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anat242 > mod 3 > Flashcards

mod 3 Flashcards

1
Q

steps of memory storage in brain

A
  1. release of neurotransmitter
  2. activation of postsynaptic receptors
  3. trafficking of receptors to PSD
  4. local translation of new proteins
  5. altered gene expression
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2
Q

sodium potassium pump pumps

A

3 Na out and 2 K in

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3
Q

calcium homeostasis

A

pumping Ca out of cell, and intracellular calcium-binding proteins and organelles: mitochondria and endoplasmic reticulum

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4
Q

influx of +ve ions

A

depolarised, excites the neurons EPSP

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5
Q

influx of -ve ions

A

hyperpolarized, inhibits the neurons IPSP

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6
Q

membrane potential changes during an action potential

A
  1. stimulus moves membrane potential to threshold
  2. opens voltage-gated Na channel, Na flows in
  3. Na channels close and voltage-gated K channels open
  4. K flows out until K equilibrium potential reached
  5. Na/K pumps return membrane to resting potential
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7
Q

spatial summation

A

multiple input neurons (EPSP) generate simultaneously at many different synapses on a dendrite

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8
Q

temporal summation

A

one input neuron strongly activated

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9
Q

chemical synapse

A

transmission via the release of a neurotransmitter

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10
Q

electrical synapse

A

transmission via electrical currents flowing from one neuron to the next at gap junctions

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11
Q

presynaptic events

A
  1. action potential reaches axon terminal and depolarises membrane
  2. voltage-gated Ca channels open and Ca flows in
  3. Ca influx triggers synaptic vesicles to release neurotransmitters
  4. neurotransmitter binds to receptors on target cell
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12
Q

visualising communication between neurons

A

through micro-periscope, in vivo. view calcium activity in subfield CA1 in excitatory neurons

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13
Q

small synaptic vesicles

A

50nm diameter, clear, membrane bound, most abundant within CNS, contain glutamate, GABA and glycine

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14
Q

small synaptic vesicles at readily releasable pool

A

docked at the active zone

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15
Q

small synaptic vesicles at reserve pool

A

distal to active zone, associated with cytoskeleton

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16
Q

small synaptic vesicles at recycling pool

A

diffusing

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17
Q

vesicle cycle

A

formed in golgi apparatus —– transport along microtubules to axons —> filled with neurotransmitter at never terminal —> release transmitter then ercycle via endocytosis to endosomes or reserve pool and refilled with transporters

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18
Q

large dense core vesicles structure

A

100nm diameter, electron dense/dark, membrane bound, contain catecholamine neuropeptides, neurotrophines, nor/adrenaline

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19
Q

large dense core vesicles function

A

local diffusion to active synaptic partners, act on g-protein-couple receptors, may contribute to presynaptic modulation in addition to postsynaptic effects, comprise of 1-2% of vesicles

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20
Q

synthesis pathway

A
  1. synthesis and modification of neuropeptides (RER and golgi apparatus)
  2. packaging pro-peptide and modifying enzymes
  3. axonal transport
  4. cleavage of pro-peptide (will dock on membrane to release contents)
  5. release
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21
Q

why prolonged stimulation of LDCV

A

not pre-docked, requires more widespread increase in Ca including activation of CaMKII via calcium - induced calcium release from ER.

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22
Q

primary locations of LDCV

A

neurosecretory and neuroendocrine cells as well as sympathetic neurons of PNS, neurohypophysis, hypothalamus

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23
Q

neurosecretory cells (location of LDCV)

A

neurons that secrete their products into pituitary portal vessels at the median eminence

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24
Q

neuroendocrine cells (location of LDCV)

A

cells which receive neuronal input and release hormones into the blood stream - chromaffin cells

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25
Q

chromaffin cells

A

neurendocrine cells: medulla of adrenal glands, enriched with LDCVs

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26
Q

chromaffin cells role

A

contain and release many substances into circulatory system: catecholamines, peptides, proteins, microRNa, neuromodulations, stress transducers

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27
Q

what are the snares involved with

A

exocytosis

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28
Q

v-snare

A

synaptopbrevin (from synaptic vesicle)

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29
Q

t-snare from cytosol

A

SNAP25

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30
Q

t-snare from embedded in plasma membrane

A

syntaxin

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31
Q

binding of snares

A

synaptobrevin binds to alpha primed end of SNAP25 while syntaxin binds to alpha helix terminal at end of SNAP25

