 Main negative symptom of schizophrenia?

A

avolition - decrease in motivated self-initated purposeful activities

297
Q

1 criteria of manic/ hypomanic episodes

A

increase in goal-directed activity

298
Q

Aberration in reward processing can lead to …

A

addiction

299
Q

What is used in the treatment of addictions?

A

extrinsic motivators to change behaviour

300
Q

cognitive/ behavioural approaches

A

creating reward contingencies that modify deficits or excesses in behaviour

301
Q

what is deep brain stimulation used for?

A 
essential tremour
parkinson's disease
treatment refractory major depression
OCD 
Chronic pain
302
Q

what are the major functions of the frontal lobe?

A 
(motor)
movement
executive control
planning
language
personality
303
Q

which part of the brain controls movement

A

frontal lobe

304
Q

which part of the brain controls executive control

A

frontal lobe

305
Q

which part of the brain controls planning

A

frontal lobe

306
Q

which part of the brain controls language

A

frontal lobe

307
Q

which part of the brain controls personality

A

frontal lobe

308
Q

what are the functional parts of the frontal cortex? how many parts are there?

A

3 part
primary motor - gross and fine movement
premotor cortex - planning and selective movement
prefrontal cortex - integrates multimodal sensory information (post gyrus)

309
Q

what is the function of the primary motor?

A

gross and fine movement

310
Q

what is the function of the premotor cortex?

A

planning and selective movement

311
Q

what is the function of the prefrontal cortex?

A

integrates multimodal sensory information (post gyrus)

312
Q

what part of the brain controls gross and fine movement

A

frontal lobe - primary motor

313
Q

what part of the brain controls planning and selective movement

A

frontal lobe - premotor cortex

314
Q

what part of the brain integrates multimodal sensory information (post gyrus)

A

frontal lobe - prefrontal cortex

315
Q

frontal lobe damage

A

problems in intellectual abstraction and concentration
problems with executive function, sequencing and speed
personality changes - instability, social difficulties, says what they think (disinhibition)
Broca’s Aphasia - difficulty producing speech, disjointed words, comprehension preserved, aware of problem
inability to find and create patterns or to change action when rules have changed.

316
Q

what causes problems in intellectual abstraction and concentration?

A

frontal lobe damage

317
Q

what causes problems with executive function, sequencing and speed

A

frontal lobe damage

318
Q

what causes personality changes - instability, social difficulties, says what they think (disinhibition)

A

frontal lobe damage

319
Q

what causes Broca’s Aphasia

A

frontal lobe damage

320
Q

what causes inability to find and create patterns or to change action when rules have changed.

A

frontal lobe damage

321
Q

what causes difficulty producing speech, disjointed words, comprehension preserved, aware of problem

A

frontal lobe damage - Broca’s Aphasia

322
Q

what is Broca’s Aphasia

A

difficulty producing speech, disjointed words, comprehension preserved, aware of problem by frontal lobe damage to Broca’s area

323
Q

what lobe controls motor function?

A

frontal

324
Q

what lobe controls senses and perception?

A

parietal

325
Q

what is the function of the parietal lobe?

A 
somatosensory with info from visual system
perception of language
attention
learning
coordination in space
326
Q

what lobe is responsible for perception of language

A

parietal lobe

327
Q

what lobe is responsible attention

A

parietal lobe

328
Q

what lobe is responsible learning

A

parietal lobe

329
Q

what lobe is responsible learning coordination in space

A

parietal lobe

330
Q

what is the importance of the functional parts of the parietal lobe?

A

primary somatosensory cortex - receives and interprets sensory information (contralateral)
somatosensory unimodal association area - further processes sensory information
multimodal sensory association area - interprets afferents from somatosensory, visual, auditory and movement in 3D space

331
Q

what part of the brain interprets movement in 3D space

A

multimodal sensory association area or parietal lobe

332
Q

what results from parietal lobe damage

A

denial/ neglect of 1/2 of the visual field (contralateral)
apraxia - inability to carry out movement
agnosias - inability to recognise words, numbers and location
difficulty integrating information from various parts of the body
difficulty with skills requiring knowledge of relations (eg numbers)
difficulty with skills requiring manipulation of objects

333
Q

how is agnosias tested?

