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Neurophysiology > Cellular Neuroscience Pt2 > Flashcards

Cellular Neuroscience Pt2 Flashcards

0
Q

What is faster in electrophysiological analysis, many cells or single excitable cell?

A

single excitable cell (msec, sec)

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1
Q

Neurophys has been a study of what?

A

electrical activity of the brain at the global and cellular level

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2
Q

What does electrophysiological analysis of nervous system activity involve?

A

cathode ray oscilloscope recording of VOLTAGE-time displays

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3
Q

Macro electrode are good for what?

A

population responses

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4
Q

What are the diagnostic tools used for population responses?

A
  • EEG, sEP, ERP (cortex & pathwways)
  • compound whole nerve potential (peripheral nerve)
  • EMG (group of muscle cells)
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5
Q

What doe micro-electrodes record?

A

single cell responses

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6
Q

What diagnostic tools are used for single cell recordings?

A
  • single unit extracellular recording
  • single unit Intracellular
  • single unit patch-clamp
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7
Q

what is an ERP?

A

event related potential for cell population recording

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8
Q

what is an EEG?

A

electoencephalogram for recording potentials on the skull

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9
Q

On a graph for ERP, EEG and WNP what is recorded on the y-axis upward

A

ERP - positive up
EEG - negative up
WNP - negative up

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10
Q

in single unit recordings what charge is upward on y-axis?

A

positive up

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11
Q

How are EEG used clinically?

A

diagnostic tool to tell abnormal from normal

identifies where pathology located

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12
Q

What defines a normal EEG?

A

alpha rhythm average around midline

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13
Q

What defines an abnormal EEG?

A

“spikes” in multiple leads

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14
Q

**What is a problem with EEG?

A

the recording cannot tell us anything about what is wrong at the cellular level but can tell us grossly normal vs abnormal

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15
Q

What are ERPs triggered by?

A

sensory input (visual, auditory, somato)

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16
Q

What is receptotopic mapping?

A

map receptor sheets on to the brain (place-to-place mapping of r/c’s to cortex)

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17
Q

****What are ERPs used for?

A

used to evaluate the general viability/functional integrity of a sensory pathway

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18
Q

What are compound whole nerve potentials used for?

A

PNS electrodiagnosis

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19
Q

What is important about graduated electrical stimulation of PNS recordings?

A
  • smallest currents activate large fibers only

- large currents activate all fibers, small and large

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20
Q

In thee PNS which fibers are myelinated and unmyelinated? what is their arrival during a CRO recording?

A

myelinated 1)Aalpha 2)Abeta 3)Adelta
unmyelinated 4) C

= order in which they appear in CRO

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21
Q

What does a abnormal PNS recording look like?

A

-diabetes/MS => demyelination and inability to produce myelinating cells => increased lag time in AP

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22
Q

***** What does peripheral neuropathy look like? significance of whole nerve potential?

A
  • slowing, failure of conducting fibers

- doesnt tel what is happening at cellular level but rather what is happening with the nerve

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23
Q

What are the functional/ clnical significance of EEGs, ERPs, WNP?

A
  • oldest brain recording tech.
  • excellent temporal, poor spatial res
  • used for differential diagnosis of CNS, PNS, sk mm.
    • inability to monitor cell-level processes
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24
Q

What are the benefits of single cell neurophysiology?

A

very fast electrical membrane communication (less than 1 sec)

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25
Q

What is involved in single unit electrophys?

A

plasma membrane

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26
Q

What are electrical membrane signalling directly and indirectly coupled to in single unit electrophys?

A

ion channels and signal transduction pathways

Energy dependent

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27
Q

What type of potential do single unit recording have?

A

all-or-none

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28
Q

What encompass the graded potentials in a neuron and the electrogenic all or none membrane?

A 
graded = dendrite and axon
all-or-none = axon
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29
Q

Are graded potentials passive or active?

A

passive electronic spread

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30
Q

Are all-or-none active or passive regenerative propagation?

A

active

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31
Q

What are some characteristics of functional dynamic polarization?

A

highly ATP dependent

needs glucose & O2 to keep up (ionotropic = fast; melanotropic = slow)

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32
Q

What are the 3 tech. of single cell recording?

A

extracellular, intracellular unit recording & patch clamp

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33
Q

What is the resting membrane potential?

A

-70mV

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34
Q

What is important about patch-clamp?

A

single/group of ion channels

- can be resting, graded, all-or-none

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35
Q

What is the physiological sequence via neuronal chains?

