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ZOO 3600 > Midterm > Flashcards

Midterm Flashcards

1
Q

animal physiology

A

study of how animal function at all levels of organization to accomplish something by considering physiology, biochemistry, morphology, and biomechanics

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2
Q

comparative animal physiology

A

in light of evolution, compare species, and bodily systems to understand the diversity of physiological systems

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3
Q

August Krogh Principle

A

there are optimally-suited animals study study most biological problems, which provide insight into principles that are highly applicable because traits are often conserved

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4
Q

2 types of physiological regulation

A

conformers and regulators

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5
Q

conformers

A

internal fluctuation matches external fluctuation as in a line of conformity

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6
Q

regulators

A

internal fluctuation is minimal with respect to external fluctuation within the zone of stability, internal fluctuation is greater with respect to external fluctuation outside the zone of stability

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7
Q

zone of stability

A

indicates physiological conditions that an animal’s physiological systems are best adapted to and work best under

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8
Q

homeostasis

A

the tendency to maintained relative internal stability in the face of external fluctuations, maintained by regulatory systems

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9
Q

homeostasis nor regulatory systems equate to

A

constancy

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10
Q

parameter specific regulation

A

whether an animal uses conformity or regulation is parameter specific – lizard conforms to external temperature but regulate water chloride concentrations

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11
Q

negative feedback

A

control system regulates a variable by opposing it deviation from a set point therefore keeping the variable within its homeostatic range

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12
Q

positive feedback

A

control system regulates a variable by rapidly deviating from a set point therefore promoting a unidirectional response that is a non-homeostatic change

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13
Q

acclimation

A

process of change in response to an isolated environmental variable in the lab, within an organism’s lifespan, largely reversible

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14
Q

acclimatization

A

process of change in response to a natural environmental variation including multiple variables, within an organism’s lifespan, largely reversible

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15
Q

adaptation

A

process of change through natural selection leading to an organism whose physiology, anatomy, and behaviour are suited to the demands of its environment by changes to the DNA, over multiple generations, largely irreversible

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16
Q

lipid bilayers separate

A

the intracellular fluid from the extracellular fluid

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17
Q

lipid bilayers composition

A

peripheral membrane proteins, integral membrane proteins, and phospholipid molecules

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18
Q

fluid mosaic

A

the lipid bilayer composition is constantly changing and is composed of multiple subunits

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19
Q

permeability of epithelial cells

A

high permeability, thin epithelium and high SA, passive diffusion of O2 and CO2 down the concentration gradient

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20
Q

permeability of integument cells

A

low permeability, thick epithelium impenetrable to water to regulate internal environment

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21
Q

integument low permeability depends on 3 possible substances

A

keratins, lipids, waxes

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22
Q

2 paths materials follow across an epithelium

A

transcellular path and paracellular path

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23
Q

transcellular path

A

larger and/or charged molecules require 2 sets of membrane transporters to cross the (1) apical and (2) basolateral membranes

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24
Q

paracellular path

A

small and/or polar molecules must be able to move the the band of tight junctions

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25
Q

heterogenous composition of lipid membranes

A

inner and outer membrane layers are distinct, lipid rafts are regions that accumulate cholesterol and glycolipids

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26
Q

lipid rafts

A

regions that accumulate cholesterol and glycolipids, they are more rigid, highly mobile, and recruit specific proteins involved in signalling pathways

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27
Q

membrane fluidity alters between 2 states

A

liquid crystalline (oil) and gel (butter)

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28
Q

general changes that allow membranes to retain their fluidity

A

homeostatic changes, changes in phospholipid composition

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29
Q

membrane fluidity state at the norm

A

liquid crystalline, allows for functional proteins

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30
Q

4 changes that can occur to alter membrane fluidity for acclimation or acclimatization

A

fatty acid chain length
saturation
polar head groups
cholesterol

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31
Q

fatty acid chain length and membrane fluidity

A

inversely related to membrane fluidity

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32
Q

saturation and membrane fluidity

A

inversely related to membrane fluidity

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33
Q

polar head groups and membrane fluidity

A

phosphatidylcholine (PC) cylinder like so more compact, phosphatidylethanolamine (PE) cone like so less compact

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34
Q

cholesterol and membrane fluidity

A

directly related to membrane fluidity

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35
Q

cholesterol has complex membrane properties for 2 reasons

A

(1) cholesterol disrupts interaction between fatty acid tails, increasing membrane fluidity and (2) cholesterol fills gaps between polar heads, decreasing membrane fluidity to small molecules

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36
Q

homeoviscous adaptation

A

under physiological conditions, animals have similar membrane fluidity, maintained by changes in phospholipid composition

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37
Q

it is of physiological important that concentrations of inorganic solutes are regulated between

A

intracellular and extracellular compartments

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38
Q

muscle cell interior of [Na+], [K+], [Ca2+], [Cl-], [A-]

A 
[Na+]	10 mM
[K+]	140 mM
[Ca2+]	<10-3 mM
[Cl-]	3-4 mM
[A-]	140 mM
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39
Q

[A-]

A

molar equivalent of negative charges carried by molecules and ions, primarily large proteins

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40
Q

simple diffusion

A

overall movement down the concentration gradient, more molecules pass through the membrane from high to low concentration by a chance process

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41
Q

Fick’s law of diffusion calculates

A

net rate of diffusion os a solute across a membrane

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42
Q

Fick’s law of diffusion variables J, D, P, MW, C1, C2, X

A

J rate of diffusion, quantity of solute diffusing per unit time
D diffusion coefficient
P permeability (pore size)
MW molecular weight
C1 value of high concentration
C2 value of low concentration
X distance separating C1 from C2 (thickness of membrane)

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43
Q

5 factors influence J, rate of diffusion

A

concentration gradient (direct), permeability (direct), molecular weight (inverse), distance (inverse), temperature (direct)

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44
Q

electrochemical gradient

A

movement of solutes across a permeable membrane determined by the electrical (charge) gradient and the chemical (concentration) gradient

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45
Q

ionic charge separation occurs where with respect to the membrane, why

A

within nanometers of the membrane (net positive and net negative charges concentrate) because the lipid bilayers can maintain separation of oppositely charged ions

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46
Q

reinforcing with respect to the electrochemical gradient

A

concentration and electrical effects support fast diffusion

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47
Q

opposing with respect to the electrochemical gradient

A

concentration and electrical effects contrasting, slow diffusion

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48
Q

osmosis

A

diffusion of water through a semipermeable membrane from a region of low solute concentration to a region of high solute concentration

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49
Q

is osmosis, water stops moving when

A

hydrostatic pressure (weight of water) equals osmotic pressure (force associated with movement of water)

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50
Q

osmolarity

A

accounts for the total concentration of penetrating and non-penetrating solutes

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51
Q

tonicity

A

accounts for the total concentration of non-penetrating solute only

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52
Q

the effect of tonicity depends on difference in 2 things

A

osmolarity and the permeability of the membrane

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53
Q

Donnan equilibrium

A

predicts the distribution of ions across a membrane will be unequal is the membrane is impermeable to one or more types of charged particles

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54
Q

3 rules dictate the distribution of ions across a membrane that is impermeable to one or more types of charged particles

A

chronological order only: (1) principle of electroneutrality, (2) product of the concentration of permeant ions inside = the concentration of permeant ions outside, (3) osmolarity in = osmolarity out

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55
Q

2 types of membrane transport

A

passive and active

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56
Q

passive transport

A

requires no energy, solute moves from high to low concentrations

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57
Q

active transport

A

requires energy, solute moves from low to high concentrations

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58
Q

2 types of passive transport

A

simple diffusion and facilitated diffusion

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59
Q

simple diffusion membrane transport

A

gases, no transporter required

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60
Q

facilitated diffusion membrane transport

A

requires either (a) channel proteins (open/close) or (b) carrier proteins (change in conformation via non-covalent bonds)

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61
Q

equations that illustrates the saturation kinetics of facilitated transport

A

Michaelis-Menton equation

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62
Q

describe facilitated diffusion curve

A

hyperbolic curve with plateau at the point of transporter saturation

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63
Q

saturation point of facilitated diffusion versus simple diffusion

A

simple diffusion does not have a saturation point

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64
Q

the substrate concentration [S] that gives 1/2 Vmax

A

Km Michaelis constant

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65
Q

3 types of transporters

A

uniporter, antiporter, symporter (co-transporter)

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66
Q

substrate transport is determined by

A

channel composition

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67
Q

transporters are driven by either

A

a concentration gradient or ATP

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68
Q

uniporter

A

glucose, Na+, unidirectional transport of 1 substrate

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69
Q

antiporter

A

Na+/K+ ATPase, Cl-/HCO3- exchanger, counter-directional transporter of 2 different subtrates

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70
Q

symporter (co-transporter)

A

KNCC (Na+, K+, 2Cl- co-transporter), K+/Cl- co-transporter, unidirectional transporter of 2 or more different substrates at the same time

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71
Q

3 types of ion channels involved in facilitated diffusion

A

voltage-gated channels, ligand-gated channels, mechanically-gated channels

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72
Q

voltage-gated channels

A

Na+ and heart contraction, open/close in response to changes in membrane potential

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73
Q

ligand-gated channels

A

acetylcholine and neurotransmission, open/close in response to presence/absence of ligand

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74
Q

mechanically-gated channels

A

pushing on skin and firing of AP to nerve for sense of touch, open/close in response to changes in cell shape

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75
Q

2 types of active transport

A

primary active transport and secondary active transport

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76
Q

primary active transport

A

energy released by ATP hydrolysis drives solute (X) movement against an electrochemical gradient

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77
Q

secondary active transport

A

energy from electrochemical gradient (X) drives co-transport of a second solute (S) against its electrochemical gradient

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78
Q

2 types of primary active transport pumps

A

electrogenic and electroneutral

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79
Q

electrogenic primary active transport pump

A

sets of a difference of electrical charge, Na+/K+ ATPase maintains electrical potential, maintains high [K+]in and [Na+]out for use in secondary transport (3Na+ for 2K+)

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80
Q

electroneutral primary active transport pump

A

does not set up a difference in electrical charge, H+/K+ ATPase responsible for secretion of stomach acid in vertebrate stomach lining, protein expressed along the canaliculi (invaginations to increase SA) of parietal cells that line stomach cavity wall (2H+ for 2K+)

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81
Q

aquaporin

A

uniporter channel protein discovered by Peter Agre who determined the DNA and amino acid sequences of the water channel AQP1 using Xenopus (frog) oocytes (eggs) to demonstrate that AQP1 is responsible for osmosis

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82
Q

Xenopus oocyte experiment

A

Xenopus oocyte is naturally water resistant. Xenopus oocyte microinjected with RNA coding for AQP1 (mammalian protein) expresses protein, tritiated water (radioactive) in hypotonic solution indicates increased permeability (cell ruptures). Xenopus oocyte microinjected with RNA coding for AQP1 (mammalian protein) and RNA inhibitor (mercury) does not express protein, absence of movement of tritiated water (radioactive) in hypotonic solution indicates no change in permeability.

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83
Q

aquaporins are abundant in

A

the kidney and RBCs

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84
Q

aquaporins in the kidney

A

Arginine vasopressin (AVP) hormone regulates kidney water permeability. The pituitary gland releases AVP in response to thirst when blood concentration in increased. AVP binds to vasopressin receptor, triggering the signalling molecule cAMP to activate protein kinase A. Protein kinase A phosphorylates storage vesicles with aquaporins, which move water from collecting duct of kidney back to blood

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85
Q

prior to Cajal’s microscopy work and drawing of

A

cells of the chick cerebellum the nervous system was though to be one elongate body

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86
Q

application of August Krogh principle and neurons

A

giant axon of the squid was the source of fundamental knowledge of the nervous system

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87
Q

fraction of neural cells that generate action potential

A

1/10, neurons

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88
Q

4 functional zones of neurons

A

dendrites, axon hillock, axon, axon terminals

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89
Q

function of dendrites

A

signal reception, input

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90
Q

function of axon hillock

A

signal integration

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91
Q

function of axon

A

signal conduction

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92
Q

function of axon terminals

A

signal transmission, output

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93
Q

synapse

A

connection between 2 nerves, or 1 nerve and 1 muscle cell (myocyte)

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94
Q

myelin sheath

A

insulation for effective transmission of AP, prevents unintended transmission between nerves

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95
Q

loss of myelin sheath associated with

A

multiple sclerosis

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96
Q

soma of the neuron

A

cell body

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97
Q

glial cells

A

majority of neural cells, do not generate AP, support neurons

98
Q

4 types of glial cells

A

Schwann cells, oligodendrocytes, astrocytes, microglia

99
Q

Schwann cells

A

form myelin in the PNS

100
Q

oligodendrocytes

A

form myelin in the CNS

101
Q

astrocytes

A

transport nutrients, regulate synaptic neurotransmitter levels (clean up released neurotransmitters to maintain rapid response), remove dead cell in CNS

102
Q

microglia

A

remove debris in CNS, remove dead cells in CNS

103
Q

neural signals are

A

unidirectional: cell body to axon terminals

104
Q

CNS

A

brain and nerves with cell body in brain case or spinal cord

105
Q

PNS

A

nerves with cell body outside of brain case or spinal cord

106
Q

PNS function

A

sends output from sensory pathways to CNS and carries out motor pathways as directed by the CNS

107
Q

3 types of motor pathways

A

(1) autonomic (involuntary: sympathetic (stress/adrenaline) and parasympathetic (relax / acetylcholine)) and (2) somatic (voluntary)

108
Q

neuromuscular junction stage 1

A

electrical potential: AP arrives to pre-synaptic cell, triggering voltage-gated Ca2+ channel to open, Ca2+ enters the pre-synaptic cell

109
Q

neuromuscular junction stage 2

A

chemical potential: Ca2+ signals vesicle filled with neurotransmitters to release ACh into synaptic cleft

110
Q

neuromuscular junction stage 3

A

chemical potential: ACh triggers ligand-gated channels to open in the post-synaptic cell, Na+ enters the post-synaptic cell which generates post-synaptic AP

111
Q

neuromuscular junction stage 4

A

electrical potential: propagation of electrical potential in the post-synaptic cell activate the myocyte to contract

112
Q

resting membrane potential

A

difference in charge across the membrane caused by differences in ion concentration across the membrane

113
Q

neurons are excitable

A

(can rapidly change their membrane potential) due to the activation of channel and carrier proteins which rapidly move ions

114
Q

changes in membrane potential act as

A

electrical signals

115
Q

the distribution of an ion across a semi-permeable membrane depends on

A

the electromotive force

116
Q

electromotive force

A

force generates by electrical gradient and chemical gradient

117
Q

potential difference across a membrane when the forces generated by the electrical and chemical gradient are in equilibrium

A

equilibrium potential

118
Q

equilibrium potential, resting Vm

A

-70 mV

119
Q

depolarization, how to return to resting potential

A

more positive than resting potential, undergo repolarization to return to resting potential

120
Q

hyperpolarization, how to return to resting potential

A

more negative than resting potential, undergo repolarization to return to resting potential

121
Q

Nernst equation

A

calculates the equilibrium potential for single ions, proportional to the ratio of the concentration of an ion X across the membrane (greater ion ratio, greater equilibrium potential), Ex

122
Q

Nernst equation variables R, T, s, F

A

R gas constant
T absolute temperature
z valence on ion (+/-)
F Faraday constant

123
Q

Nernst equation is standardized at

A

18˚C

124
Q

Goldmann equation

A

calculates the final membrane potential Vm for all contributing ions, proportional to the ratio of the concentrations of ions across the membrane and the permeability (depending on presence / number of ion channels) of the membrane to the ions (greater ion ratio, greater equilibrium potential)

125
Q

Goldmann variables R, T, F, P

A

R gas constant
T absolute temperature
F Faraday constant
P permeability

126
Q

Goldmann equation is standardized at

A

18˚C, use proportionality of permeability: low permeability to Cl- and Ca2+, permeability of Na+ is 1/100 of K+

127
Q

Vm (-92 mV) of a cell is relatively close to Ek (-101 mV)

A

(1) cell membranes have a higher permeability to K+ than to other ions, (2) the Na+/K+ ATPase pump indirectly contributes to the Vm by maintaining high internal [K+] (move negative inside cell than outside because 3Na+ out for every 2K+ in)

128
Q

neurons have massive amount of 2 things

A

mitochondria and ribosomes to produce neurotransmitters

129
Q

ligands are released from neurons in proportion to

A

AP

130
Q

neurons are organized into

A

functional circuits

131
Q

functional circuits

A

rapidly conduct information to a target

132
Q

information through neuronal circuits alternate between 2 signal types

A

graded signals (dendrites, soma) and all-or-none- signals (axon hillock, axon, axon terminals)

133
Q

information is carried through neuronal circuits via

A

alternating electrical signals (AP) and chemical signals (neurotransmitters)

134
Q

sensory neurons

A

afferent fibres, carry information inward toward interneurons

135
Q

motor neurons

A

efferent fibres, carry information outward toward effectors (ie. muscle)

136
Q

grade potential

A

electrical signals generated by ligand-gated channels in the dendrites and soma, the ion carries the charge down the electrochemical gradients, net movement stops when equilibrium potential is reached

137
Q

ligand-gated ion channels convert chemical signals in electrical signals

A

by changing membrane potential

138
Q

the magnitude of grade potentials is proportional to

A

stimulus strength (ie. concentration of the neurotransmitter)

139
Q

graded potential can either

A

depolarize the cell (less negative via Na+ and Ca2+ channels) or hyperpolarize the cell (more negative via K+ and Cl- channels)

140
Q

3 reasons graded potential travel short distances

A

membrane permeability, cytoplasmic resistance, decremental spread (electrotonic conduction)

141
Q

membrane permeability impacts graded potential

A

leakage of charge ions across the membrane

142
Q

cytoplasmic resistance impacts graded potential

A

inherent resistance to current flow, ion entry difficulty, friction of medium

143
Q

decremental spread (electrotonic conduction) impacts graded potential

A

net charge decreases further away from ion entry

144
Q

local charge does not equal

A

axon hillock charge

145
Q

in order for the exon to fire an AP, graded potentials in the axon hillock need to depolarize the membrane beyond

A

threshold potential

146
Q

spatial summation

A

graded potentials from different locations can interact to influence the net change in membrane potential at the axon hillock (consider inhibition and activation signals)

147
Q

temporal summation

A

graded potentials occurring at slightly different times can interact to influence the net graded potential at the axon hillock (sub-threshold potentials that do not overlap in time do not summate, sub-threshold potentials that overlap in time summate and may trigger an AP – even though same number of ions involved in each scenario)

148
Q

sub-threshold stimulus induce

A

proportional response in voltage threshold

149
Q

supra-threshold stimulus induce

A

uniform action potential

150
Q

instead of increasing AP, multiple action potentials are fired in series in response to

A

chronic stimulation

151
Q

AP triggered

A

when membrane potential at axon hillock reach threshold (~55 mv)

152
Q

AP are charcertistically

A

large (~△100 mV), brief (2-3 msec), and carry an all-or-none response

153
Q

current is carried by

A

ions

154
Q

ion concentration is restored by

A

Na+/K+ ATPase pump

155
Q

Na+/K+ ATPase pump versus AP formation and ATP

A

Na+/K+ ATPase pump requires ATP, AP formation does not require ATP

156
Q

structure and function of the startle response in cockroaches

A

mechanically-gated channels in the filiform hair receptors are stimulated by wind and initiate AP across the giant interneuron, leg motor neurons fire a series of AP to effectors in response to chronic stimulus, muscle tension is controlled in 1/10 sec

157
Q

single cell patch clamp rig

A

isolated neurons bathed in mimic extracellular solution, glass micro-pipette electrode containing mimic extracellular solution uses suction to remove membrane patch containing singular channel and surrounding membrane, bathed in mimic intracellular solution, path-clamp recording of a single-channel currents using amplified to detect fine change in voltage by using electrons to quantify sodium current

158
Q

use the single cell path clamp rig to

A

map the relative timing or opening and closing of voltage-gated channels to the characteristic phases of the AP

159
Q

in the single cell patch clamp rig, conductance equates to

A

membrane permeability

160
Q

Na+ and K+ channels are activated by the same AP but

A

exhibit different timings of response

161
Q

following initial depolarization, inward current of Na+ is

A

‘instant’ and short-lived, depolarization involves 30x increase in Na+ conductance (gNa)

162
Q

following initial depolarization, outward current of K+ is

A

delayed and longer-lived, repolarization involves a decrease in gNa and a delayed increase in K+ conductance (gK)

163
Q

hyperpolarization follows AP initial repolarization

A

because gK remains elevated for some time after the AP

164
Q

2 gates in voltage-gated Na+ channels

A

voltage-dependent activation gate (open/close) and voltage-dependent time-delayed inactivation gate (open/close)

165
Q

conformation states in voltage-gated Na+ channels

A

(1) activation gate closed (capable of opening), (2) open (activated), (3) inactivation gate closed (inactivates, not capable of opening)

166
Q

Na+ channel gates

A

activation gate (fast, ‘stick’) and inactivation gate (slow, ‘ball’)

167
Q

1 gate in voltage-gated K+ channels

A

voltage-dependent time-delayed gate (open/close)

168
Q

conformation states in voltage-dependent K+ channels

A

(1) closed, (2) open

169
Q

refractory period

A

prevents back flow of sodium channel activation

170
Q

absolute refractory period

A

the inactivation gate of the Na+ channel closes to prevent backward signalling, no AP can be triggered

171
Q

relative refractory period

A

K+ channel opens to return membrane to rest, difficult for AP to be triggered because charge is hyperpolarized

172
Q

propagation of AP

A

Na+ local currents spread longitudinally via electrotonic conduction depolarizing adjacent patches

173
Q

AP at nodes of Ranvier via

A

voltage-gated channels

174
Q

electronic conduction along internode via

A

diffusion of ions carrying charge

175
Q

AP is triggered at

A

axon hillock

176
Q

why does axonal conduction use a combination of electrotonic current flow and APs

A

electrotonic flow is faster but graded and can only travel short distances, AP increase efficiency but is slow

177
Q

saltatory conduction

A

the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials: combination of electronic (passive diffusion) and action potential

178
Q

2 factors affecting conduction speed

A

length constant and time constant

179
Q

length constant λ

A

length taken for Vm to reach 63% of its maximal value, but electrotonic conduction enhanced by high membrane resistance Rm and low longitudinal (axoplasmic) resistance Rl

180
Q

time constant τ

A

times taken for V, to reach 63% of its maximal value, but membrane voltage changes are reduced by high membrane resistance Rm and high membrane capacitance (ability to absorb / store electric charge) Cm

181
Q

axon myelination increases

A

speed of propagation of an AP because myelination increase the length constant because insulation inhibits loss of charge (Rm increases)

182
Q

increasing axonal diameter increases

A

speed of propagation of an AP because increasing axonal diameter increases the length constant because with increased diameter there is less interaction between the ions and cell walls which reduced resistance and flow distance increases (Rl increases)

183
Q

myelination increases rate of conduction velocity in lieu of

A

a larger axon diameter, smaller axon diameter allow for more nerves per cubic area allowing for more complex neuronal processing

184
Q

2 types of signals across the synapse

A

electrical and chemical

185
Q

electrical synapse

A

transfer information between cells directly via ionic coupling via gap junctions: connexon proteins

186
Q

how to connexon proteins of gap junctions help transfer information between cells directly via ionic coupling

A

by narrowing the gap between cells and lowering the resistance between cells

187
Q

advantage of electrical synapse

A

faster response than chemical synapse because of discrete bridges between cells

188
Q

disadvantage of electrical synapse

A

current decays between neurons exist, decremental charge spread across cells leads to reduced voltage in postsynaptic cells

189
Q

crayfish escape circuit

A

electrical synapses first demonstrated between ventral nerve cord giant axons and motor neurons responsible for tail-flip reponse

190
Q

chemical synapse

A

transfer information between cells indirectly via neurotransmitters, involves a signal transmission zone consisting of a presynaptic cleft, a synaptic cleft, and a post-synaptic cell (either neuron, muscle, or endocrine glands)

191
Q

advantage of chemical synapse

A

induce APs so long as the threshold potential is reached, efficient transduction

192
Q

disadvantage of chemical synapse

A

slower response than electrical synapse because of indirect bridging between cells, energetically expensive to (1) make dendritic spines, (2) prepare ACh in vacuoles – high demand for mitochondria