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32
Q

what drives the dissociation of the SNARE complex

A

ATPase N-ethylmaleimide-sensitive fusion (NSF)

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33
Q

Rab proteins

A

small GTP binding proteins

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34
Q

rab protein function

A

involved in vesicle guiding and docking at membrane. GTP is hydrolysed which results in fusion of vesicle and release of neurotransmitter

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35
Q

what results in the fusion of vesicles and release of neurotransmitter

A

GTP hydrolysis

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36
Q

exocytosis

A

synaptic vesicle protein, calcium sensor, docking, vesicle fusion+release, ca influx

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37
Q

clathrin-mediated endocytosis

A

the process by which vesicular membrane is retrieved back into the cytoplasm

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38
Q

clathrin

A

assists in the formation of a coated pit on the inner surface of the plasma membrane of the cell which buds into cell to form a coated vesicle

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39
Q

clathrin structure

A

subunits comprise 3 large and 3 small polypeptide chains that form a triskelion and assemble into basket-like frameworks.

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40
Q

dynamin

A

a GTPase, binding to form a bud on membrane. forms a helical collar around the neck of the bud

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41
Q

what do dynamin spirals undergo

A

a length-wise extension which pinches or pops the vesicle from the parent membrane

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42
Q

synaptic vesicle cycle exocytosis

A

Rabs, v-SNARE, t-SNARE, synaptotagmin

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43
Q

synaptic vesicle cycle endocytosis

A

clathrin, dynamin

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44
Q

botulinum toxin

A

blocks release of acetylcholine at the NMJ resulting in muscle paralysis lasting 3 months

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45
Q

one of the most poisonous biological substances

A

botulinum toxin (produced by clostridium botulinum)

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46
Q

heavy chain toxin binds to what

A

binds selectively and irreversibly to presynaptic receptors on cholinergic neurons

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47
Q

behaviour of heavy chain - preventing muscle contraction

A

binded with cholinergic neurons, it is endocytosed during which the light chain is cleaved and released from heavy chain to bind to SNAP25. this prevents exocytosis.fusion of vesicles so no acetylcholine is release and muscles cannot contract

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48
Q

tetanus toxin

A

cleaves synaptic vesicles associated proteins synaptabrevin in cytosol. meaning glycine or gaba cannot be secreted nor acetylcholine so no muscle contraction will be halted resulting in spastic paralysis

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49
Q

what does botulinum toxin cause

A

muscle paralysis

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50
Q

what does tetanus toxin cause

A

spastic paralysis

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51
Q

tetanus toxin pathway

A

binds to presynaptic membrane of NMJ, then transports back to CNS by axon to bind to inhibitory neurons by endocytosis, then leaves vesicle and goes into cytosol to cleave

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52
Q

alpha latrotoxin

A

derived from widow spiders - causes release of small synaptic vesicles, via forming a calcium channel - causes spasms?

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53
Q

synapsin

A

a phosphoprotein controlling synaptic vesicle mobility and post-docking steps of exocytosis
- maintain the SSV reserve pool and contribute to synaptic plasticity

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54
Q

most abundant isoform of synapsin

A

SYN1

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55
Q

ca activation of CaMKii / protein kinase results in what

A

phosphorylation of synapsin

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56
Q

what does the phosphorylation of synapsin result in

A

reduction of synapsin binding to the actin cytoskeleton. this makes vesicles now available for exocytosis

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57
Q

what happens in the absence of synapsin

A

binding disperses the distal cluster of SV’s, while docked SV’s remain intact. synaptic depression is hastened following peptide injection

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58
Q

cellular changes from excitatory synapses

A

synapsin deletion reduces size of reserve pool of synaptic vesicles. this impairs the glutamate release and delayed recovery from synaptic transmission with relatively normal basal transmission

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59
Q

cellular changes from inhibitory synapses

A

knockout of synapsins inhibitory neurons result in a loss of synaptic vesicles from both the readily releasable and the reserve pool (excitatory is just reserve pool only)

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60
Q

knockout phenotype

A

deletion of SYN gene produces epileptic phenotype

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61
Q

synapsin in terms of autism

A

those autistic have many mutations in genes which encode synaptic proteins

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62
Q

knockout mouse results of synapsin 2 deletion mouse

A

displayed deficits in short-term social recognition and increased repetitive self-grooming behaviour

