Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Organisms And Their Environment > Essential neuroscience (A) > Flashcards

Essential neuroscience (A) Flashcards

1
Q

Why do animals have nervous systems

A

Sense and respond to their environment Homeostatic regulation of internal functions (homeostasis = maintenance of a relatively stable internal environment). 2 major regulatory systems:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

endocrine v nervous system - system tyoe

A

endocrine - wired, nervous - wireless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

endocrine v nervous system - - target

A

endocrine - specificity of target cell binding, nervous - anatomical connection with target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

endocrine v nervous system - distance

A

endocrine - hormones carried in the blood over a long distance. nervous - neurotransmitters diffuse through a short distance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

endocrine v nervous system - response time

A

endocrine - slow and long-lasting. nervous - rapid and brief response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

endocrine v nervous system - what does it coordinate

A

endocrine - long lasting activities (growth, etc) nervous - coordinates fast and precise responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

endocrine v nervous system - voluntary or involuntary

A

endocrine - involuntary. nervous - voluntary/involuntary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

endocrine v nervous system - influence

A

endocrine - influences CNS output. nervous system - influences endocrine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is gyrification

A

folding of the cortex - allows a larger cortical surface area and hence greater cognitive functionality to fit inside a smaller cranium. Enhances efficient neural processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 2 divisions of neural tissue

A

grey matter and white matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is grey mattter

A

neuronal cell bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is white matter

A

myelinated neurites projecting from neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What division is the CNS

A

Sensory/afferent division – brings sensory information to the CNS from receptors in peripheral tissues and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What makes up the preipheral nervous system

A

Cranial nerves: 12 pairs

Spinal nerves: 31 pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What division is the peripheral nervous system under

A

Motor/efferent division – sends motor commands from the CNS to target organs (muscles, glands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 parts of the peripheral nervous system

A

SOMATIC AND AUTONOMIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the somatic nervous system

A

motor neurons to skeletal muscle. Voluntary control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the autonomic nervous system

A

neurons to visceral organs (e.g., heart). No voluntary control. Sympathetic and parasympathetic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is a neuron’s function anatomically compartmentalised

A

input, intergrative, conductive, output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the cell body

A

contains nucleus, golgi and most organelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are neurites

A

long, filamentous extensions responsible for propagating action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are synpases

A

responsible for transmitting information between neurons via neurotransmitter signalling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do synapses allow for

A

information to pass between neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does the pre-synapse release

A

neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does the post-synapse carry

A

carries neurotransmitters sensitive ion channel receptors that can have excitatory or inhibitory effect on the target neuron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

sensory neuron function

A

detection of external and internal information: light, vibration, temperature, pressure and stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

motor neuron function

A

Outputting information from the central nervous system to muscles, driving behavioral response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

interneuron function

A

connecting neurons to each other, amplifying and attenuating activity of a neuronal circuit by integrating additional data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which cells support neurons

A

glial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are astrocytes

A

‘Star-shaped’ glia, supporting neuron function and delivery of molecules to/from the vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

when are astrocytes activated

A

Activate in response to injury, neuroinflammation or degeneration in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

non-reactive astrocytes

A

trophic support of neurons, synapase formation and maintenance, clearance of neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

reactive (inflamed) astrocytes

A

damage neurons, activate microglia, some phagocytic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are microglia

A

Resident immune cell of the brain, surveying for pathogens and damaged material. Important roles in development and pruning of excess synpases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When do microglia become inflamed

A

in response to pathogens (virus, bacteria, etc) injury and neurodegeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

morphological and functional changes of microglia when activated

A

increased motility, phagocytosis and release of immune factors (cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how do myelinating glia myelinate neurons

A

by insulating them in multiple layers of sphingolipids, increasing axon potential speed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what do oligodendrocytes do

A

myelinate multiple axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what do schwann cells do

A

myelinate single axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which axons are myselinated

A

All motor axons are myelinated, and some sensory axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Different cell culture models to measure the function of the nervous system

