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KINE 3670 > Final > Flashcards

Final Flashcards

1
Q

Is acetylcholine (ACh) excitatory or inhibitory?

A

excitatory

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2
Q

What is the function of ACh in the PNS?

A

activates skeletal muscles via ionotropic

inhibits muscles via metabotropic

helps w/autonomic NS (release adrenaline etc)

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3
Q

WHat is the function of the ACh in the CNS?

A

invoved w/synapses in short term memory

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4
Q

What is AChE inhibitors?

A

enhance ACh levels, used in elderly patients w/memory issues

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5
Q

What enzyme synthesizes ACh?

A

choline acetyltransferase (CAT)

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6
Q

What does CAT use to make ACh?

A

choline and acetate (from acetyl CoA)

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7
Q

How is choline transported back to presynaptic?

A

Na+ depedent choline co-transporter (ChT)

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8
Q

What breaksdown ACh?

A

acetylcholinesterase (AChE)

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9
Q

What is Sarin? How does it work??

A

nerve gas

inhibits AChE, causes muscle spasms + neuromuscular paralysis

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10
Q

What is atropine?

A

works as antidote to nerve gas (Sarin, insecticides)

blocks ACh muscarinic receptors

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11
Q

What are the two types of ACh receptors?

A

nicotinic (ionotropic) and muscarinic (metabotropic)

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12
Q

What inhibits nicotinic ACh receptors?

A

curare

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13
Q

Where are nicotonic receptors found?

A

neuromuscular junctions of skeletal muscles

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13
Q

Where are muscarinic receptors found?

A

neuromuscular junctions of smooth and cardiac muslce, glands

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13
Q

Is nicotonic receptors selective?

A

no, non selective channels

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13
Q

Where does ACh bind on nicotonic receptors?

A

on both of the alpha subunits

need both

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14
Q

What does black widow venom do?

A

stimulates release of ACh, causes muslce spasms and cramps

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15
Q

What does alpha-bungarotoxin do?

A

irreversibly binds to nAChR

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16
Q

What is the structure of nicotine similar to?

A

ACh

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17
Q

What does nicotine cause changes in?

A

number of cholinergic receptos and sensitivity of these receptors

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18
Q

How does nicotine trigger reward?

A

stimulates release of dopamine, directly and indirectly

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19
Q

What is myasthenia gravis?

A

autoimmune disease that disrupts nerve muscle signal transmission

attacks acetylcholine receptors

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20
Q

Myasthenia gravis most often affects?

A

women under 40 and men over 60

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21
Q

What are the symptoms of myasthenia gravis?

A

weakness and rapid fatigue in muscles that control the eye/eyelid, facial expressions, chewing, talking, swallowing, breathing, neck/limb movement

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22
Q

What gland is abnormal 75% of the time in myasthenia gravis patients?

A

thymus gland

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23
Q

What damage is seen in cells of person w/myathenia gravis?

A

lymphocyte aggregates, widening of synaptic cleft

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24
Q

What can cause myasthenia gravis?

A

some drugs, some viruses/infections

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25
Q

How can you diagnose myasthenia gravis?

A

blood tests, edrophonium test, nerve conduction studies

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26
Q

What are the treatments for myasthenia gravis?

A

AChE inhibitors, immunosuppresants, plasmaphersis, thymectomy

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27
Q

What is the main inhibitory neurotransmitter in brain?

A

GABA

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28
Q

Are GABAergic synapses or glutamergic synapses formed first?

A

gaba-ergic

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29
Q

Early in development GABA is?

A

main excitatory NT

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30
Q

In immature neurons the intracellular concentration of chloride is?

A

relatively high

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31
Q

The activation of GABA receptors in mature neurons generates?

A

an influx of chloride

in immature its oppossite

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32
Q

NKCC1 is?

A

Na/K/Cl co transporter

in immature neurons

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33
Q

KCC2 is?

A

K/Cl co-transpoer

in mature neurons

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34
Q

What is GABA synthesized from?

A

from glutamate

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35
Q

What syntehsizes GABA?

A

glutamic acid decarboxylase (GAD)

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36
Q

What is GAD’s cofactor?

A

pyridoxal phosphate

form of B6 vitamnin

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37
Q

What types of GABA receptors are ionotropic?

A

GABAa and GABAc

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38
Q

What GABA receptor is metabotropic?

A

GABAb

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39
Q

GABA receptors are found where on neuron?

A

soma

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40
Q

Glutamate receptors are found where on neuron?

A

on denrdrites

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41
Q

Where do benzodiazepines bind?