A

electrical => chemical => electrical…etc.

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36
Q

What did Sherrignton discover?

A

stop and go synapses

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37
Q

What is synaptic delay?

A

2msec for synaptic signal to move across synaptic cleft

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38
Q

What controls the actions at the synapse?

A

go (excitatory) and stop (inhibitory) messages

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39
Q

What is the importance of Go and Stop?

A

contraction and relaxation of mm groups etc

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40
Q

What kind of n.t. is Acetylcholine?

A

inhibitory

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41
Q

How do you quiet down striated mm?

A

quiet down CNS (Ach)

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42
Q

What is an excitatory amino acid?

A

glutamate

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43
Q

What is an inhibitory amino acid?

A

GABA

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44
Q

What is thee membrane of excitable cells permeable to?

A

lipid-soluble substances, NOT charged ions

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45
Q

A thin unit membrane acts as a good battery plate & stacks electrical charge, what does it show?

A

capacitance

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46
Q

Electrically charged entities can only get across membrane via what?

A
  • slow crossing via transport proteins

- rapidly via ion channels

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47
Q

Define leakage in p.m.

A

passive ion channels
always open
single ion selective
responsible for RMP or neurons, mm & glia

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48
Q

What are gated ion channels responsible for?

A

graded & all-or none AP for neurosecretion

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49
Q

What are the diffusional tendencies for Na, K, Cl, Ca?

A

Na, Cl, Ca = inward

K = outward

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50
Q

How are conc. differences maintained with Na, Cl, Ca, K?

A

pumped by ion exchange

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51
Q

What are the tendencies of Na?

A

transport = Na-K pump
Intracellular conc = low
Ion diffusion = inward

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52
Q

What are the tendencies of K?

A

transport = Na-K pump
intracellular conc = high
ion diffusion = outward

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53
Q

What are the tendencies of Ca?

A

Transport = Ca pumps
intracell conc = low
ion diffusion = inward

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54
Q

What are the tendencies of Cl?

A

transport = KCC2 co transport
Intracell conc = low
ion diffusion = inward

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55
Q

What does KCC2 K-Cl cotransport involve?

A

1 K and 1 Cl => outside cell = K moving with conc gradient and Cl against

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56
Q

What forces act on ions dissolved in solution?

A
  • diffusional

- electrostatic

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57
Q

What is the electrochemical equilibrium?

A

diffusion stops when at equilibrium - dictated by NERNST equation

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58
Q

What is the rule for intracellular membrane voltage?

A

set closest to the equilibrium potential of the most permeant ion
- ion with the greatest # of open channels

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59
Q

What are the Eion for Ca, Cl, Na, K?

A 
Ca = +246
Na = +60
Cl = -70
K = -90
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60
Q

What are the general features of RMP?

A
  • always inside negative

- found throughout the unit membrane but vary across types of excitable cells

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61
Q

What are the RMP of small, large neurons and mm, glial cells?

A 
small = -60mV
large = -70mV
mm = -80mV
glial = -90mV
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62
Q

What is the significance of RMP?

A
  • ***RMP in neurons & mm is the background against which all electrical signaling is produced
  • glial cells have an RMP but do not generate electrical signals on cell membrane
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63
Q

What is the mechanism of RMP?

A
  • RMP in glial cells is pure K diffusion potential

- neurons & mm = predominantly K diffusion but Na ion inward leakage very small contribution

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64
Q

Is there a leakage channel for Ca in skeletal mm.?

A

NO

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65
Q

What is the importance of Na?

A

takes away negativity => establishes -70mV

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66
Q

What are the functions of leak current ion channels?

A
  • single ion selective
  • open at rest
  • produce the resting membrane potential
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67
Q

What is the structure of leak current ion channels?

A

2 pore, 4 sided tetramere topolgy

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68
Q

Alpha and Beta proteins make up leak current ion channels, what is their function?

A
  • alpha helix (4) form the channel

- Beta form the anchoring protein

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69
Q

What are the importance of leak channels?

A
  • expressed throughout entire excitable cell (K>Cl>Na)

- produce RMP

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70
Q

What are depolarizing excitatory effects?

A

loss of polarization => positive and continuation of AP

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71
Q

What are the pathways of graded synaptic potentials?

A

ionotropic and metabotropic signal transduction pathways

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72
Q

What are the hyperpoarization inhibitory effects?