A
  1. Stable cell lines – easy to grow, derived from tumors
  2. Primary neuronal cultures (derived from model organisms)
  3. Human stem cell derived cultures (derived from skin cells of living patients)
  4. Advances in cell culture technique now allow researchers to grow 3D ‘mini brains’
  5. Powerful tools for pharmacological testing, genetic screening and electrophysiology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

common model organisms in neuroscience research

A
  1. Rodents (mouse, rat)
  2. Zebrafish (Dario renio)
  3. Zebra finch (Taeniopygia guttata)
  4. Fruitfly (drosophilia melanogaster)
  5. Nematode worms (caenorhabditis elegans)
  6. Ethical considerations – must have justification for use of vertebrates, strict regulation of experiments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how can behavioural responses be manipulated

A

pharmacologically and genetically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what can excitable cells do

A

Excitable cells can propagate an action potential across their membrane and include: muscle (myocytes, cardiomyocytes), endocrine cells, neuronal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the important properties of a membrane

A
  1. composed of hydrophobic lipids, impermeable to water soluble molecules
  2. Channels/pumps facilitate cross membrane transport of ions and molecules
  3. Channels/pumps are selective, based on size, charge and solubility of substrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How do ions move down an electrical gradient

A

positive to negative charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

electrophysiological activity

A

Important, widely used technique for measuring neuron activity in cell culture and model organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what does and intracellular microelectrode and an extracellular electrode measure

A

intra - measures internal voltage. extra - extracellular voltage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how can we record the membrane potential of the cell of interest

A

The difference in voltage recorded between intra- and extracellular electrodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is resting potential

A

the point at which difference in ion concentrations are stable across a membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Under resting potential neuronal membranes are:

A
  1. Permeable to passive diffusion by K+, Na+ and Cl-. Ions pass through ‘leaky’ channels (not through the lipid bilayer)
  2. Impermeable to intracellular large anions, organic acids, sulphates, phosphates, amino acids. Too large to pass through the membrane channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how are ion concentration gradients maintained

A

by active transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how do active transporters utilize energy

A

Active transporters utilize energy from ATP hydrolysis, pump ions against the chemical gradient. Na+ - K+ pump exchanges 3 intracellular Na+ ions for 2 extracellular K+ ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

where is there high K+

A

in the neuronal cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

where is there high Na+

A

in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how is neuronal K+ buffered

A

by membrane impermeable organic anions (negative charge), but membranes are permeable to K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

how is a steady chemical and electrical gradient established

A

combined passive diffusion and active transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what prevents K+ diffusion at resting potential

A

negative intracellular electrostatic forces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

at rest what is yhe K+ equilibrium potential

A

-90mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Sodium ions at resting potential

A

positive charge with low permeability across the neuronal membrane (Ena = +55mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Sodium ions at resting potential

A

positive charge with low permeability across the neuronal membrane (Ena = +55mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Sodium ions at resting potential

A

positive charge with low permeability across the neuronal membrane (Ena = +55mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Chloride ions at resting potential

A

negative charge, passively distributed and dependent of Na+ and K+ distribution (ECl = -60mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the resting potential of the neuronal membrane

A

-70 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What triggers an action potential

A

by input stimulation of inward current, caused by activation of post-synaptic receptors on the neuronal membrane. inwards flow of positive ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what triggers neurotransmitter release

A

stimulated by action potentials reaching the pre-synaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what triggers neurotransmitter release

A

stimulated by action potentials reaching the pre-synaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Why can information travel long distances

A

Cascading reversal of membrane potential transmits a signal across neurite membranes to the synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the 4 phases of an action potential