A

maze

334
Q

what is apraxia?

A

inability to carry out movement

335
Q

what is the name of the illness characterised by the inability to carry out movement?

A

apraxia

336
Q

what is agnosias?

A

inability to recognise words, numbers and location

337
Q

what is the name of the illness characterized by the inability to recognise words, numbers and location?

A

agnosias

338
Q

what causes denial/ neglect of 1/2 of the visual field (contralateral)

A

parietal lobe damage

339
Q

what causes apraxia

A

parietal lobe damage

340
Q

what causes inability to carry out movement

A

parietal lobe damage

341
Q

what causes agnosias

A

parietal lobe damage

342
Q

what causes inability to recognise words, numbers and location

A

parietal lobe damage

343
Q

what causes difficulty integrating information from various parts of the body

A

parietal lobe damage

344
Q

what causes difficulty with skills requiring knowledge of relations (eg numbers)

A

parietal lobe damage

345
Q

what causes difficulty with skills requiring manipulation of objects

A

parietal lobe damage

346
Q

what is lobe of the brain is involved in vision?

A

occipital

347
Q

what is the importance of the functional parts of the occipital lobe?

A

Primary visual cortex - initial processing of visual information from thalamus
Visual unimodal Association area - further Processing of the visual information from primary visual cortex

348
Q

where does visual information go after being processed by the occipital lobe?

A

Multimodal sensory Association areas of the parietal and temporal lobe

349
Q

Where are the multimodal sensory Association areas located in the brain?

A

Parietal and temporal lobe

350
Q

Visual information from the occipital lobe goes to which lobes?

A

Parietal and temporal lobe

351
Q

What results from occipital lobe damage?

A

Cortical blindness - lesion in primary visual cortex, normal eye, visual stimuli received but cannot be interpreted - confabulates the response
Inability to recognise what is seen, cannot draw what is in front of them.

352
Q

what causes Cortical blindness

A

occipital lobe damage

353
Q

what causes lesion in primary visual cortex, normal eye, visual stimuli received but cannot be interpreted -confabulates the response

A

occipital lobe damage

354
Q

what causes Inability to recognise what is seen, cannot draw what is in front of them.

A

occipital lobe damage

355
Q

what is cortical blindness?

A

lesion in primary visual cortex, normal eye, visual stimuli received but cannot be interpreted - confabulates the response

356
Q

what is the function temporal lobe?

A 
auditory 
memory
language comprehension
taste 
smell
facial recognition
357
Q

what part of the brain is responsible for language comprehension

A

temporal lobe

358
Q

what part of the brain is responsible for facial recognition

A

temporal lobe

359
Q

what part of the brain is responsible for taste

A

temporal lobe

360
Q

what part of the brain is responsible for smell

A

temporal lobe

361
Q

what are the functional regions if the temporal lobe?

A

primary auditory cortex
auditory unimodal association areas
visual unimodal association (also in occipital)
multimodal sensory association areas
limbic association areas - memory, learning, feelings, emotions associated with senses (visual and auditory stimuli)
amygdala and hippocampus - components of limbic system

362
Q

what results from temporal lobe damage?

A

Wernicke’s aphasia - loss of comprehension, silent reading, speaks fluently with no meaning
memory difficulties - left damage - impaired verbal memory, right damage - impaired non-verbal memory (music)
difficulty recognizing faces
inability to characterize objects

363
Q

what causes Wernicke’s aphasia

A

temporal lobe damage

364
Q

what causes loss of comprehension, silent reading, speaks fluently with no meaning

A

temporal lobe damage - Wernicke’s aphasia

365
Q

what causes memory difficulties

A

temporal lobe damage

366
Q

what causes impaired verbal memory

A

temporal lobe damage left damage to memory

367
Q

what causes impaired non-verbal memory (music)

A

temporal lobe damage - right damage to memory

368
Q

what causes difficulty recognizing faces

A

temporal lobe damage

369
Q

what causes inability to characterize objects

A

temporal lobe damage

370
Q

what is Wernicke’s aphasia

A

loss of comprehension, silent reading, speaks fluently with no meaning

371
Q

what illness is characterised by loss of comprehension, silent reading, speaks fluently with no meaning

A

Wernicke’s aphasia

372
Q

is a person with Wernicke’s aphasia aware of their problem?