A

excess negativity (negative) => arrest the AP

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73
Q

What are the processes through which information is sent through a cell?

A

transduction -> transformation -> propagation -> translation

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74
Q

What are the membrane domains and associated electrical events in a cell?

A

dendrites & soma = graded, synaptic potentials
axon hillock, impulse trigger zone = all-or-none
axon = impulse propagation/conduction
axon terminals = excitation secretion coupling

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75
Q

Match the processes with the appropriate membrane domain

A 
transduction = dendrites & soma
transformation = axon-hillock and impulse trigger zone
propagation = axon
translation = axon terminals
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76
Q

What happens when n.t release occurs at the synapse?

A

r/c binding => ion channels open or close => conductance change => postsynaptic potential changes => excited or inhibited postsynaptic cells

77
Q

What are EPSPs?

A

excitatory postsynaptic potentials => voltage depolarization by excitatory n.t (neurotrophin), neuropeptide ligands, neuromodulator substance

78
Q

What happens when 2 EPSPs elicited in rapid succession?

A

sum to produce a larger EPSP (temporal summation)

79
Q

All excitatory synapses have 2 mechanisms, what are they?

A

ionotropic and metabotropic

80
Q

What are all excitatory synapses calles?

A

Grey Type 1 synapses

81
Q

What are some characteristics of Grey Type 1 Synapse (excitatory)?

A
  • round presynaptic vesicles
  • large presyn bulb with electron dense inside
  • wide synaptic cleft
  • dense postsyn basement membrane
  • large extensive postsyn density
82
Q

What are type 1 synapses known as beside Grey Type 1?

A

assymetrical junction

83
Q

What are some functions, structure of ligand-gated ion channels?

A
  • 1 pore, 4TM, 5 subunit pentameres
  • gated open or closed by ligands
  • especially like Na but selective to Cl, Ca, K too
84
Q

What happens to the ligand-gated ion channel with glutamate presentation?

A

glutamate goes out = resting state = closed

glutamate attaches = open

85
Q

ligand - gated channels have 5 subunits, whats the importance?

A

selective filter

86
Q

What did Sutherland discover?

A
  • signalling molecules that control nerve cell function do so via 2 types of membrane signal transduction mechanisms: 1) IONOTROPIC 2) METABOTROPIC
87
Q

WHat is direct/ ionotropic synaptic action?

A
  • direct, selective binding of n.t. to surface r/c of ion channel
  • rapid & reversible change in electrophysiology
  • new addition to the cellular control arsenal
  • ***OPEN or CLOSE membrane ion channels
88
Q

What is the difference between ionotropic vs. metabotropic?

A 
ionotropic = ligand gated ion channel
metabotropic = G protein coupled receptors
89
Q

What is the system of activation for metabotropic r/c’s?

A

nt => binds r/c => G-protein activated => effector protein => intracellular messengers => ion channel opens => ions flow across membrane

90
Q

What is the special about indirect/ metabotropic synaptic action?

A
  • slower & indirect
  • G-protein/ P coupled
  • turn on slowly => dephospo => turn off slowly
91
Q

Where is the metabotropic motif commonly employed in?

A

the neural networks of the brain

92
Q

What are CAMs?

A

cell-adhesion “docking” molecules which bind the cells together (ie. Neurexins & Neurligans)

93
Q

What is the postsynaptic organization?

A

1) CAM
2) Ionotropic STPs
3) Metabotropic STPs

94
Q

What is the AP threshold in a cell?

A

-65mV

95
Q

What happens when EAA - Gutamate is introduced to ionotropic - STP?

A
  • AMPA-r => open => increase conductance permeability => Increase Na in => Icrease EPSc => Graded Depol fast EPSP
96
Q

What happens when EAA - Gutamate is introduced to metabotropic - STP?

A

mGlu-r => close => decrease conductance permeability => Decrease K out => Increase EPSc => Graded depol slow EPSP

97
Q

What happens if the summation between iono and metabo STP is greater than or equal to 5mV above RMP (-70mV)?

A

trigger zone impulse and AP begins

98
Q

What happens with channel opening?

A

Increased ionic permeability (Pion), Increased conductance (G), decreased membrane resistance (Rm)

99
Q

What happens when a channel closes?

A

Decreased Pion, Decreased G, Increased Rm

100
Q

What happens with an indirect closing of K metabo channel?

A

rebound depol postsyn (EPSP)

101
Q

What happens with an indirect closing of sodium metabo channel?