A

outside the pore (GABA)

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42
Q

What do benzodiazepines do?

A

increase GABA binding, reduces anxiety

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43
Q

Where do barbituates bind?

A

inside the pore (GABA)

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44
Q

What are barbituates used for?

A

anaesthesia, treatment for epilepsy

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45
Q

What does alcohol do? (GABA)

A

increases the effects of the inhibitory GABA ligand

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46
Q

WHat is GHP?

A

date rape drug

naturally produced in CNS in small amounts, GABA derivitive, acts on GABAb

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47
Q

What is GHP used to treat?

A

insomnia, clinical depression, narcolepsy, alcoholism

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48
Q

How is glycine synthesized?

A

from serine by transhyrdroxy-methylase

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49
Q

What is major inhibitory neurotransmitter in CNS?

A

glycine

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50
Q

What is hyperglycinemia xaused by?

A

mutation in glycine reuptake transporter

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51
Q

What are symptoms of hyperrglycinemia?

A

lethargy, seizures, mental retardation

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52
Q

Can glutamate cross thee BBB?

A

no

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53
Q

How is glutamate syntehsized?

A

in neurons from glutamine, also could be from glucose

by glutaminase

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54
Q

What are the ionotropic gluatmate receptors?

A

AMPA, NMDA, kainate

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55
Q

What pushes Mg2+ out of NMDA receptors?

A

depolarization

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56
Q

NMDA receptors open when?

A

glutamate binds, and strong depolarization of postsynaptic membrane

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57
Q

Where are metabotropic glutamate receptors found?

A

hippocampus, cerebellum, cerebral cortex

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58
Q

What is serotonin synthesized from?

A

tryptophan

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59
Q

What is SERT?

A

serotonin reuptake transporter

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60
Q

Serotonin receptors are all?

A

metabotropic receptors

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61
Q

What does raphe nucleu regulate?

A

mood, sleep, emotions, body temp, appetite, mempry processing

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62
Q

What is the biosynthetic pathway of catecholamines?

A

tyrosine -> L-DOPA -> Dopamine -> Norepinephrine -> Epinephrine

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63
Q

What is tyrosine made from?

A

phenylalanine

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64
Q

What enyme makes l-dopa?

A

tyrosine hydroxylase

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65
Q

What produces norepinehprine?

A

locus coeruleus

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66
Q

What is the fight or flight hormone?

A

epinephrine

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67
Q

Where does epinephrine go in the brain?

A

medulla, hypothalamus, thalamus

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68
Q

All epinephrine and norepinerhine receptors are?

A

metabotropic

69
Q

Both NE and E affect ______ nerves?

A

sympathetic

70
Q

Whatt converts L-dopa to dopamine?

A

dopa decarboxylase

71
Q

What does the substantia nigra project to?

A

striatum

72
Q

What does the ventral tegmental area project to?

A

prefrontal cortex and the basal forebrain including the nucleus accumbens

73
Q

What is the role of dopamine?

A

coordination of body movements, pleasure and motivation, reward, moods, emotions

74
Q

What does MAO do?

A

breakdown dopamine

75
Q

What does cocaine do in the body?

A

inhibits DAT, increases dopamine in synaptic cleft

76
Q

What does amphetamine do in the body?

A

forces dopamine out of their storage vesicles, increase DA concentration

77
Q

What does D1 do?

A

binds Gs protein, activates adenylyl cyclase, cAMP levels is increased

78
Q

What does D2 do?

A

binds Gi protein, inhibits adenylyl cyclase, cAMP levels is decreased

79
Q

What is included in basal ganglia?

A

caudate & putamen (striatum), globus pallidus, substantia nigra, subthalamic nucleus

80
Q

What damage is first seen in parkinsons?

A

damage to dopaminergic neurons in substantia nigra pars compactaW

81
Q

What damage is first seen in huntingtons?

A

degeneration of striatum, starts w/GABA and dopamine neurons

82
Q

Tyrosine hydroxylasse levels are lower in?

A

parkinsons patients

83
Q

What genetic defect is seen in huntingtons?

A

37+ CAG repeats in huntingtin gene

84
Q

The number of repeats in huntingtin gene decides?

A

if they develop disease and how old they will be

more repeats, younger onset

85
Q

Addiction is characterized by?

A

compulsive behaviour, reinforcing behaviour, loss of control

86
Q

Drug addiction can be considered drug-induced ____ ______?

A

neural plasticity

87
Q

Repeated exposure to drug alters?

A

gene expression in specific brain regions, behavioural abnormalities

88
Q

What are the 3 major structures in the reward pathway?