A

NOPE

373
Q

What do the characteristics of light govern?

A

wavelength - colour (ROYGBIV) (780-550-400)

amplitude - brightness

374
Q

what is the wavelength of red light?

A

780

375
Q

what is the wavelength of violet light?

A

400

376
Q

what is the wavelength of green light?

A

550

377
Q

what is the relationship of wavelength, frequency and energy?

A

wavelength is inversely proportional to frequency and energy

378
Q

significance of choroid

A

nutritional

pigments

379
Q

significance of retina

A

photoreceptors and neurons

380
Q

significance of cornea

A

2/3 of the light converges

381
Q

what produces aqueous humour

A

ciliary

382
Q

significance of iris

A

adjusts pupil diameter by the contraction of radial and circular muscles

383
Q

what is responsible for the adjustment of pupil size

A

radial and circular muscles

ie dilator and sphincter pupillae

384
Q

significance of lens

A

adjusts focal length

385
Q

how does the lens adjust focal length

A

by changing the curvature by the suspensory ligaments and the ciliary apparatus

386
Q

significance of macula

A

region containing fovea

387
Q

significance of fovea

A

only cones

most photoreceptors at this point

388
Q

what structure of the eye converges light?

A

cornea (2/3)

lens (1/3)

389
Q

what alters the shape of the lens?

A

ciliary muscles of the PNS (III)

390
Q

what is the shape of the lens?

A

biconcave

391
Q

explain the alteration of the shape of the lens in viewing a distant image?

A

distant vision –> relax –> flatten lens –> increase in focal length –> no stimulation

392
Q

explain the alteration of the shape of the lens in viewing a near image?

A

near vision –> contracts –> more convex –> decrease in focal length –> PNS stimulation

393
Q

stimulation of the PNS is involved in ______ vision.

A

near

394
Q

the lens flattens when viewing a ____ object.

A

distant

395
Q

the lens takes on a more convex shape when viewing a ______ object.

A

nearby

396
Q

the ciliary muscles ____ in distant vision

A

relaxes

397
Q

the ciliary muscles ____ in near vision

A

contracts

398
Q

the focal length _____ in distant vision

A

increases

399
Q

the focal length _____ in near vision

A

decreases

400
Q

is the pupil a hole?

A

YES

401
Q

what induces a change in pupil diameter?

A

change in light intensity

402
Q

how does a change in light intensity affect the pupil?

A

change is diameter

403
Q

explain the alteration of pupil diameter in response to light intensity.

A

PNS –> pupil constriction –> circular muscle (sphincter pupillae) –> reduces light –> increase DoF (depth of focus) and decrease FoV (field of view)

SNS –> pupil dilation –> radial muscles (dilator pupillae) –> increases light –> decrease DoF and increase FoV

404
Q

what NS is responsible for pupil constriction

A

PNS

405
Q

what NS is responsible for pupil dilation?

A

SNS

406
Q

what changes in DoF and FoV result from the pupil constriction?

A

increase DoF (depth of focus) and decrease FoV (field of view)

407
Q

what changes in DoF and FoV result from the pupil constriction?

A

decrease DoF and increase FoV

408
Q

what is the retina

A

it is the part of the eye where the image is focused on and is comprised of 3 layers

409
Q

how many layers does the retina had?

A

3

410
Q

what are the layers of the retina

A

photoreceptors - rods and cones (graded potential to bipolar cells)
bipolar cells - receives graded potential from photoreceptors and releases NTs from ganglion cells
ganglion cells - axons of which form the optic nerve and send out action potential

411
Q

photoreceptors

A

rods and cones (graded potential to bipolar cells)

412
Q

bipolar cells

A

receives graded potential from photoreceptors and releases NTs from ganglion cells

413
Q

ganglion cells

A

axons of which form the optic nerve and send out action potential

414
Q

the axons of which cell type directly contact the optic nerve?

A

ganglion cells

415
Q

where are NTs in the eye released from?

A

ganglion cells

416
Q

what cell causes the release of NTs

A

bipolar cells

417
Q

what cells in the eye generate a graded potential?

A

photoreceptors

418
Q

what cells in the eye generate an action potential

A

ganglion cells

419
Q

parts of retina

A

neural - deals with perception and transduction of light into electrical signals
pigmented - lines retina

420
Q

function of neural part of retina

A

deals with perception and transduction of light into electrical signals

421
Q

what part of the retina deals with perception and transduction of light into electrical signals

A

neural part

422
Q

what is the thinnest part of the retina

A

fovea

423
Q

what is the center if the retina

A

fovea

424
Q

what part of the retina has the highest density of photoreceptors?

A

fovea

425
Q

what part of the retina has only cones?

A

fovea

426
Q

what part of the retina has no blood vessels

A

fovea

427
Q

what part of the retina has no photorecptors?

A

optic disc

428
Q

what does the optic disc contain?

A

optic nerve

central retinal artery and vein

429
Q

compare the central and peripheral retina

A

central retina has less photoreceptors per ganglion cells

430
Q

melanopsin

A

light sensitive pigment that only absorbs 720-480 nm

contributes to circadian rhythm in SCN of the hypothalamus

431
Q

what wavelength of light can melanopsin absorb?

A

720-480 nm

432
Q

what is the name give to the light sensitive pigment in the eye?

A

melanopsin

433
Q

What pigment in the eye contributes to the circadian rhythm?

A

circadian rhythm

434
Q

function of rods

A

light intensity

435
Q

quantity of rods

A

very high except in fovea

436
Q

structure of rods

A

outer segment has more discs

437
Q

what part of the rods have more discs?

A

outer segment

438
Q

distribution of rods

A

mostly in peripheral areas

439
Q

what do rods detect

A

single photons

440
Q

what is an important characteristic of rods that allows it to detect single photons?

A

high sensitivity to light

441
Q

describe the acuity of rods

A

low acuity as they converge onto the same ganglion

442
Q

do rods contribute to colour vision?

A

NO

443
Q

function of cones

A

colour and sharp image production

444
Q

quantity of cones

A

less except at fovea

445
Q

structure of cones

A

outer segment has less discs - discs contain photopigments

446
Q

what do the discs of cones contain?

A

photopigments

447
Q

where are cones mostly found?

A

macula (includes fovea)

448
Q

describe the sensitivity to light of a cone

A

low

449
Q

compare rods and cones in terms of pigments and signal amplication

A

cones have less pigments (less discs) and less signal amplification

450
Q

types of cones

A

3
short - blue - 430
medium - green - 530
long - red - 690 (MOSTLY)

451
Q

what is the most abundant type of cone?

A

long - red - 690

452
Q

significance of types of cones

A

allow for high absorption of light in 3 distinct regions

453
Q

how does the brain interpret colour

A

there is overlap where the incoming light stimulates each cone differently
the brain compares relative stimulation of each type of cone to interpret the colour

454
Q

difference in process of phototransduction of rods and cones

A

no difference in process
rods - rhodopsin
cones - iodopsin

455
Q

explain the process of phototransduction

A
  1. light triggers conformational change of retinal from cis to trans and activates it into rhodopsin
  2. the activated opsin activates transduction which activates PDEs (phosphodiesterases)
  3. the activated PDE converts cGMP to GMP and this decrease in cGMP levels causes closure of the Na+ channels which can only be opened when cGMP is present
  4. the closure of the channels leads to the decrease in Nt release (eg. glutamate) which causes hyperpolarization (-40 to -70). The degree in reduction of glutamate release determines light intensity/ brightness.
  5. graded potentials are then presented to bipolar cells. the decrease in glutamate, increases depolarisation.
  6. depolarisation of bipolar cells leads to release of another graded potential to ganglion cells which send action potential through its axons
456
Q

where is rhodopsin found?

A

rods

457
Q

where is iodopsin found?

A

cones

458
Q

what is rhodopsin

A

chromophore

composed of retinal (vitamin a derivative) and opsin protein

459
Q

what substance inhibits bipolar cells?