A

rebound hyperpol postsyn (IPSP)

102
Q

Metabo ion channel closing “gating themes”show passive decay, which is?

A

the excitatory voltages/currents die out as they move away from the postsyn membrane region

103
Q

What happens to depol of postsyn membrane?

A

+ charges cancel out negative charge which causes a pushing effect away from postsyn membrane (see pg 58)

104
Q

Why is the location crucial for testing electronic decay of graded EPSP?

A

the closer to the synapse = more powerful current; therefore the more powerful the message

105
Q

What is temporal summation in a neuron?

A

repeated impulse over a short period of time from a cell produces temporal summation EPSCs/ EPSPs at that synapse

106
Q

What is spatial summation in a neuron?

A

sensory summation that involves stimulation of several spatially separated neurons at the same time

107
Q

If >5mV graded potential, what does this trigger at the AH-IS/T.Z areas?

A

Transformation = all-or-none AP

108
Q

What are the characteristics of EPSPs?

A
  • graded in size
  • summate both temporally and spatially
  • display passive electronic decay
109
Q

At the axon hillock what happens to the signal in terms of graded synaptic membrane response?

A

transduced => transformed

110
Q

What are IPSPs?

A

inhibitory postsyn potentials = hyperpolarize (SILENCE EFFECT)

111
Q

What are the events from n.t release to postsyn excitation/inhibition?

A

nt release => r/c binding => ion channels open or close => conductance change (ion current flow) => post syn potential changes (EPSPs, IPSPs) => excited or inhibited postsyn cells

112
Q

What can happen with 2 IPSPs elicited in rapid succession?

A

sum to produce a larger (-‘ve) IPSP

113
Q

What are Grey Type II Synapses?

A

inhibitory with IAA being GABAergic

114
Q

Grey Type II Synapse are location specific, wher?

A

tend to cluster at specific locations toward axon hillock

115
Q

What are some specifications of Inhibitory synapses?

A
  • flattened oval presyn vesicles
  • small, multiple presyn active zones
  • narrow syn cleft
  • modest postsyn basement membrane
  • multiple, restricted postsyn densities
116
Q

Are Inhibitory synapses asymmetrical?

A

NO, they are symmetrical (in terms of density)

Grey type I are asymmetric

117
Q

Where is the binding site on GABAa r/c Cl complex?

A

2 alpha subunits

118
Q

All the ionotropic site is how many sided?

A

5 - ion selectivity because of this

119
Q

What is the difference between Greys Type I and II in terms of ionotropic and metabotropic at active zone?

A

Greys Type II uses GABAa for both metabotropic and ionotropic and ionotropic are direct but slow!

120
Q

Metabotropic signal transduction in Inhibitory synapses utilize what 2 GABA subtypes which correlate to which ions?

A

GABAb -> K (-90mV)

GABAa -> Cl

121
Q

How is the signal inhibitory when Cl- equilibrium is -70mV and GABAa is for above -70mV?

A

due to GABAb and the use of K efflux which equilibrium is -90mV (see pg 65) - essentially draws the equilibrium below -70mV

122
Q

what is the neuropeptide for inhibitory synapses?

A

Eukephalin

123
Q

What happens with GABA presentation for iono-STP?

A

GABAa => Increased conductance (open) => Increased Cl- IN => graded hyperpol FAST IPSP

124
Q

What happens with GABA presentation for metabo-STP?

A

GABAb => Increased conductance (open) => Increased K+ OUT => graded hyperpol SLOW IPSP

125
Q

Passive electronic decay for inhibitory synaptic voltages die out where?

A

prior to hillock, die out fast

126
Q

IPSPs do what at the AH-IS trigger zone to suppress impulse production?

A

push voltages away from impulse threshold => postsyn inhibition

127
Q

What happens if IPSP = EPSP; IPSP > EPSP; IPSP<EPSP?

A

IPSP = EPSP => cancel each other out and no AP
IPSP > EPSP => inhibitory effect (hyperpol) no AP
IPSP < EPSP => excitatory effect (depol) AP (>5mV)

128
Q

What is neuronal integration?

A

IPSP + EPSP to determine whether an AP occurs

129
Q

At the axon bulb what does the AP stimulate?

A

Ca to be released

130
Q

What are the channels on the axon?

A

all or none impulse + voltage gated ion channel

131
Q

What aa/nt stimulates excitatory actions? inhibitory? both?