193
Q

fast and slow chemical synapses are defined by and not by

A

their post-synaptic mechanisms and not their neurotransmitters

194
Q

fast chemical synapses

A

act through ionotropic receptors on the post-synaptic membrane

195
Q

slow chemical synapses

A

act through metabotropic receptors on the post-synaptic membrane

196
Q

ionotropic receptors

A

ligand-gated ion channels, fast change in charge because voltage-gated channels are near ligand-gated channels on postsynaptic cell

197
Q

metabotropic receptors

A

neurotransmitter binds to either a channel or not a channel (eg. ligand binds to G Protein Coupled Receptor (GCPR), activates G Protein, activates Effectors – memory, gene expression, growth (hormones))

198
Q

primary neurotransmitter at the vertebrate neuromuscular junction

A

ACh

199
Q

signal strength across the neuromuscular junction influenced by 2 things

A

neurotransmitter amount and receptor activity

200
Q

neurotransmitter amount

A

rate of release (primarily) vs rate of removal (by enzyme)

201
Q

receptor activity

A

density of receptors on postsynaptic cell

202
Q

site of synthesis and recycling of ACh for the neuromuscular junction

A

synapse

203
Q

post-synaptic cell manipulation and the neuromuscular junction

A

manipulates the response of the post-synaptic cell and creates a highly controlled system response

204
Q

pre and post synaptic specializations and the neuromuscular junction

A

pre-synaptic terminal boutons, Schwann cell sheath. basement membrane, junctional folds, mitochondria, synaptic vesicles, high concentration of ACh receptors activate adjacent voltage-gated channels

205
Q

pre-synaptic terminal boutons and the neuromuscular junction

A

branching termini to simultaneously innervate multiple muscle cells to activate contraction, insulated by Schwann cells

206
Q

basement membrane and the neuromuscular junction

A

invaginations into muscle cells

207
Q

junctional folds and the neuromuscular junction

A

invaginations into muscle cells

208
Q

synaptic vesicles and the neuromuscular junction

A

pre-packaged ACh available for instant release

209
Q

7 neuromuscular junction events

A
  1. presynaptic cell voltage-gated Ca2+ channels are opened by AP
  2. Ca2+ concentration increases, signals synaptic vesicles to bind to docking protein
  3. vesicles release neurotransmitter: ACh exocytosis
  4. neurotransmitter binds to ligand-gated channel on post-synaptic cell
  5. current is induced, produces end plate potential
  6. induction of postsynaptic AP
  7. acetylcholine esterase catalyze the breakdown of acetylcholine, delivers choline back to pre-synaptic cell
210
Q

excitatory and inhibitory postsynaptic potentials are based on

A

manipulation of the stimulus and manipulation of pre and post synaptic cells

211
Q

ESPS

A

excitatory postsynaptic potentials move the membrane potential toward the threshold potential (hypopolarize)

212
Q

ISPS

A

inhibitory postsynaptic potentials move the membrane potential away from the threshold potential (hyperpolarize)

213
Q

EPSPs and IPSPs can

A

summate

214
Q

ESPS and ISPS impact depends on relative closeness to

A

stoma and axon hillock

215
Q

whether a neurotransmitter is excitatory and inhibitory depends on

A

properties of its receptor
eg. ionotropic ACh nicotinic receptors – impacts channel protein, eg. metabotropic ACh muscarinic receptors – impacts channel protein or some other cellular process pathway

216
Q

plasticity is rooted in the diversity at

A

the chemical synapse

217
Q

plastcity

A

ability to change synaptic strength over time via synaptic connections and functional properties of neurons: ↑plasticity, ↑complexity, ↑specificity, ↑response

218
Q

example of plasticity of chemical synapse

A

use and production of neurotransmitters and receptors

219
Q

neurons can synthesize more than one kind of neurotransmitter and receptor, including

A

biogenic amines, amino acids, neuropeptides, others…

220
Q

learning and memory are based on

A

modification of neuropathways based on experience

221
Q

learning

A

process of acquiring new information

222
Q

memory

A

retention and retrieval of information

223
Q

synaptic transfer of information depends on

A

its history

224
Q

facilitation

A

strength of response increases despite signal remaining the same, unknown mechanism, opposite of habituation