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63
Q

knockout mouse results of synapsin 1 and 3 deletion

A

displayed an impaired social transmission of food preference

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64
Q

knockout mouse results of synapsin 1 and 2 deletion

A

displayed a decreased environmental interest

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65
Q

four classes of neurotransmitters

A
  1. amino acids (glutamate excit, GABA inhib)
  2. amines and purines (actyl, nor/adren, serotonin)
  3. neuropeptides (opioids, substance P, neuropeptide Y)
  4. gases (NO, CO)
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66
Q

where amines and purines found

A

small synaptic vesicles

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67
Q

where neuropeptides found

A

large dense core vesicles

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68
Q

dopamine

A

a catecholamine - involved in regulation of movement, attention, mood, cognition, addiction, reward

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69
Q

parkinsons prevalence

A

age of onset 55 to 65 years
1 in 100 people >60 years of age

70
Q

arvid carlsson

A

discovered that circuits that control movements dont work properly when dopamine levels are decreased

71
Q

parkinsons is a loss of what

A

dopamine and substantia nigra

72
Q

tyrosine to epinephrine process

A

tyrosine -> L-Dopa -> dopamine -> norepinephrine -> epinephrine

73
Q

synaptosomes

A

are a synaptic terminal isolated from a neuron, involved in reuptake

74
Q

bromocriptine

A

an agonist approved to treat parkinson’s disease, hyperprolactinemia and related conditions

75
Q

haloperidol

A

an antagonist that is used in treating schizophrenia, bipolar disorder and stimulant-induced psychosis

76
Q

L-Dopa treatment for Parkinson’s disease

A

L-dopa treatment does not stop neurodegeneration but might enhance the activity of the neurons remaining

77
Q

what side effects does prolonged L-DOPa treatment result in

A

L-DOPA-induced dyskinesia and psychosis

78
Q

NO - what its not

A

not stored in lipid vesicles, not released by exocytosis, not bind to receptors, not metabolized by hydrolytic enzymes

79
Q

NO

A

a gas derived from arginine, synthesized on demand, an important retrograde messenger involved in the long-term potentiation model for memory

80
Q

fast acting receptors

A

ligand-gated ion channels (glutamate receptors)
milliseconds
excitatory or inhibitory, depending on ion involved and its direction of movement

81
Q

slow acting receptors

A
  1. g-protein coupled receptors
  2. D1 - like receptors (D1 and D5)
  3. D2 - like receptors (D2, D2, and D4)
82
Q

g-protein coupled receptors

A

metabotropic receptors
7-transmembrane domains
directly regulates ion channels
generate second messengers

83
Q

D1 like receptors

A

stimulation of adenylate cyclase, coupled to Gs, mediate excitatory neurotransmission

84
Q

D1 like receptors

A

stimulation of adenylate cyclase, coupled to Gs, mediate excitatory neurotransmission

85
Q

D2 like receptors

A

inhibition of adenylate cyclase, couple to Gi/Go, mediate inhibitory neurotransmission

86
Q

dopamine sites of actions

A

substantia nigra to striatum circuit
ventral tegemental area to cortex
limbic system
dopamine can be in SSV and LDCV

87
Q

ventral tegemental area dopamine system

A

projects to the nucleus accumbens
is a reward system which reinforces desirable behaviours - opiates and nicotine stimulate VTA neurons

88
Q

what do opiates and nicotine stimulate

A

VTA neurons

89
Q

cocaine and amphetamines do what

A

block reuptake which increases dopamine at synapses

90
Q

what does prolonged activity of VTA result in

A

down-regulation, drug tolerance, and with any removal - withdrawal

91
Q

ATP a neurotransmitter

A

acts on purinergic receptors it is co-stored and co-released with classical neurotransmitters, are both ion channel and G-protein coupled

92
Q

brain derived neurotropic factor

A

high levels found in hippocampus, has a role in neuronal plasticity

93
Q

proBDNF

A

BDNF is synthesized as the precursor proBDNF but proBDNF is not an inactive precursor, it is a signalling protein in its own right

94
Q

proBDNF

A

BDNF is synthesized as the precursor proBDNF but proBDNF is not an inactive precursor, it is a signalling protein in its own right

95
Q

BDNF action

A

undergoes Ca influx-dependent release from pre and post synaptic sites, act on ligand-gated ion channels, voltage-gated ion channels, second-messenger pathways

96
Q

what activates CB1 receptors which are coupled to G-protein

A

endocannabinoids

97
Q

how many transmembrane domains does each unit of an enzyme-linked receptor usually have?