A 
excitatory = 75% Glutamate (E.A.A); 25% Ach, Adenosine, NA, serotonin
inhibitory = 90% GABAa/GABAb  (I.A.A)
both = histamine, Ach
132
Q

From threshold to peak what are the # in mV?

A

-65=>0=>+20

133
Q

What is the Na dependent process in the all or none impulse?

A

rising depol phase

134
Q

What is the K dependent process in the all or none impulse?

A

repol phase

135
Q

What is the AP threshold?

A

-65mV

136
Q

What causes the difference in AP from nerve to nerve?

A

axon hillock graded EPSP + summation time

137
Q

What did Hodgkin and Huxley test on to prove ion movement through membrane pores?

A

squid giant axon

138
Q

What causes the impulse that occurs at the TZ and subsequent opening of ion selective and voltage gated ion channels?

A

****positive, graded cationic generator currents supply the depolarizing voltage to trigger these events!

139
Q

What happens when Na influx pushes charge inside the cell to positive?

A

inactivated state of r/c (AMPA) => refractory period

140
Q

What happens when K efflux outside cell?

A

hyperpol. => cell need to repol to -90mV => refractory period

141
Q

What is the spike freq upper limit?

A

800 spikes/sec

142
Q

What can selectively block Na channel?

A

tetrodotoxin (TTX) & saxitoxin (STX)

143
Q

What is saxidomus?

A

a specific toxin that inhibits depol of neuron (Na channel) therefore fatal to humans - from clams

144
Q

What can selectively block K channels?

A

tetraethylammonium (TEA) from outside the cell & 4-Aminopyridine from inside after migration into the cell

145
Q

Do the K and Na voltage gated channels differ in transmembrane segments?

A

No they both have 6TM, 1 pore and 4 sided tretramers

146
Q

What is the difference between absolute and relative refractory periods?

A

absolute => no AP from second stimulus

relative => second impulse fails to elicit an impulse of normal size or amplitude

147
Q

What does the Na influx during thee rising depol phase of the AP spike produce?

A

local cationic (+) circuit current (LCC)

148
Q

What is LCC?

A

helps to depol the next patch of membrane with Na voltage gated channels until reaches end of axon or fiber

149
Q

What happens to the speed of conduction when you increase/ decrease axonal size in small, unmyelinated axons?

A

Increase axon size => decrease resistance => Increase speed of LCC => faster conduction velocity
Decrease axon size => increase resistance => decrease speed of LCC => slower conduction velocity

150
Q

What is the conduction velocity in small unmyelinated axons?

A

0.3-4.0m/s

151
Q

What is the conduction velocity of large myelinated axons?

A

5-120m/s

152
Q

What is salidatory conduction? where does it take place at?

A

hopping conduction at the Nodes of Ranvier in myelinated axons

153
Q

What are the characteristics of All-or-None Law?

A
  • threshold voltage
  • magnitude from threshold to peak voltage
  • duration
  • voltage waveform
  • conduct/ propagate
  • electrogenic -> self-regenerative
154
Q

What does a high freq stimulation lead to in the axon bulb in terms of Ca?

A

general increase of Ca => release of peptide nt from large dense-core vesicles, as well as small molecule nt from small clear-core vesicles

155
Q

What are stored in small vesicles in axon terminal?

A

small mol transmitter (glutamate, aspartate, GABA, Ach)

156
Q

What is the sequence of events of AP arriving at axon terminal in terms of Ca?

A

AP => LCC opens Ca voltage gated channel => Increase in Ca => glutamate release => Glutamate bind to postsyn => Glutamate reuptake by glial cells or presyn cells

157
Q

What is the Katz’s Quantal Hypothesis of Transmitter Release?

A
  • a single impulse forces many small vesicles to release their contents into synaptic cleft and then diffuse to postsyn and bind to recognition sites and open ligand-gated ion channels
158
Q

What happens in silent chemical synapses, with no invading all or none impulse?

A

few “quanta” (small vesicles) release spontaneously and form a spontaneous miniature postsynaptic potential mPSP

159
Q

What determines the amount of quanta released by the neuron?

A

Ca levels in the presynaptic terminal

160
Q

where are neuropeptides generated and stored in a neuron?

A

generated in the neuron cell body from precursor molecules

stored in large dense-core vesicles

161
Q

What happens once the NP of a dense-core vesicle enters the synaptic cleft?