A

depolarisation , repolarisation, hyperpolarisation, afterpolarisation

69
Q

what happens during depolarisation 1

A

rapid positive change in membrane potential from –70mV to ~+30mV

70
Q

What happens during repolarisation

A

rapid negative change in potential

71
Q

How long does the depolarisation - repolarisation spike last

A

~1ms

72
Q

What happens during hyperpolarisation

A

membrane potential becomes more negative than resting potential

73
Q

What happens during afterpolarisation

A

membrane potential returns to resting potential state

74
Q

What is a threshold stimuli

A

stimulation needed to achieve an action potential. every cell has a different threshold. ~15mV below resting potential

75
Q

what is the absolute refractory period

A

During the spike, a neuron cannot be stimulated

76
Q

hat is the relative refractory period

A

During hyperpolarisation and afterpolarisation, a suprathreshold stimulus (I,e,. Larger) is required to trigger an action potential

77
Q

hat do refractory periods allow for

A

unidirectionality (blocks them from travelling in the reverse dircetion) of action potentials and an upper limit on firing rate

78
Q

How are action potentials unidircetional

A

Action potentials create an active zone region of local difference in membrane potential. Differences in membrane induce a local circuit. Current spreads from the negative active zone to positively charged surrounding membrane

79
Q

How does ion flow occur

A

through specialised transmembrane voltage dependent ion channels

80
Q

what are the key properties of voltage dependent ion channels

A
  1. Ion specific – generally only one specific ion can pass through a channel
  2. Voltage sensitive – channels open/close in response to changes in membrane potential
81
Q

Where on the axon are action potentials triggered

A

axon hillock - has the lowest threshold across the cell

82
Q

What does the stimulus threshold being released cause

A

Na+ channels opening triggering an action potential

83
Q

Ion movement - depolarisation

A

voltage gated Na+ channels open rapidly – Na+ enters the cell, voltage gated K+ channels slowly open

84
Q

ion movement - repolarisation

A

Na+ channels close slowly. Voltage gated K+ channels continue to open – K+ leaves the cell

85
Q

Ion movement - hyperpolarisation

A

K+ continues to enter the cell, K+ channels close slowly

86
Q

Ion movement - afterpolarisation

A

K+ and Na+ actively transported, membrane returns to resting potential

87
Q

What are the 2 forms of synapses

A
  1. Electrical synapses – transmission by current
  2. Chemical synpases – transmission by chemical
88
Q

Features of electrical transmission

A

instantaneous, bidirectional transmission of signal via ion current . Allow for electrical coupling of adjacent cells. Rapid repsonse. Highly synchronised neuronal firing

89
Q

Electrical synapse - gap junction

A

Gap junction connections composted of hemichannels on pre and post synaptic side of membrane, each formed by six connexin proteins

Gap junctions close in response to elevated Ca2+

Also have important roles in glia (astrocyte Ca2+ signalling. Schwaan cell layers)

90
Q

Chemical synaptic junctions

A

Signal transduction is not facilitated through direct cell contact. A chemical signal is transmitted across a cleft, or gap between cells. Diffusion of a chemical signal across the cleft is slower than electrical transmission across gap junctions. Chemical transmission allows for amplification of signal to the target neuron

91
Q

What defines a neurotransmitter

A
  1. Synthesized in the presynaptic neuron
  2. Can be released into the synaptic cleft and elicit a response in target neurons when present in sufficient concentration
  3. Can be experimental added to a target neuron and cause same response as endogenous transmitter release
92
Q

What type of signal is given by the chemical synaptic junction

A

excitory or inhibitory - depends on type of receptor

93
Q

Where are axodendritic synpases usually found

A

synapses are most common in the brain, with pre-synapses trageting post-synpatic receptors in dendrites

In ‘spiny’ neurons, axo- dendritic post-synapses form on specialised spine structures

94
Q

Where can post-synaptic receptors be found

A

in other compartments of the target neuron

95
Q

What is axosomatic

A

synapsing at the cell body

96
Q

What is axoaxonic

A

synapsing at the axon (or presynapse)

97
Q

What do pre-synaptic terminals contain

A

synaptic vesicles (specialised vesicles loaded with neurotrnsmitters)