A

one

98
Q

GABA-A receptors

A

ionotropic

98
Q

GABA-A receptors

A

ionotropic

99
Q

GABA-B receptors

A

metabotropic

100
Q

what is GABA

A

an amino acid, not found in proteins, is synthesized in GABA’ergic neurons by glutamatic acid decarboxylases

101
Q

GABA-A distribution

A

widespread CNS, PNS, limbic system, eye, amygdala, nuerons, oligodendrocytes, NMJ

102
Q

activation of GABA gated ion channels cause a

A

IPSP via opening chloride ion channels and resulting influx of Cl.

103
Q

substances that enhance the natural effect of GABA

A

benzodiazepines and ethanol enahnce the natural effect of GABA

104
Q

phasic inhibition

A

GABA is released from presynaptic terminals and binds to postsynaptic GABA-A R’s

105
Q

tonic inhibition

A

ambient extracellular GABA binds to extrasynaptic GABA-A r’s and modulates resting membrane potentials and cell excitability

106
Q

drugs that enhance GABA action are what

A

anxiolytic - they reduce anxiety or panic

107
Q

GABA - B distribution

A

both pre and post synaptically

108
Q

GABA-B receptor associated with

A

epilepsy, spasticity, schizophrenia, anxiety, depression, cognitive deficits, and addiction

109
Q

acetylcholine receptor distribution

A

transmitter at NMJ, autonomic ganglia, postganglionic parasympathetic synapses

110
Q

acetylcholine synthesization

A

AcH is synthesized by choline acetyltransferase and transported into vesicles. following synaptic release, AcH degraded by acetylcholinesterase

111
Q

muscarinic AchR

A

metabotropic - sensitive to muscarine, G-protein couples, found in: glia, heart muscle, salivary glands

112
Q

nicotinic AchR

A

ion channels - sensitive to nicotine, ligand-gated channel, mediate fast synaptic transmission, occur in high density at neuromuscular junction, sensitive to alpha-bungarotoxin

113
Q

ligand-gated ion channels

A

results in depolarisation of muscle cell, opening of voltage-gated sodium channels; action potential and muscle contraction

114
Q

in vitro

A

molecular and cellular events: cells in culture, acute brain slices, organotypic brain slices

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

115
Q

in vivo

A

simple invertebrate models, vertebrate rodent models

116
Q

nonassociative learning: behavioural responses

A

habituation and sensitization

117
Q

aplysia california models learning and memory with example of what reflex

A

siphon-gill-withdrawal refex, undergoes either habituation or sensitization when a stimulus is applied

118
Q

presynaptic facilitation (gill-withdrawal response)

A

stimuli activate interneuron L29. this enhances neurotransmitter release from the sensory neuron presynaptic terminal and alters gene expression

119
Q

single tailed shock

A

L29 releases serotonin activates its receptors on presynaptic nerve terminals as well as stimulates formation of cAMP, which activates protein kinase A and the release of neurotransmitter

120
Q

PKA increases what

A

phosphorylation of Ca and K+ channels

121
Q

multiple tailed shock

A

same as single except PKA moves to nucleus, alters gene expression and new proteins stimulate synapse growth

122
Q

drosophila melanogaster

A

small genome and nervous system, rapid life cycle, easy to identify circuits

123
Q

aplysia california

A

small nervous system, large neurons, easy to identify individual neurons and circuits

124
Q

AMPA receptors

A

ligand-gated, mediate fast depolarisation, na channel

125
Q

NMDA receptor subtypes

A

ligand and ion-gated, slightly slower response, ca and na channel

126
Q

long term potentiation summary

A

ca influx into dendritic spine activates protein kinases such as Ca calmodulin-dependent protein kinase II. it phosphorylates the AMPA receptor to increase conduction.
AMPA receptors get trafficked to the membrane, and long term changes are made to gene expression

127
Q

long term depression summary

A

repetitive low frequency stimulation results in a low level Ca influx through NMDARs
low levels of Ca activate protein phosphatases, removing phosphates from AMPA receptor and other targets, results in long-term changes to gene expression