A

diffuses to the postsyn cell, the NP binds to a r/c/ which INDIRECTLY activates a signal transduction pathway and coupled postsynaptic cellular response

162
Q

What happens to the NP in the synaptic cleft with decreased amounts of Ca?

A

the peptide diffuses out of the synaptic cleft

altered by endopeptidases

163
Q

What is Dales Rule?

A

a single neuron transcribes, constructs, packages, and releases the same chemical transmitter at ALL of its synaptic terminals (for both small and large vesicles)

164
Q

What are the inhibitory NP for Glutamate and GABA?

A

Glu => Subs-P

GABA => Enkephalin

165
Q

Which r/c’s do small molecule n.t. activate?

A

Iono & Metabo

166
Q

What r/c’s do NPs activate?

A

metabo ONLY!

167
Q

Is there retrograde signalling with impulse-based signal release?

A

NO

168
Q

What r/c’s do non-impulse bases, continuous/constitutive signal release (growth factors) activate?

A

NGF, BDNF => Metabo-TrK-R

169
Q

What are ways to terminate transmitter action?

A
  • active transmitter re-uptake
  • diffusion
  • degradative processes
  • autoreceptor inhibition of release
170
Q

How are small molecule transmitters take up in the synaptic cleft? whats the effect?

A
  • avid reuptake in glia & terminal via specific n.t. transporter
  • rapid/fast decrease of conc. in the synaptic cleft which provides rapid termination of synaptic action
171
Q

What Neuromodulator has different mechanism of termination of transmitter in the synaptic cleft than small molecule transmitter?

A

Ach = degradative enz - Ach-E in synaptic cleft

Dopamine, serotonin, noradrenaline have same mech and effect as small molecule transmitter (Glu, Asp, GABA, Gly)

172
Q

How are neuropeptides terminated in the synaptic cleft?

A
  • ednopeptidases in synaptic cleft and diffusion

- very slow breakdown and diffusion decreases # of NP in cleft - allows for prolonged action

173
Q

What are special about autoreceptor actions in terms of n.t.?

A

provide negative feedback to decrease small mol n.t. release into snyaptic cleft - to stop synaptic action

  • Glu comes back and binds to mGlu-R which inhibits release
  • GABA binds to GABAb-R
174
Q

What is presynaptic inhibition?

A

decrease n.t. release

175
Q

What is presynaptic facilitation?

A

Increase n.t release

176
Q

What is the mechanism of neuromodulation?

A

induced change in axon terminal Ca ion levels/ conc.

177
Q

What n.t. is released from neuromusculare junctions?

A

Ach

178
Q

Where is Ach released from in NMJ?

A

prejunctional component (active zone)

179
Q

What are the 2 types of release from NMJ?

A
  • spontaneous release

- evoked release

180
Q

Is an AP evoked with spontaneous release at NMJ?

A
  • small depol of the post-junctional end plate region do not spread beyond the end-plate and do not excite the mm cell = NO!; however do produce mEPPs (miniature end plate potentials)
181
Q

What is special about an EPP?

A

20-40mV with 1 release; graded response; very big and dont usually summate

182
Q

Do evoked release at NMJ form an AP?

A

YES! form an EPP (end plate potential) which gives rise to an AP => tension generation

183
Q

Is the NMJ Ca dependent?

A

YES!

184
Q

How is Ach blocked?

A

ACh-E degrades Ach in cleft

185
Q

**The motor end plate of the NMJ has specific characteristics, what are they?

A
  • direct, ionotropic system
  • nicotinic-Ach ion channel
  • ligand gated ion channel
  • 5 sided pentamer
186
Q

What cause an End Plate Potentials (EPP)?

A
  • binding of 2 Ach => gates open
  • Increased conductance => depol
  • large (20-40mV) event
  • 2 ion voltage (Na influx (mostly) K efflux)
187
Q

What are the characteristics of an NMJ?

A
  • high-fidelity and high safety factor chemical synapse

=> obligatory and reliable 1-1 transmission of motorneuron impulse leads to mm impulse (“twitch”)

188
Q

What are special about electrical synapses in CNS?

A
  • allows for unhindered passage of electrical ionic currents
  • bidirectional communication
  • mediates synchronized electrical activation of some cell types (neocortex, thalamus, brainstem (inhibitory) neurons, cardiac & smooth mm)
189
Q

What is the structure of electrical synapses (gap junctions)?

A

6-seded hemi channels called connexons

4 alpha helixes per subunit

Neurophysiology (3 decks)

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