98
Q

Where do synpatic vesicles release their content

A

dock with the synaptic membrane, releasing their conetent across the synaptic cleft (~20nm)

99
Q

what are chemical synapses enriched for

A

energetically demanding, and enriched for energy producing mitochondria

100
Q

How can post-synapses be identified

A

by a post-synaptic density, a region enriched from receptors and associated machinery

101
Q

Function of glia found at the synaptic junction

A

support synpase function, particularly clearance of transmitters from the cleft

102
Q

What stimulates neurotransmitter release

A

action potentials recahing the pre-synaptic bouton and triggering a Ca2+ influx through voltage-dependent calcium channels

103
Q

What does increased calcium in the terminal activate

A

fusing of synaptic vesicles with the presynaptic terminal

104
Q

What do the released neurotransmitters do when they have crossed the synaptic cleft

A

, bind their type specific receptors and trigger ion influx to either stimulate or supress an action potential in the target neuron

105
Q

Synaptic vesicle neurotransmitter release - neurotransmitter uptake (1)

A

neurotransmitters are loaded into synaptic vesicales by active transporters. Active transporters are selective for specific neurotransmitters

106
Q

Synaptic vesicle neurotransmitter release - reserve pool (2)

A

synaptic vesicles loaded with neurotransmitters are intially tethered to the actin cytoskeleton by snapsin 1. Reserve pool synaptic vesicles can be released from the cytoskelton by Ca2+ dependent phosphorylation of synapsin 1

107
Q

Synaptic vesicle neurotransmitter release - docking (3)

A

synaptic vesicles are recruited from the reserve pool to a reasable pool at the pre-synaptic membrane. Reserve pool vesicles are released from the cytoskeleton by calcium depndent phosphorylation of synapsin 1 (by kinases including PKC). Releasable pool synaptic vesicles are located at the active zone

108
Q

Synaptic vesicle neurotransmitter release - priming (4)

A

ATP dependent process partially fusing synaptic vesicles with the pre-synaptic membrane. Priming and subsequent fusion are facilitated by ‘SNARE’ proteins. V – snare: located on the synaptic vesicle synaptobrevin. T-snare: located on the presynaptic terminal syntaxin, SNAP-25. Without Ca2+ bound, synaptotagmin blocks fusion

109
Q

Synaptic vesicle neurotransmitter release - calcium influx (5)

A

action potentials trigger a rapid influx of Ca2+ through voltage dependent channels. Activates calcium dependent proteins. Fusion: calcium binding to synaptotagmin causes a confirmational changes, allowing SNARE facilitated membrane fusion to occur. Synaptic vesicle neurotransmitter contents are released into the cleft

110
Q

Synaptic vesicle neurotransmitter release - step 6

A

Synaptic vesicles are coated with endocytic proteins clathrin. Mmembrane bending recovers the synaptic vesicle membrane. Dynamin facilitates scission of the vesicle from in the membrane (activated through GTP -> GDP + P hydrolysis. Clathrin is removed from the vesicles.

111
Q

Synaptic vesicle neurotransmitter release - step 7

A

Recovered synaptic vesicles are acidified by active pumping of H+ for neurotransmitters via specific vesicular transporters:
1. VGLUT: vesicular glutamate transporter
2. VMAT: vesicular monoamine transporter (serotonin, dopamine, adrenaline, noradrenaline, histamine)
3. VAchT: vesicular acetylcholine transporter
4. VGAT: vesicular GABA transporter

112
Q

what can block neurotransmitter relase

A

toxin target SNARE proteins

113
Q

What is botulinum neurotoxins

A

peptide toxins composed of a heavy and light chain. Derived from Clostridium botulinum

114
Q

How can botulinum prevent neurotransmitter release

A
  1. BoNTs bind synaptic terminals of aetyl-choline releasing neurons and internalised by endocytosis
  2. Once within the cytoplasm, light chains of BoNTs A and E bind and cleave the c-terminal of t-SNARE SNAP25 via metalloprotease activity
  3. Disruption of SNAP 25 results in failure of neurotransmitter vesicles to fuse at the synaptic terminal
115
Q