A

glutamate

460
Q

phototransduction - ______ triggers conformational change of retinal from cis to trans and activates it into rhodopsin

A

light

461
Q

phototransduction - light triggers conformational change of _________________ and activates it into rhodopsin

A

retinal from cis to trans

462
Q

phototransduction - the activated opsin activates ______ which activates PDEs (phosphodiesterases)

A

transduction

463
Q

phototransduction - the activated opsin activates transductuction which activates _________

A

PDEs (phosphodiesterases)

464
Q

phototransduction - light triggers conformational change of retinal from cis to trans and activates it into _______

A

rhodopsin

465
Q

phototransduction - the activated PDE converts ______ and this decrease in cGMP levels causes closure of the Na+ channels which can only be opened when cGMP is present

A

cGMP to GMP

466
Q

phototransduction - the activated PDE converts cGMP to GMP and this decrease in cGMP levels causes closure of the _____ which can only be opened when cGMP is present

A

closure of the Na+ channels

467
Q

phototransduction - the closure of the channels leads to the _________ which causes hyperpolarization (-40 to -70).

A

decrease in Nt release (eg. glutamate)

468
Q

phototransduction - The degree in reduction of glutamate release determines _________.

A

light intensity/ brightness

469
Q

phototransduction - graded potentials are then presented to ____ cells.

A

bipolar

470
Q

phototransduction - the decrease in glutamate, ______ depolarisation.

A

increases

471
Q

phototransduction - depolarisation of bipolar cells leads to _______ to ganglion cells which send action potential through its axons

A

another graded potential

472
Q

Colour blindness

A

inherited absence of one or more types of cones

473
Q

types of colour blindness

A

protanope - red cone cells defective
deuteranope - green cone cells defective
tritanope - blue cone cells defective

474
Q

protanope

A

red cone cells defective

475
Q

deuteranope

A

green cone cells defective

476
Q

tritanope

A

blue cone cells defective

477
Q

red cone cells defective

A

protanope

478
Q

green cone cells defective

A

deuteranope

479
Q

blue cone cells defective

A

tritanope

480
Q

what determines the eye’s sensitivity to light?

A

the amount of photosensitive pigments

481
Q

dark adaptation

A

light –> dark
insufficient light to activate cones
must wait for regeneration of rhodopsin
scotopic vision

482
Q

light adaptation

A

dark –> light
rod cells are bleached
brain switched to cone-only information processing

483
Q

light –> dark
insufficient light to activate cones
must wait for regeneration of rhodopsin
scotopic vision

A

dark adaptation

484
Q

dark –> light
rod cells are bleached
brain switched to cone-only information processing

A

light adaptation

485
Q

outline the visual pathway

A

eye –> optic chiasm –> lateral geniculate nucleus of thalamus –> primary visual cortex –> 2 pathways

1) parietal lobe –> perception of movement
2) temporal lobe –> perception of shape and colour

486
Q

incoming light affects what side of eye

A

nasal of the same eye
temporal of the opposite
they cross over at the optic chiasm

487
Q

where do neurons involved in the visual pathway synapse

A

lateral geniculate nucleus of thalamus

488
Q

which axons in the visual pathway decussate?

A

nasal

489
Q

which axons in the visual pathway do not decussate?

A

temporal

490
Q

what structure cortically processes neurons of the visual pathway?

A

lateral geniculate nucleus of thalamus

491
Q

what is the result of the cortical processing of neurons?

A

topographical maps from patterns of illuminations in order to vender movement (parietal), shapes and movement (temporal) in 3D space

492
Q

significance of topographical maps from patterns of illuminations made by the brain

A

result of the cortical processing of neurons

fxn - to vender movement (parietal), shapes and movement (temporal) in 3D space

493
Q

pupil light reflex

A

shining a light in the eye –> optic nerve sends info to occipital lobe but goes to the edinger-westphal nucleus in the midbrain before going to the lateral geniculate nucleus –> parasympathetics of CN III travel with Va where it synapses at the ciliary ganglion before continuing to the sphincter pupillae which causes the pupil to constrict in both eyes

Finals (17 decks)

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