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Neurophysiology > Quiz #2 > Flashcards

Quiz #2 Flashcards

0
Q

What processes occur during experimental phase of neural development?

A
  • experience changes synapses from the time of birth throughout and individuals life
  • wiring by firing = Hebb’s rule
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1
Q

What processes occur during the developmental phase of neural darwinism?

A
  • genetics present before birth of child

- neural darwinism and apoptosis

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2
Q

What is Neural Darwinism?

A
  • theory of neuronal group selection
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3
Q

What is Developmental Selection?

A
  • genes generate a hugee population of neural and glial cells to select for network building (making network larger through life and death of neural and glial cells)
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4
Q

What is Experiential Selection?

A
  • experience leads to changes in connection strength of synapses, which favour some pathways and weaken others
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5
Q

What are the 2 forms of Neural Darwinism?

A
  • Developmental

- Experiential

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6
Q

What is the organization of the ocular dominance column?

A

the columns are found in layer 4 of the striate cortex (of the monkeys)

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7
Q

In ocular dominance column, what is the distribution of LGN and where do the zones appear?

A
  • LGN serves one eeye

- zones appear in patches within layer 4 (zebra stripes if superficial 1-3 layers peeled away)

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8
Q

What do dark bands get information from? light bands?

A

dark bands - get information from one eye
light bands - get information from the other eye
* alternating stripes - ZEBRA LOOK

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9
Q

Input from the LGN serving the 2 eyes are intermingled in where? over time?

A
  • layer 4

- over time - ocular dominance columns in layer 4

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10
Q

The zebra stripes begin to form due to what?

A

competition dominance

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11
Q

What is the critical period?

A
  • if eye covered at birth then lose segregation and sending of information from that eye => lack of dominance and see black shapes (due to lack of information from the monocular eye development)
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12
Q

What does monocular input beginning at birth lead to?

A

complete eye dominance

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13
Q

When is the process of ocular dominance column formation?

A

complete by 6 week

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14
Q

What is monocular deprivation in the early stages post birth?

A

lose eye information and less striping in layer 4 of the cortex

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15
Q

What does deprivation at 2,3,6 weeks have on monocular deprivation?

A

weaker effect on the ocular dominance columns since they become more segregated with time

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16
Q

What is the Hebbs synaptic learning/plasticity rule for LTP and LTD?

A

when an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased

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17
Q

What is a Hebbs synapse?

A
  • pre and post synaptic simultaneous/ concurrent activity
  • produces increased synaptic transmission efficiency/strength
  • initially signal is only strong enough so that A fires
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18
Q

What is an Anti-hebbian synaptic process?

A
  • an unused connection decays
  • triggered by non-concident pre and post synaptic activity
  • produces a weakening r decrease in synaptic strength and efficiency, if depression is persistent (LTD)
  • initially cell A or B doesnt fire (silent) => synapse A-B weakened
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19
Q

What does LTD stand for?

A

Long Term Depression

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20
Q

What does an inactivation of cell B do to an active cell A?

A

depression

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21
Q

What does an active cell B do to an active cell A?

A

potentiation

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22
Q

What does and inactive cell B do to an inactive cell A?

A

no change

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23
Q

What is Hebbs view?

A

chief mechanisms of learning and memory is simply the strengthening of synaptic connections between brain cells of an assembly

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24
Q

What are the different processing streams in neural circuits?

A

divergence
convergence
hierarchical

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25
Q

What is divergence?

A

one source cell can send info to multiple targets in the same area, or multiple targets in 2 different areas

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26
Q

What is convergence?

A

many sources converge onto one neuron. source signal can come from multiple neurons in one area or multiple neurons in different areas

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27
Q

What 4 types of processing occur in hierarchical circuits?

A

serial information processing
parallel information processing
reciprocal information processing
local circuit connections

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28
Q

What is serial information processing?

A

information handed from area to area in a sequence at each level processing is regulated by other kinds of local circuits

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29
Q

What are parallel information processing?

A

information flows through hierarchy in a side by side fashion

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30
Q

What is reciprocal information processing?

A

information may flow back and forth within circuits

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31
Q

what are local circuit connections?

A
  • both feedforward and feedback as well as excitatory and inhibitory
  • information alters the processing at each hierarchical stage determining the nature of information that will be sent to the next stage
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32
Q

What is feed forward excitation?

A

helps to sustain the excitatory discharge response over time

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33
Q

What is elicited inhibition?

A

produces on/off gating by the effected nerve cell

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34
Q

What are feedforward excitation and inhibition?

A

elicited excitation

elicited inhibition

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35
Q

What are feedback excitation and inhibition

A

recurrent excitation

recurrent inhibition

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36
Q

What is recurrent excitation?

A

accelerates the original outputs overtime - feedback amplification

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37
Q

What is recurrent inhibition?

A

feedback signal from post synaptic cell comes back to slowly suppress cell output over time

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38
Q

What is a disinhibition circuit?

A

inhibition of inhibition that leads to the release of excitation

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39
Q

Where are feedback inhibition, feedforward inhibition and dis-inhibitory connections found?

A

spinal cord motor circuitry

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40
Q

What are Principal cells?

A

pyramidal cell

spiny stellate cell

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41
Q

What are pyramidal cells?

A

converge multiple signals and then send one signal out to an excitatory cell

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42
Q

What are spiny stellate cells?

A

one neuron sends out to multiple signals

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43
Q

What are the features of principal cells

A
  • ~80% circuit neurons
  • Glutaminergic
  • excitatory synaptic actions
  • electrical synapses are absent
  • local intrinsic and projection extrinsic targets
  • reciprocal connection with other principal cells, interneurons and with themselves
  • dendritic spines on both cell types
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44
Q

What is the electrophysiology of principal cells?

A

each type of principal “excitatory” neuron expresses a specific combination of membrane ion channels, produces certain numbers of each channel, uniquely modifies each channels molecular structure. And distributes signal in a characteristic pattern across the membrane surface to generate a specific type of electrical behav

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45
Q

What are special about glutamatergic principal cells?

A

can be modifies by experience = hebbian plasticity

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46
Q

What are the features of interneurons?

A
  • GABAergic
  • inhibitory synaptic actions: feedforward, feedback and recurrent
  • interneuron subtypes: form reciprocal synaptic connections with other inhibitory interneurons and principal cells and with themselves
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47
Q

What are the subtypes of interneurons based upon?

A
  • molecular diversity and related electrophysiology
  • distinguished based on post synaptic targets, dendritic patterns and expression of key molecular markers
  • distinct inhibit netweorks - exxist as a result of gap junctional electrical coupling
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48
Q

What do interneurons perform on principal cells?

A

disinhibition

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49
Q

What are the function of interneurons?

A

inhibitory interneurons produce rapid alterations in time windows of synaptic convergence in targeted cells that allows coincident time binding across large numbers of neurons constituting hebbiaan assembly/cognitive network.

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50
Q

What are the old views of brain function?

A
  • brain structure is stable
  • brain circuitry is hard wired
  • cognitive functions and memory are localized
  • brain activity is driven by excitatory sensory input
  • information processing involves serial processing only
  • functions vulnerable to single site injury/lesion
  • limited clinical explanatory power
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51
Q

What are the new views of brain function?

A
  • brain structure is changeable
  • cognitive functions and memories are distributed
  • info processing involves SP, PP, RP streams together at the same time
  • brain activity is driven by internal intrinsic cycles
  • functions resistant to degradation by single site injury
  • excellent clinical explanatory power
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52
Q

What are the major nuclei of Ach?

A

nucleus basalis, pontopedunuclear-tegmental nuclei

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53
Q

What is the transmitter for Ach modulatory network?

A

Ach

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54
Q

What is the Ach synaptic action?

A

excitatory&inhibitory

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55
Q

What is the duration of Ach network?

A

fast/slow

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56
Q

What are the signal transduction for Ach?

A

nicotinic (iono (2))

muscarinic (metabo (5))

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57
Q

What does Ach control?

A

learning, memory, emotion, REM sleep

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58
Q

What are the major nuclei of NE network?

A

locus ceruleus of rostral pons

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59
Q

What is the transmitter of NE network?

A

norepinephrine

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60
Q

What is the synaptic action of NE?

A

excitatory & inhibitory

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61
Q

What is the duration of NE?

A

slow

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62
Q

What is the signal transduction of NE?

A

noradrenergic (metab (9r/c))

63
Q

What does NE control?

A

attention, supports learning & memory, emotions and deep slow wave sleep

64
Q

What are the major nuclei of DA network?

A

substantia nigra, ventral tegmental area, arcuate nuclei

65
Q

What is the transmitter for DA network?

A

dopamine

66
Q

What is the synaptic action of DA?

A

excitatory & inhibition

67
Q

What is the duration of DA?

A

slow

68
Q

What is the signal transduction of DA?

A

dopaminergic (metabo (5r/c))

69
Q

What does DA control?

A

emotion, learning, memory, movement regulation, positive reward system

70
Q

What are the major nuclei for 5HT (serotonin) network?

A

raphe nuclei

71
Q

What is the transmitter for 5HT?

A

serotonin

72
Q

What is the synaptic action of 5HT?

A

excitatory & inhibitory

73
Q

What is the duration of 5HT?

A

fast & slow

74
Q

What is the signal transduction for 5HT?

A

serotinergic (metabo (13r/c))

ionotropic (1r/c/)

75
Q

What does 5HT control?

A

inhibition of behaviour, emotion, learning, memory, deep sleep

76
Q

What are the major nuclei of HIS network?

A

tuberomammillary nuclei (MTn)

77
Q

What is the transmitter for HIS?

A

histamine

78
Q

What is the synaptic action of HIS?

A

excitatory

79
Q

What is the duration of HIS?

A

slow

80
Q

What are the signal transduction of HIS?

A

histaminergic (metabo (3r/c))

81
Q

What does HIS ccontrol?

A

attention, body energy stores, stress, learning and memory

82
Q

NE graph shows what when intern levels of arousal cognitive performance is the highest?

A

inverted U

83
Q

What are drugs of abuse?

A

psycho-stimulants that act to rapidly and abnormally increase 3 modulatory squad transmitters NE, 5HT, DA

84
Q

What are the short term effects of drug abuse?

A

euphoria, suppression of fatigue and appetite

85
Q

What are withdrawal symptoms of drug abuse?

A

dysphoria, depression, anxiety, fear, fatigue, exhaustion, hyperphagia

86
Q

What does cocaine do?

A

block dopamine uptake at synaptic cleft and increases potential dopamine transmission in nucleus accumbens

87
Q

What does amphetamine do?

A

increase dopamine release from vesicles in presynaptic terminal

88
Q

What does PCP do?

A

blocks input from other areas causing down regulation. blocks excitatory glutaminergic input to cortex decrease nucleus accumbens

89
Q

What do opiates do?

A

inhibit GABA neuron, reducing tonic inhibition of DA, thus increasing their firing increasing nucleus accumbens

90
Q

What does nicotine/alcohol do?

A

increase DA reward system within brain

91
Q

What is the pre-synaptic site of action of addictive drugs acting on dopamine reward network?

A
  • dis-inhibition action - heroin and THC decrease GABA release => increased VTA dopamine
  • presynaptic facilitation - of glutamate release by nicotine => leads to VTA dopamine neuron spiking
92
Q

What is ARAS?

A

Ascending reticular activating system

93
Q

What does ARAS regulate?

A

arousal and sleep/wake transitions

94
Q

What does ARAS relay input to?

A

relays sensory input to non specific areas of he brain (thalamus relays to specific areas)

95
Q

What are the functions of ARAS?

A
  • to alert/wake up cortex and prepare for more specific stimuli
  • tells the entire cortex to pay attention
  • brain stem ARAS makes diffuse connections to thalamic ARAS and cortex
  • damage to ARAS would result in deep coma
96
Q

What is the function of the thalamus?

A
  • tells and isolated area about a specific stimuli

- makes connections to specific cortical projections

97
Q

What type of input passes through the thalamus on its way to the cortex?

A

all sensory input except smell

98
Q

What are the nuclei of the thalamic ARAS?

A

(see notes)

99
Q

What is a cortical column?

A

information processing unit within a cortical module

100
Q

What are the cortical columns comprised of?

A

narrow chain of neurons that extend vertically across cellular layers 2-4

101
Q

What are the diameters of cortical columns?

A

sensory/motor = 100-500micrometers

association fibers = 200-500 micrometers

102
Q

What are the related properties and selectivities that neurons within a column show?

A
  • place - peripheral RF

- modality - nature of adequate stimuli that change discharge of cell

103
Q

What is the EJ Jones Rule?

A

inputs to column layer 4, outputs to layers 2 and 3 to other cortical columns/layers 5 and 6 to subcortical targets

104
Q

Can cortical columns be linked together?

A

yes. by short and long range horizontal intracortical synaptic connections to form larger groupings (modules)

105
Q

What is the sleep induction hypothesis?

A

when glial cell glycogen stores are depleted by repeat n.t. release during wakefulness, adenosine is released from glia and initiates non REM sleep (NREM).
Increased adenosine binds to specific r/c in cortex, thalamus and brainstem where they promote sleep induction.

106
Q

What is NREM?

A

deep or slow wave sleep

107
Q

What does the anabolic nature of sleep suggest?

A

a rest and restorative function - sleep conservation of energy. repair of injury, isolation and immobility as a defence from predation

108
Q

What is REM sleep?

A

dream sleep

109
Q

What occurs during REM sleep with the brain?

A

consolidation of daytime info into long term memory.
this stage of sleep prevents interference in the consolidation process by suppressing further sensory input and motor input

110
Q

What cortical area control working memory?

A

controlled by the prefrontal cortex

111
Q

What is the relationship between working memory and attention?

A

(see notes)

112
Q

What is working memory?

A

The ability to remember/retain certain “task” information and then recall it after a certain time period (delayed matching)

113
Q

What are the stages of a working memory model?

A
  • 1-cue period (10sec)- visual
  • 2-delay period (2min) - auditory
  • 3-response - visual motor
114
Q

What is selective attention?

A

Attention is the cognitive process of selectively concentrating on one aspect of the environment while ignoring other things. Attention has also been referred to as the allocation of processing resources.

115
Q

What is a STROOP test?

A

name the colours of the words, but do not read the words

116
Q

What brain area controls selective attention?

A

cingulate gyrus

117
Q

What brain areas regulate positive and negative emotions?

A

positive - ventral tegmental area

negative - locus ceruleus and nucleus raphe

118
Q

What are the neuro-modulators of positive and negative emotions?

A

positive - increased nucleas accumbens, and decreased amygdala
negative - increased amygdala, decreased nucleus accumbens

119
Q

What do we see with major depression?

A
  • abnormally increased rCBF in prefrontal cortex
  • abnormally increase of rCBF in amygdala
  • abnormal decrease in rCBF in caudate nucleus
  • these features relate to a patients excessive negative feelings and their inability to develop a strategy to escape from or solve the problem
120
Q

What are some examples of antidepressant drugs?

A

MAOIs, tricyclics, SSRIs

121
Q

What is the effects of MAOIs?

A

inhibitors enhance the action of NE and serotonin by preventing their enzymatic destruction

122
Q

What are the action of tricyclics and serotonin?

A

blocking uptake

123
Q

What is the effect of SSRIs?

A

selective for serotonin by preventing uptake

124
Q

What is the Theory of the Mind?

A

the ability to infer what others are thinking and feeling, inferring motive or intention on the part of others

125
Q

What are the features of TOM?

A
  • sensitive to understand emotional state of others
  • operates when you have positive emotion of love aand compassion for others, feelings of empathy
  • only observable in humans and appears at age 4-5
  • not working in autism or schizo or with sociopathic personalities
126
Q

What modulatory network supports TOM?

A

anterior paracingulate cortex activated awareness of mental state of self (desire, emotion, thought) and social interaction

127
Q

Where is the hippocampus located?

A

temporal lobe

128
Q

Whats the function of the hippocampus?

A

transferring short term memories into long term memories

129
Q

Specifically where does the hippocampus lie?

A

at the tail end of the fornix in the floor of the lateral ventricle

130
Q

What is the mossy fiber pathway?

A

connects with the pyramidal cells in areas CA3, where CA3 cells project to pyramidal cells in CA1 by schaeffer collaterals

131
Q

What happens when schaeffer collateral fibre pathway sends information from CA3 to CA1

A

see long term potentiation to CA1 region

132
Q

What is the perforant pathway?

A

major excitatory pathway with granule cells that give rise to form the mossy fiber pathway

133
Q

How can the features of hippocampal long term potentiation be demonstrated?

A

by stimulating two different fiber pathways converging onto a single CA1 pyramidal neuron

134
Q

How does LTD conduction occur?

A
  • glutamate binds to NMDA r/c
  • post synaptic neuron is strongly depolarized releasing Mg block of the NMDA r/c allowing Ca to flow through the channel
  • through Ca/calmodulin kinase and protein kinase see a retrograde messenger is triggered and causes increased glutamate release by presynaptic cell => enhance n.t. release
135
Q

What does LTP result in?

A

multiplication of synapses

136
Q

Where are most synapses located?

A

on dendritic spines

137
Q

What is the mechanism of synaptic modifications supporting NMDA r/c mediated LTP?

A
  • post synaptic density expands, perforates and splits into multiple densities
  • the presynaptic active zone splits into corresponding regions
  • perforated synapse further divides spine branches
  • branched spine ultimately become two spines each cntaining a synaptic region
138
Q

What are synaptic modifications supporting NMDA r/c mediated LTP in terms of AMPA r/cs?

A

strengthening individual synapses by increasing the number of AMPA r/c on the post synaptic membrane which increases the cells response to glutamate

  • Ca activates CaMK enzyme
  • 2nd messenger signal transduction pathways are activated - new AMPA r/c inserted into membrane
139
Q

What is cooperativity?

A

tetanize the weak and strong inputs individually. the weak input does not potentiate but the strong input does

140
Q

What is associativity?

A

tetanize the weak nd strong inputs simultaneous - both weak and strong inputs potentiate

141
Q

What is specificity?

A

tetanize the strong input alone - the weak input doesnt potentiate but the strong input

142
Q

What happens to the post synaptic activity when you inject EGTA?

A

no LTP

143
Q

What happens to the post synaptic activity when you raise extracellular Ca?

A

see LTP increase

144
Q

What happens to the post synaptic activity when prevent depolarization through intracellular hyperpolarization current inject?

A

no LTP

145
Q

What happens to the post synaptic activity when pair weak input with intracellular depolarization current injection?

A

increases LTP

146
Q

What does AVP do to LTP?

A

its an NMDA antagonist and blocks LTP

147
Q

What happens to LTD with low freq stimulation?

A
  • with small post synaptic depol

- not temporal summation of EPSPs

148
Q

What happens to LTD with postsynaptic depolarization?

A

strong hyperpolarization = no LTD

149
Q

What happens to LTD with a change in post synaptic Ca?

A
  • inject BAPTA (Ca chelator) = no LTD

- lower extracellular Ca - induce LTD instead of LTP

150
Q

Does AVP block LTD?

A

yes

151
Q

How can you convert LTD to LTP by adjusting membrane potential of post synaptic cell?

A

by changing depolarization in extracellular fluid

152
Q

What causes the conversion of LTD to LTP?

A

strong depol of post synaptic cell

153
Q

What is a serial scheme?

A

a lesion at B prevents information from A to be transmitted to C,D,E

154
Q

What is a Distribution scheme?

A

if a lesion at B, will have minimal impact on transfer of info from A to C,D,E

155
Q

What does a distribution scheme tell us?

A

time, location, quality, and magnitude of signal

Neurophysiology (3 decks)

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