What applications does botulinum neurotoxins have

A

theraputic application beyond cosmetics, treatment of epileptic seizures and muscle spasms

116
Q

What is tetanus toxin (tetanospasmin)

A

peptide toxins derived from Clostridium tetani

117
Q

What does teatnus toxin bind to

A

s pre-synaptic membrane glycoprotein/lipids in neuromuscular junction and enters motor neuron through endocytosis

118
Q

Where is tetanus toxin transported to

A

the central nervous system and released into synaptic clefts, where it is internalised by inhibitory interneurons. Tetanus toxins access the presynaptic membrane, then binds and cleaves synaptobrevins VAMP 1 / 2

119
Q

Tetanus toxin causes a loss of regulatory GABA release, what does this result in

A

overactivity of motor neuron and powerful, dmaaging muscle spasms

120
Q

How are neurotransmitters produced

A

through enxymatic metabolism of precursors

121
Q

Where are small amino acid neurotransmitters synthesised

A

enzymatic processing occurs in the cytosol (cell body or pre synaptic terminal). Transmitters are packaged into synaptic vesicles

122
Q

Where are large neuropeptide neurotransmitters synthesised

A

Produced as pre-peptides in the soma ER-Golgi. Packaged into dense-core vesicles. Transported to presynaptic terminal for processing and secretion

123
Q

What is the most common excitatory neurotransmitters

A

glutamate - CNS. pyramidal neurons - cortex. granule cells - cerebellum

124
Q

How is glutamate synthesised

A

Metabolised by cytosolic Glutaminase enzyme from precursor Glutamine

125
Q

How is glutamate loaded into synaptic vesicles

A

VGLUT transporter

126
Q

How is glutamate cleared from the synaptic cleft

A

by neuronal and astrglial glutamate transporters

127
Q

What do neurons do to glutamate

A

return to metabolic pool or reloaded into synaptic vesicles

128
Q

What do astrocytes do to glutamate

A

Glutamate converted to glutamine by glutamine synthetase. Secreted from astrocytes and taken up by neuronal glutamine transporters

129
Q

What is the most common inhibitory neurotransmitter in mammalian CNS

A

GABA

130
Q

How is GABA synthesised

A

from glutamate by glutamic acid decarboxylase (GAD)

131
Q

What produces GABA

A

lpha-ketoglutarate, a produce of the mitochondria Krebs cycle

132
Q

What loads GABA into synaptic vesicles

A

VGAT - vesicular GABA transporter

133
Q

What clears GABA from the synaptic cleft

A

be neuronal and astroglial GABA transporters

134
Q

GABA and neurons

A

GABA return to metabolic pool or reloaded into synaptic vesicles

135
Q

GABA and astrocytes

A

GABA converted to glutamine and enters the glycine processing pathway to return to neurons

136
Q

Fast transmission

A

ligand gated ion channels induce changes in post-synaptic membrane potential in milliseconds

137
Q

Slow transmission

A

Metabotropic receptors coupled to secondary messengers. Slowe (milliseconds-minutes) and long lasting (minutes-days) changes

138
Q

What do ionotrophic receptors allow for in EPSPs

A

influx of Na+, K+ and Ca+ membrane depolarisation

139
Q

How many excitatory post-synaptic potentials are needed to stimulate an action potential

A

Many EPSPs stimulating a post-synaptic membrane within ~10ms are required to overcome threshold and induce an action potential

140
Q

What are IPSPs

A

inhibitory post synaptic potentials

141
Q

What do iontrophic receptors allow for in IPSPs

A

allow influx of Cl-. Reduced change of membrane reaching threshold.