128
Q

AMPAR subunit GluA1-GluA4

A

assemble as dimers-of-dimers to form hetero-tetrameric or homomeric receptors (GluA1)

129
Q

GluaA2 permeability

A

impermeable when containing AMPAR, permeable without

130
Q

what would create more long term significant change

A

homomeric receptors (AMPA)

131
Q

what would create more short lasting changes

A

properties of phosphorylation

132
Q

polyribosomes

A

found in spines, translocate from dendritic shafts to spines in response to activity

133
Q

mRNA

A

found in dendrites, translated in response to activity

134
Q

immediate early genes

A

are fast responding genes that are altered in response to activity. they are transcription factors and will also mediate target genes. these target genes will mediate significant changes

135
Q

secondary response genes

A

receptors and many others, new and larger synapses, re-structured synapses

136
Q

amyloid beta causing an initial hyperexcitability of neurons leads to what

A

excessive levels of glutamate in the extra-synaptic space, leading to overstimulation of NMDA receptors and subsequently synaptic loss and cell death

137
Q

what does AB-induced endocytosis of the AMPA-type glutamate receptors lead to?

A

long-term depression

138
Q

what does disruption to actin dynamics from AB cause

A

impairments in the trafficking of AMPA, NMDA

139
Q

memantine

A

antagonist of the NMDA receptor subtype of glutamate receptor. it is used to slow neurotoxicity

140
Q

what did researchers at Genetech find?

A

a small molecule that enhances GluN2A function to boost synaptic NMDAR signalling. found that abnormal low-frequency oscillations and epileptiform bursts were reduced and morris water maze performance impoved

141
Q

sAPPalpha

A

enhances plasticity, protein synthesis, GluA1 synthesis

142
Q

hypothalamus

A

a hypophysis that secretes many hormones and regulates the function of other hormone-secreting glands

143
Q

lateral and medial zones of the hypothalamus

A

project to brain stem and telencephalon

144
Q

periventricular zone of the hypothalamus

A

multiple functions including regulation of the pituitary

145
Q

magnocellular

A

release neurohormones, oxytocin and antiduretic hormone into the capillary bed

146
Q

oxytocin involved in

A

uterine contraction and milk ejection

147
Q

antidiuretic hormone

A

regulates extracellular fluid volume and acts on kidney to increase water retention and constricts blood vessels

148
Q

magnocellular neurons project to where

A

posterior lobe of pituitary

149
Q

what neurons regulate the anterior lobe of the pituitary

A

parvocellular neurons

150
Q

parvocellular neurons

A

secrete hypophysiotropic hormones into the hypothalamic pituitary portal circulation

151
Q

follicle stimulating hormone (FSH)

A

stimulates estrogen secretion, egg production, sperm production

152
Q

luteinizing hormones (LH)

A

triggers ovulation, progestin production (females), androgen production (males).

153
Q

LH and FSH collectively known as

A

gonadotrophins

154
Q

thyroid stimulating hormone (TSH)

A

triggers thyroid hormone release called thyroxine

155
Q

adrenocorticotropic hormone (ACTH)

A

stimulates glucocorticoid release from the adrenal gland

156
Q

growth hormone (GH)

A

stimulates growth via somatomedins released from liver

157
Q

prolactin

A

stimulates mammary gland development and milk secretoin

158
Q

gonadotropin-releasing hormone (GnRH)

A

is released by hypothalamus and travels to anterior pituitary where it causes the release of LH/FDH and travels to target tissues testes/ovaries to produce estrogen/androgen

159
Q

absence of gonadotrophins in females

A

means ovaries are inactive (e.g. childhood)

160
Q

estrogen distribution

A

distributed in CNS, concentrated in pituitary and hypothalamus and also in cortex, midbrain and cerebellum

161
Q

estrogen

A

alters the intrinsic excitability of neurons via modulating the flow of potassium ions, depolarisation and more potentials. fast action

162
Q

estrogen role

A

development and regulation of female reproductive system as well as physiological roles in males

163
Q

estrogen receptors

A

intracellular

164
Q

reverse transcription-polymerase chain reaction (4)

A
  1. isolate (purify) RNA
  2. convert RNA to DNA by process of reverse transcription
  3. amplify target DNA (PCR)
  4. analyse products

anat242 (4 decks)

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