225
Q

habituation

A

strength of response decreases despite signal remaining the same, unknown mechanism, opposite of facilitation

226
Q

sensitization

A

strength of response increases in response to a novel stimulus, ‘restores’ habituation effects

227
Q

potentiation

A

strength of response increased in response to a strong chronic stimulus

228
Q

2 types of short-term neuromodulation

A

habituation (post-synaptic) and sensitization (post-synaptic)

229
Q

Eric Kendel and the sea slug

A

August Krogh principle example, insight into the brain and learning: stimulation of the mantle or siphon leads to gill withdrawal, this reflex habituates with repeated stimulation (to mantle), this reflex is sensitized (enhanced) with novel stimulation (to head) – observe relatively increased gill withdrawal following novel stimulus, and subsequent habituation

230
Q

reduction and enhancement of motor-neuron EPSP mirror the behaviour of

A

habituation and sensitization, respectively

231
Q

sensitization involves

A

as secondary facilitating interneuron (head sensory neuron: indirect (secondary) contact with motor neuron, axon termini in contact with axon termini of skin sensory neuron)

232
Q

in short-term habituation, there is a reduction in

A

neurotransmitter release by the skin sensory neuron: Ca2+ voltage-gated channel opens less with each tap, less Ca2+ enters the cell, less protein kinase is activated, fewer neurotransmitters vesicles are phosphorylated, fewer ligands are available to bind to ligand-gated channels on the postsynaptic cell, lesser response

233
Q

in short-term sensitization, there is an increase in

A

neurotransmitter release by the skin sensory neuron as a result of presynaptic facilitation from the head sensory neuron: serotonin binds to serotonin receptors in the axon termini, activating a metabotropic pathway which activates cAMP synthesis and increases [cAMP] in the cell, which activates cAMP dependent protein kinase, which phosphorylates channel proteins: Ca2+ channel stays open longer and more Ca2+ is transported into the cell, K+ channel stays closed longer and less K+ is transported into the cell to broaden action potential

234
Q

1 type of long-term neuromodulation

A

potentiation (or long-term potentiation) (post-synaptic)

235
Q

tetanic stimulation simulates

A

strong emotion, repetition of events

236
Q

tetanic stimulation of neurons in the hippocampus leads to

A

increased EPSPs

237
Q

normal synaptic transmission: 1 pule per second

A

Ca2+ is unable to enter the cell via NMDA receptor channel because NMDA Glu receptors are blocked at resting potential by Mg2+ ions even if bound to the ligand Glu, AMOA Glu channel receptors are open at resting potential to produce fast ESPS

238
Q

long-term potentiation induction: 100 pulse per second

A

tetanic stimulation results in strong depolarization of the postsynaptic cell, NMDA Glu receptors release bound Mg2+ so Ca2+ enters the NMDA Glu receptor channel – Ca2+ influx activates Ca2+ dependent protein kinase C which phosphorylates AMPA Na+ channel receptors stored in vesicles stimulating the fusion of the vesicles to the cell membrane, new AMPA Glu channel receptors results in increased capacity to respond to the neurotransmitter Glu

239
Q

long-term sensitization is characterized by

A

increase in neuroreceptors (protein synthesis), as a result of chronic kinase activity: with a strong chronic stimulus, protein kinase C chronically (‘permanently’) phosphorylates AMPA Glu receptors to deliver receptors to the cell membrane, and can activate ↑ gene expression for such receptors at the level of the nucleus

240
Q

what is responsible for the effects of LTP

A

differential gating properties of NDMA and AMPA glutamate receptors and the events regulated by Ca2+ in the postsynaptic neuron

241
Q

glutamate uncaging on a single dendritic spine

A

glutamate is packaged, uncaged by UV light, causes significant depolarization of dendrite, activates protein kinase, which phosphorylates vesicles, which are incorporated into the membrane, resulting in a larger dendritic spine and greater possible response because more ligand-gated channels are available

242
Q

stress hormones encode

A

neurotransmitters, stimulating system consolidation (ie. long term potentiation)

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