142
Q

What ligan-gated ion channels are included in the cys-loop family

A

Ionotrophic channels including those for acetylcholine, GABA, Glycine and serotonin

143
Q

What are all cys loop receptors

A

pentamers of subunits forming a pore

144
Q

What defines channel activity

A

Combinations of alpha, beta, gamma and delta subunits defines channel activity (physiological function, pharmacology)

145
Q

How can we see what channels actually look like

A

Advanced ‘cryo’ electron microscopy

146
Q

How are glutamate receptors defined

A

by selective inhibitors - are all tetrameric

147
Q

What are the 3 categories of glutamate receptors

A
  1. AMPA - GluR1, GluR2 (voltage gating, Ca2+ slectivity), GluR3, GluR4
  2. Kainate – GluR5, GluR6, GluR7. Functions less well described, more limited distribution
  3. NMDA – heterotetramer of NR1 (8 isoform), NR2 (4 isoforms) NR3 confers inhibitory activity. Voltage gated – depolarisation requires to activate. Allow large Ca2+ permeable, allowing activation of secondary messengers. Roles in long term potentiation and long term depression
148
Q

What blocks the NMDA receptors at resting potential

A

voltage gated Mg2+ ions, removed by membrane depolarisation

149
Q

How can NMDA receptor activity be potentiated

A

by binding of co-agonists, D-serine and glycine

150
Q

Why can NMDA receptors allow for longer term activation of secondary messengers

A

because they are permeable to Ca2+

151
Q

What does modulation of AMPA receptor activity allow for a role in

A

long-term potentiation and long-term depression

152
Q

what activates metabotropic receptors

A

neurotransmitters

153
Q

Why do metabotropic receptors have slow transmission

A

indirect activation of ion channels

154
Q

What does activation of metabotropic receptors lead to

A

a down stream signalling cascade

155
Q

What effect on neuronal activity do metabotropic receptors have

A

excitatory or inhibitory

156
Q

Metabotropic receptors long-term effects

A

neuronal function and morphology

157
Q

What is homosynaptic depression

A

reduced activity within the pathway - I.e., not requiring a modifying cell

158
Q

Short-term habituation

A

Aplysia exposed to 10 stimuli = habituated response lasts several minutes

159
Q

Long-term habituation

A

Aplysia exposed to 10x stimuli x 4 sessions = habituated response lasts several weeks

160
Q

What is sensitisation

A

learning to avoid a noxious stimulus

161
Q

What is facilitisation

A

increased strength of post-synaptic potential to a stimulus if closely paired with a prior stimulus

162
Q

What is dishabituation

A

overcoming a habituated response

163
Q

What is heterosynaptic processing

A

synapse activity altered by a modifying neuron

164
Q

What do modulatory inter-neurons release in the short-term sensitization signaling cascade

A

serotonin (5-HT) onto G-coupled 5-HT receptors on presynaptic terminals of sensory neurons

165
Q

short-term sensitization signaling cascade - pathway 1

A
  1. Secondary messenger cyclic adenosine monophosphate produced in presynapse
  2. Activation of cAMP dependent protein kinase A (PKA) [NB PKA has 2 catalytic and 2 regulatory subunits]
  3. Phosphorylation induced closing of outwards K+ channel extend action potential, increasing presynaptic Ca2+ levels
  4. Increased calcium promotes increased neurotransmitter release
166
Q

short-term sensitization signaling cascade - pathway 2

A
  1. Enhanced activation of phospholipase C (PLC)
  2. Increased production of diacylglycerol (DAG) activates protein kinase C (PKC)
  3. Phosphorylation of presynaptic proteins increases mobilisation of reserve glutamate vesicles to releasable vescile pool
167
Q

What does short-term sensitization do

A

increase synaptic release for minutes - hours

168
Q

Consolidation

A

Long-term sensitization requires more stable changes in synaptic function and architecture

169
Q

Long-term sensitization - what causes altered gene expression

A

Sustained activation 5-HT metabotropic receptors

170
Q

Long-term sensitization - result of activation of CREB regulated genes

A

results in increased production of synpases, changing the morphology of neurons and strengthening its activity

Organisms And Their Environment (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions