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
What gland is abnormal 75% of the time in myasthenia gravis patients?
thymus gland
23
What damage is seen in cells of person w/myathenia gravis?
lymphocyte aggregates, widening of synaptic cleft
24
What can cause myasthenia gravis?
some drugs, some viruses/infections
25
How can you diagnose myasthenia gravis?
blood tests, edrophonium test, nerve conduction studies
26
What are the treatments for myasthenia gravis?
AChE inhibitors, immunosuppresants, plasmaphersis, thymectomy
27
What is the main inhibitory neurotransmitter in brain?
GABA
28
Are GABAergic synapses or glutamergic synapses formed first?
gaba-ergic
29
Early in development GABA is?
main excitatory NT
30
In immature neurons the intracellular concentration of chloride is?
relatively high
31
The activation of GABA receptors in mature neurons generates?
an influx of chloride in immature its oppossite
32
NKCC1 is?
Na/K/Cl co transporter in immature neurons
33
KCC2 is?
K/Cl co-transpoer in mature neurons
34
What is GABA synthesized from?
from glutamate
35
What syntehsizes GABA?
glutamic acid decarboxylase (GAD)
36
What is GAD's cofactor?
pyridoxal phosphate form of B6 vitamnin
37
What types of GABA receptors are ionotropic?
GABAa and GABAc
38
What GABA receptor is metabotropic?
GABAb
39
GABA receptors are found where on neuron?
soma
40
Glutamate receptors are found where on neuron?
on denrdrites
41
Where do benzodiazepines bind?
outside the pore (GABA)
42
What do benzodiazepines do?
increase GABA binding, reduces anxiety
43
Where do barbituates bind?
inside the pore (GABA)
44
What are barbituates used for?
anaesthesia, treatment for epilepsy
45
What does alcohol do? (GABA)
increases the effects of the inhibitory GABA ligand
46
WHat is GHP?
date rape drug naturally produced in CNS in small amounts, GABA derivitive, acts on GABAb
47
What is GHP used to treat?
insomnia, clinical depression, narcolepsy, alcoholism
48
How is glycine synthesized?
from serine by transhyrdroxy-methylase
49
What is major inhibitory neurotransmitter in CNS?
glycine
50
What is hyperglycinemia xaused by?
mutation in glycine reuptake transporter
51
What are symptoms of hyperrglycinemia?
lethargy, seizures, mental retardation
52
Can glutamate cross thee BBB?
no
53
How is glutamate syntehsized?
in neurons from glutamine, also could be from glucose by glutaminase
54
What are the ionotropic gluatmate receptors?
AMPA, NMDA, kainate
55
What pushes Mg2+ out of NMDA receptors?
depolarization
56
NMDA receptors open when?
glutamate binds, and strong depolarization of postsynaptic membrane
57
Where are metabotropic glutamate receptors found?
hippocampus, cerebellum, cerebral cortex
58
What is serotonin synthesized from?
tryptophan
59
What is SERT?
serotonin reuptake transporter
60
Serotonin receptors are all?
metabotropic receptors
61
What does raphe nucleu regulate?
mood, sleep, emotions, body temp, appetite, mempry processing
62
What is the biosynthetic pathway of catecholamines?
tyrosine -> L-DOPA -> Dopamine -> Norepinephrine -> Epinephrine
63
What is tyrosine made from?
phenylalanine
64
What enyme makes l-dopa?
tyrosine hydroxylase
65
What produces norepinehprine?
locus coeruleus
66
What is the fight or flight hormone?
epinephrine
67
Where does epinephrine go in the brain?
medulla, hypothalamus, thalamus
68
All epinephrine and norepinerhine receptors are?
metabotropic
69
Both NE and E affect ______ nerves?
sympathetic
70
Whatt converts L-dopa to dopamine?
dopa decarboxylase
71
What does the substantia nigra project to?
striatum
72
What does the ventral tegmental area project to?
prefrontal cortex and the basal forebrain including the nucleus accumbens
73
What is the role of dopamine?
coordination of body movements, pleasure and motivation, reward, moods, emotions
74
What does MAO do?
breakdown dopamine
75
What does cocaine do in the body?
inhibits DAT, increases dopamine in synaptic cleft
76
What does amphetamine do in the body?
forces dopamine out of their storage vesicles, increase DA concentration
77
What does D1 do?
binds Gs protein, activates adenylyl cyclase, cAMP levels is increased
78
What does D2 do?
binds Gi protein, inhibits adenylyl cyclase, cAMP levels is decreased
79
What is included in basal ganglia?
caudate & putamen (striatum), globus pallidus, substantia nigra, subthalamic nucleus
80
What damage is first seen in parkinsons?
damage to dopaminergic neurons in substantia nigra pars compactaW
81
What damage is first seen in huntingtons?
degeneration of striatum, starts w/GABA and dopamine neurons
82
Tyrosine hydroxylasse levels are lower in?
parkinsons patients
83
What genetic defect is seen in huntingtons?
37+ CAG repeats in huntingtin gene
84
The number of repeats in huntingtin gene decides?
if they develop disease and how old they will be more repeats, younger onset
85
Addiction is characterized by?
compulsive behaviour, reinforcing behaviour, loss of control
86
Drug addiction can be considered drug-induced ____ ______?
neural plasticity
87
Repeated exposure to drug alters?
gene expression in specific brain regions, behavioural abnormalities
88
What are the 3 major structures in the reward pathway?
VTA, nucleus accumbens, prefrontal cortex
89
What are the 4 general categories of drugs?
narcotics, stimulants, hallucinogens, sedative-hypnotics
90
What are some examples of narcotics?
opium, morphine, heroin, codeine
91
What do narcotics do?
euphoria, pain relief, depresses CNS
92
What are examples of stimulants?
cocaine, amphetamines
93
What do stimulants do?
DA reuptake inhibitors, heightened activity, excitability, manic behaviour, cardiovascular failrue
94
What are examples of hallucinogens?
LSD, shrooms
95
What do hallucinogens do?
usually serotonin agonists, hallucinations
96
What are examples of sedative-hypnotics?
alcohol, barbiturates, benzodiazepines
97
What do sedative-hypnotics do?
act on GABAa receptors, relaxation, impair motor control, impaired judgement, respiraotry depression
98
What are the functions of serotonin pathways?
mood, memory processing, sleep, cognition
99
Where does cocaine concentrate in the brain?
caudate, VTA, nucleus accumbens
100
The icnreased activation of dopamine receptors causes?
increase cAMP production, abnormal firing patterns, continuous activation of reward pathawy
101
How does prolonged use of cocaine change feelings about reward?
loss of pleasurable feelings of natural rewards (food, sex, etc)
102
What three neurons participate in opiate action?
dopamine terminal, gabaergic neuron, cell w/dopamine receptors
103
Inhibiting GABA neurons allows dopamine to?
fire mroe
104
How does fentanyl increase dopamine levels?
blocks GABA release in VTA, causes less inhibition in nucleus accumbens, therefore more DA
105
What is anandamide?
endogenous cannabinoid neurotransmitter in the brain
106
What is THC?
active component of marijuana
107
What does THC cause?
induces cell death w/shrinkage of neurons, dna fragmentation in the hippocampus
108
Where does marijuana concentrate in the brain?
VTA, nucleus accumbens, caudate nucleus, hippocampus, cerebellum
109
How can nicotine directly trigger reward?
through interaction with the nACh receptors on the VTA dopaminergic neurons which project to the NAc
110
How does nicotine indirectly trigger reward?
by stimulating the nACh receptors on the glutamatergic nerve terminals
111
What does ΔFosB trigger?
a series of transcription events that produce an addictive state also it has a long half life
112
What does chronic exposure to cociane, amphetamines, morphine do?
upregulates the cAMP pathway and CREB in the NAc
113
Chronic exposure to drugs of abuse has been shown to decrease?
new neurons in adult hippocampus
114
WHat are the treatments for addiction?
withdrawal therpay, psychological therapy, long term pharmacological treatment
115
What are positive symptoms in schizophrenia?
behaviours not seen in normal people hallucinations, delusions, movement disorders
116
What are negative symptoms in schizophrenia?
absence of normal behaviour social withdrawal, flat affect, lack of pleasure, not speaking
117
What are the cognitive symptoms of schizophrenia?
poor executive function, trouble focusing, problems w/working memory
118
Who is more frequently and severly affected in schizophrenia?
males
119
What is the genetic inheritance like in schizophrenia?
non-mendelian, polygenic (~20 genes)
120
What are environmental risks for schizophrenia?
urban residence in upbringing, labour complications, retroviral activation, maternal infection during pregnancy
121
How is eye movement different in schizophrenics?
40-80% have abnormal smooth pursuit eye movements
122
What do PET and MRI show in schizophrenic patientss?
frontal lobe hypometabolism increased vetnricle volume, decfreased volume of hippocampus, prefrontal cortex, and thalamus`
123
What is the two hit hypothesis?
1st: developmental defects in neuron formation and/or migration/synapse formation 2nd: stress during adolescence
124
What are silent synapses?
synapses w/no ampa receptors only nmda
125
WHat is the major difference between early and late LTP?
early LTP does not have new proteins being synthesized
126
Phosphates causes _______ to AMPA?
internalization of the postsynaptic ampa
127
LTD causes _______ sensitivity?
decreased sensititivtiy to glutamate from Schaffer collaterla terminas
128
NO is a ________?
retrograde messanger released by postsynaptic
129
How is the neurotransmitter nitric oxide produced?
nitric oxide synthase converts arginine and citrulline to NO
130
What is hebb's hypothesis?
synpases are strengthened when pre/post synaptic terminals are stimulated at same time
131
WWhat is procedural memroy?
skills, habits, procedures, how to knowledge
132
What is asssociative learning?
classical conditioning
133
What is non-associative learning?
habituation and sensitization
134
What is episodic memory?
memroy of events
135
What is semantic memory?
memory of facts
136
Where is long term storage of non declarative memory?
cerebellum, basal ganglia, premotor cortex
137
Where is short term storage of declarative memory?
hippocampus and related structures
138
Where is long term storage of declarative memroy?
medial temporal lobe, wernickes area, + a variety of cortical areas
139
What is a MCI assessment?
mild cognitive impairment assessment
140
What is karyotyping?
evaluates the number and structure of a person's chromosomes in order to detect abnormalities
141
What is FISH?
Fluorescence in situ hybridization detect and map specific genes or gene sequences
142
What can look at entire genome?
microarray analysis
143
How is the cerebral cortex different in autism?
medial prefrontal region is less active
144
How is the amygdala different in autism?
decreased volume/cell size, less active
145
How is the hippocampus different in autism?
decreased volume/cell size
146
How is the cerebellum different in autism
decreased size/number of purkinje cells
147
How is brain growth different in people w/autism?
early brain overgrowth at beginning of life, possible decline/degen later in life
148
What are possible reasons for brain overgrowth in autism?
disruption of early neurodevelopment, premature myelination, excess neurons, reduced pruning, excess glia
149
When is the critical period of development for autism?
embryonic stage
150
What are 5 factors related to autism risk?
maternal rubella infection, ethanol, thalidomide, valproic acid, misoprostol
151
Mifepristone and misoprostol work together to?
terminate prgnancy
152
Misoprostol is structurally similar to?
prostaglandin E2 (PGE2)
153
Schaffer collaterals are the axons of?
pyramidal cells in the hippocampus
154
Tetanus is referred to as?
high-frequency bursts of presynaptic action potential
155
CA1 and CA3 are two major regions of the?
hippocampus
156
Hyperphosphorylate tau protein forms tangles _______ neurons?
within
157
Where do beta-amyloid plaques first appear in brain?
neocortex
158
Do calcium ions flow through AMPA receptors?
no
159
People w/down sydrome who develop alzheimers develop it by what age?
40 ish
160
What 3 envrionmental factors correlate with alzherimers?
poor early education, serious head injury, aluminum in drinking water
161
First signs of alzheimers?
slight memory loss, change in personality
162
What is tau protein important for?
axon and dendrite remodeling involved in forming and storing memories stablizies microtubules
163
Where do neurofibrillary tangles form?
in soma
164
What makes tau go bad?
when its hyperphosphorylated
165
What do normal beta amyloid precursor proteins do?
protect against glutamate toxciity
166
What is the bad form of beta amyloid?
AB42
167
42aa beta amyloid aggregattion causes?
disruption in calcium homeostasis, mitochondrial damage, inflammatory response, impaired energy metabolism, loss of neuronal function
168
Tau pathology first appears in the?
entorhinal cortex
169
Tau and B-amyloid 42 form __________?
indenpendently
170
What parts of the brain does alxheimers affect in order?
entorhinal cortex, limbic system, neocrotex
171
What is anti-acetylcholinesterase?
slows down progression of AD, conserves ACh as they get destroyed
172
What do iron and copper chelators do?
reduces iron/copper which contributes to peroxide formation caused by β-amyloid 42aa aggregation
173
What are some treatments for alzheimers?
anti-acetylcholinesterases, iron/copper chelators, target gamma and beta secretases, beta amyloid vaccine