A

VTA, nucleus accumbens, prefrontal cortex

89
Q

What are the 4 general categories of drugs?

A

narcotics, stimulants, hallucinogens, sedative-hypnotics

90
Q

What are some examples of narcotics?

A

opium, morphine, heroin, codeine

91
Q

What do narcotics do?

A

euphoria, pain relief, depresses CNS

92
Q

What are examples of stimulants?

A

cocaine, amphetamines

93
Q

What do stimulants do?

A

DA reuptake inhibitors, heightened activity, excitability, manic behaviour, cardiovascular failrue

94
Q

What are examples of hallucinogens?

A

LSD, shrooms

95
Q

What do hallucinogens do?

A

usually serotonin agonists, hallucinations

96
Q

What are examples of sedative-hypnotics?

A

alcohol, barbiturates, benzodiazepines

97
Q

What do sedative-hypnotics do?

A

act on GABAa receptors, relaxation, impair motor control, impaired judgement, respiraotry depression

98
Q

What are the functions of serotonin pathways?

A

mood, memory processing, sleep, cognition

99
Q

Where does cocaine concentrate in the brain?

A

caudate, VTA, nucleus accumbens

100
Q

The icnreased activation of dopamine receptors causes?

A

increase cAMP production, abnormal firing patterns, continuous activation of reward pathawy

101
Q

How does prolonged use of cocaine change feelings about reward?

A

loss of pleasurable feelings of natural rewards (food, sex, etc)

102
Q

What three neurons participate in opiate action?

A

dopamine terminal, gabaergic neuron, cell w/dopamine receptors

103
Q

Inhibiting GABA neurons allows dopamine to?

A

fire mroe

104
Q

How does fentanyl increase dopamine levels?

A

blocks GABA release in VTA, causes less inhibition in nucleus accumbens, therefore more DA

105
Q

What is anandamide?

A

endogenous cannabinoid neurotransmitter in the brain

106
Q

What is THC?

A

active component of marijuana

107
Q

What does THC cause?

A

induces cell death w/shrinkage of neurons, dna fragmentation in the hippocampus

108
Q

Where does marijuana concentrate in the brain?

A

VTA, nucleus accumbens, caudate nucleus, hippocampus, cerebellum

109
Q

How can nicotine directly trigger reward?

A

through interaction with the nACh receptors on the VTA dopaminergic
neurons which project to the NAc

110
Q

How does nicotine indirectly trigger reward?

A

by stimulating the nACh receptors on the glutamatergic nerve terminals

111
Q

What does ΔFosB trigger?

A

a series of transcription events that produce an
addictive state

also it has a long half life

112
Q

What does chronic exposure to cociane, amphetamines, morphine do?

A

upregulates the
cAMP pathway and CREB in the NAc

113
Q

Chronic exposure to drugs of abuse has
been shown to decrease?

A

new neurons in adult hippocampus

114
Q

WHat are the treatments for addiction?

A

withdrawal therpay, psychological therapy, long term pharmacological treatment

115
Q

What are positive symptoms in schizophrenia?

A

behaviours not seen in normal people

hallucinations, delusions, movement disorders

116
Q

What are negative symptoms in schizophrenia?

A

absence of normal behaviour

social withdrawal, flat affect, lack of pleasure, not speaking

117
Q

What are the cognitive symptoms of schizophrenia?

A

poor executive function, trouble focusing, problems w/working memory

118
Q

Who is more frequently and severly affected in schizophrenia?

A

males

119
Q

What is the genetic inheritance like in schizophrenia?

A

non-mendelian, polygenic (~20 genes)

120
Q

What are environmental risks for schizophrenia?

A

urban residence in upbringing, labour complications, retroviral activation, maternal infection during pregnancy

121
Q

How is eye movement different in schizophrenics?

A

40-80% have abnormal smooth pursuit eye movements

122
Q

What do PET and MRI show in schizophrenic patientss?

A

frontal lobe hypometabolism

increased vetnricle volume, decfreased volume of hippocampus, prefrontal cortex, and thalamus`

123
Q

What is the two hit hypothesis?

A

1st: developmental defects in neuron formation and/or migration/synapse formation

2nd: stress during adolescence

124
Q

What are silent synapses?

A

synapses w/no ampa receptors only nmda

125
Q

WHat is the major difference between early and late LTP?

A

early LTP does not have new proteins being synthesized

126
Q

Phosphates causes _______ to AMPA?

A

internalization of the postsynaptic ampa

127
Q

LTD causes _______ sensitivity?

A

decreased sensititivtiy to glutamate from Schaffer collaterla terminas

128
Q

NO is a ________?

A

retrograde messanger

released by postsynaptic

129
Q

How is the neurotransmitter nitric oxide produced?

A

nitric oxide synthase

converts arginine and citrulline to NO

130
Q

What is hebb’s hypothesis?

A

synpases are strengthened when pre/post synaptic terminals are stimulated at same time

131
Q

WWhat is procedural memroy?

A

skills, habits, procedures, how to knowledge

132
Q

What is asssociative learning?

A

classical conditioning

133
Q

What is non-associative learning?

A

habituation and sensitization

134
Q

What is episodic memory?

A

memroy of events

135
Q

What is semantic memory?

A

memory of facts

136
Q

Where is long term storage of non declarative memory?

A

cerebellum, basal ganglia, premotor cortex

137
Q

Where is short term storage of declarative memory?

A

hippocampus and related structures

138
Q

Where is long term storage of declarative memroy?

A

medial temporal lobe, wernickes area, + a variety of cortical areas

139
Q

What is a MCI assessment?

A

mild cognitive impairment assessment

140
Q

What is karyotyping?

A

evaluates the number and
structure of a person’s chromosomes in order to detect abnormalities

141
Q

What is FISH?

A

Fluorescence in situ hybridization

detect and map specific genes or gene sequences

142
Q

What can look at entire genome?

A

microarray analysis

143
Q

How is the cerebral cortex different in autism?

A

medial prefrontal region is less active

144
Q

How is the amygdala different in autism?

A

decreased volume/cell size, less active

145
Q

How is the hippocampus different in autism?

A

decreased volume/cell size

146
Q

How is the cerebellum different in autism

A

decreased size/number of purkinje cells

147
Q

How is brain growth different in people w/autism?

A

early brain overgrowth at beginning of life, possible decline/degen later in life

148
Q

What are possible reasons for brain overgrowth in autism?

A

disruption of early neurodevelopment, premature myelination, excess neurons, reduced pruning, excess glia

149
Q

When is the critical period of development for autism?

A

embryonic stage

150
Q

What are 5 factors related to autism risk?

A

maternal rubella infection, ethanol, thalidomide, valproic acid, misoprostol

151
Q

Mifepristone and misoprostol work together to?

A

terminate prgnancy

152
Q

Misoprostol is structurally similar to?

A

prostaglandin E2 (PGE2)

153
Q

Schaffer collaterals are the axons of?

A

pyramidal cells in the hippocampus

154
Q

Tetanus is referred to as?

A

high-frequency bursts of presynaptic action potential

155
Q

CA1 and CA3 are two major regions of the?

A

hippocampus

156
Q

Hyperphosphorylate tau protein forms tangles _______ neurons?

A

within

157
Q

Where do beta-amyloid plaques first appear in brain?

A

neocortex

158
Q

Do calcium ions flow through AMPA receptors?

A

no

159
Q

People w/down sydrome who develop alzheimers develop it by what age?

A

40 ish

160
Q

What 3 envrionmental factors correlate with alzherimers?

A

poor early education, serious head injury, aluminum in drinking water

161
Q

First signs of alzheimers?

A

slight memory loss, change in personality

162
Q

What is tau protein important for?

A

axon and
dendrite remodeling involved
in forming and storing memories

stablizies microtubules

163
Q

Where do neurofibrillary tangles form?

A

in soma

164
Q

What makes tau go bad?

A

when its hyperphosphorylated

165
Q

What do normal beta amyloid precursor proteins do?

A

protect against glutamate toxciity

166
Q

What is the bad form of beta amyloid?

A

AB42

167
Q

42aa beta amyloid aggregattion causes?

A

disruption in calcium homeostasis, mitochondrial damage, inflammatory response, impaired energy metabolism, loss of neuronal function

168
Q

Tau pathology first appears in the?

A

entorhinal cortex

169
Q

Tau and B-amyloid 42 form __________?

A

indenpendently

170
Q

What parts of the brain does alxheimers affect in order?

A

entorhinal cortex, limbic system, neocrotex

171
Q

What is anti-acetylcholinesterase?

A

slows down progression of AD, conserves ACh as they get destroyed

172
Q

What do iron and copper chelators do?

A

reduces iron/copper which contributes to peroxide formation caused by β-amyloid
42aa aggregation

173
Q

What are some treatments for alzheimers?

A

anti-acetylcholinesterases, iron/copper chelators, target gamma and beta secretases, beta amyloid vaccine

KINE 3670 (2 decks)

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