synapse Flashcards

1
Q

action potential

A

rapid, large depolarisation from threshold mem potential

threshold potential more +ve > basal (RMP)

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2
Q

when does AP occur?

A

1) when external stimulus applied
2) info is transferred to neuron

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3
Q

steps to Action potential depolarisation

A

1) rest mem potential of -80/60mV (based on K, Na, Cl distribution)

2) AP begins: excitatory neurotransmitter, open ligand -gated channels (NMJ, synapse of CNS)

depolarising potential reach trigger zone, depolarise mem

3) voltage gated Na channels activated, mem more permeable to Na (EXTRACELL –> INTRA)

4) Na entry, depolarise cell

5) inside more +ve > outside, reverse mem potential polarity

6) voltage gated Na+ channels inactivated. VG K+ channels open, mem potential more permeable to K+

K+ move out, mem potential repolarises

7) VG K+ channels close. mem potential returns to normal (Na-K pump: 2 Na+ out and 3K+ in)

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4
Q

electrochemical gradient

A

ionic distribution across mem at rest (resting mem potential)

K+ (intracell > extracell)

Ca2+ (intracell < extracell)
Na+ (intracell < extracell) ** ASM
Cl- (intracell < extracell)

electrochemical gradient determines equilibrium potential

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5
Q

resting mem potential is usually +/-ve ??

A

more neg than threshold mem potential

mem must be depolarised –> threshold mem for AP signal to be evoked

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6
Q

forces acting on K that affects its movement

A

1) conc gradient favour EFFLUX of K (intracell –> extracell)

2) electrical gradient PULLS +ve K+ (extracell –> intracell)

2 gradients oppose each other

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7
Q

equilibrium potential

A

equilibrium potential (where OUT = INWARD gradients, no net movement of ion across mem

balanced at eg: -97mV, no net movement of K+

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8
Q

eqm potential eqn

A

E = 58 log (conc of ION outside/ conc of ION inside)

specific for each ion: K, Na. Given ion will either move IN/OUT cell to push mem potential towards E value

different from mem potential

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9
Q

mem potential

A

reflects conc and permeability of K, Na, other ions that are distributed across the mem

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10
Q

at rest, normal state movement

A

K move outward (push mem potential towards -97mV)

Na move inward (push mem potential towards +75mV)

mem potential maintained at -80/60mV (more neg reflects greater permeability for K+ = leak K channels)

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11
Q

alter K conc outside (incr extracell conc)

A

E value = 58 log (50/ 140) = -25mV vs -97mV

favour K outflow but now less steep than before
less K move out since E is more +ve now

greater accumulation of +ve charges inside mem.
Resting mem potential becomes less negative, closer to threshold

Depolarisation easier as less stimulus needed to initiate action potential

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12
Q

hypernatremia

A

still favour inflow of Na+ intracellularly

more positive rest mem potential

reach threshold easier, depolarisation easier as less stimulus needed to initiate AP

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13
Q

hypokalemia

A

low extracell K

more -ve E value. still favour K outflow, more steep now, more K move out

less accumulation of +ve charges inside mem.
Resting mem potential becomes MORE negative, further from threshold

Depolarisation harder as more stimulus needed to initiate action potential (less excitable)

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14
Q

synaptic transmission

A

communication b. cells (b. neurons, nerves, muscles)

3 components:
1) presynaptic terminal
2) postsynaptic cell
3) synaptic cleft

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15
Q

2 types synaptic transmission

A

electrical – current generated in presynaptic neuron FLOWS DIRECTLY into postsynaptic cell through gap-junction channels

chemical – has synaptic cleft, neurotransmitters released, receptors on postsynaptic cleft

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16
Q

chemical synapse

A

has synaptic cleft 20-40nm

1) action potential in presynaptic cell release chemical transmitters in cleft

2) transmitter diffuse across cleft, interact with specific receptors

3) depolarise/ hyperpolarise postsynaptic cell

4) depo: reach threshold mem, leads to generation of action potential in postsynaptic cell

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17
Q

neuromuscular junction definition

A

NMJ synapse/ junction of axon terminal of motoneuron with motor end plate (motor neuron excites skeletal muscle fiber)

highly excitable region of muscle fiber

plasma mem: initiates AP across muscle surface = contract muscle

CHEMICAL SYNAPSE

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18
Q

how depolarisation occurs at neuromuscular junction

1) transmitting (AP presynaptic)
2) receptive (Ach)

A

1) synaptic transmission involve release of acetylcholine from presynaptic axon terminal (open VG Ca2+ channel)

2) Ach binds to nicotinic receptor (postsynaptic mem/ muscle mem – ligand gated)

3) initiate depol of postsynap mem (influx of Na+) result in muscle contraction (motor end plate)

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19
Q

release of Ca2+ in presynaptic axon

A

presence of Ca2+ in axon terminal cause synaptic vesicles to fuse with mem

Ca2+ act on Ca2+ sensitive vesicle mem poteins (VAMPs) –> vesicle docking to presynapse –> fuse with presynaptic mem –> exocytosis

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20
Q

transmitters for diff synapse and their effects

A

Ach – excitatory at NMJ
glutamate – excitatory in CNS

GABA – inhibitory in CNS & NMJ

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21
Q

facilitate depolarisation at threshold mem potential

A

block efflux of intracell K+
incr influx of extrcell Na+
decr influx of extracell Cl-

release Ach at NMJ
incr nicotinic receptor agonist at NMJ

22
Q

type of channels at membrane

A

ligand-gated channels (AP begins, NMJ to motor end plate)

voltage-gated channels (depol, repol)

23
Q

sensation

A

conscious awareness of external stimuli (touch, pressure)

signal generated: external stimulus reach sensory cortex (along label line)

24
Q

sensory receptor embedded in skin

A

specialised sensory nerve ending/ specialised epithelial cells – recognise stimulus

initiate sensory transduction by action potential in same cell/ adjacent one

sensory receptor send info –> CNS via afferent nerve fibers (1* afferents)

25
Q

pacinian corpuscle
enclosed nerve ending has layers of connective tissue

A

1) receptive field: specific area of receptor that monitors non pain frequencies (vibration)

2) converts physical energy to signal

26
Q

1* afferent

A

carry nerve impulses from receptors/ sense organs –> CNS

27
Q

mechanoreceptor sensory receptors

A

sensitive to mechanical energy

touch, pressure (vibration), stretch, sound

28
Q

nociceptor

A

free nerve ending, sensitive to tissue damage

noxious stimuli

eg: capsaicin (chemical) – Trpv1 receptor

29
Q

chemoreceptor

A

sensitive to chemicals

O2, pH, various organic molecules – glucose

30
Q

photoreceptor

A

responsive to light

photos of light

31
Q

thermoreceptor

A

sensitive to hear and cold

varying degrees of heat
(> 44-45*C = noxious stimuli)

32
Q

proprioceptor

A

sense position of body in space

33
Q

types of 1* afferent

A

A: skeletal muscle within body
Ab: mechanoreceptor of skin

Ad: pain, temp
C: temp, pain itch

34
Q

degree of myelination

A

A, Ab: largest diameter, thickest myelin

Ad: thinly myelinated
C: free nerve ending, unmyelinated

35
Q

sensory transduction

A

sensory receptor converts energy (in a STIMULUS) –> AP (change in electrical potential across mem)

cause receptor mem to depolarise = AP generation (signal relayed to brain)

36
Q

steps in sensory transduction

A

1) Application of stimulus to receptor in periphery that generally results in depolarisation of receptor mem

2) Receptor potential travels to trigger zone of associated primary afferent
a. Depolarisation, when it reaches trigger zone generates action potential generation adzone

3) Action potential discharge propagated along the axon

4) Action potential discharge reaches the axon terminal stimulate the release of transmitter
a. Affect next neuron in line in the CNS

37
Q

Trigger zone

A

axon hillock

sum of total signals (inhibitory & excitatory)
if > threshold = trigger AP

38
Q

label lines

A

the brain perceives the info arriving from specific neuronal tract as the adequate stimulus of the 1st order sensory receptor (afferent),

only respond to one type of stimulus even if diff stimulus activates it

39
Q

common somatosensory pathways

A

1* afferent (peripheral axon) –> 2* afferent (spinal cord or brain stem nucleus)

decussation (cross to other side below thalamus)

all have thalamic nucleus

end in parietal lobe of cerebral cortex

40
Q

nociceptors (C, Ad 1* afferents)

A

sensory receptor that responds to potential damaging stimuli

BY send nerve signals to spinal cord and brain
- nociception = perception of pain

internal and external nociceptors

41
Q

external nociceptors

A

cell bodies of these neurons located in either Dorsal root ganglion/ Trigeminal ganglia

TGM ganglia: specialised nerves for face
DR ganglia: associated with rest of body

axons extend into PNS, terminate in branches (receptive fields)

42
Q

intensity of stimulus incr when incr in

A

number of AP generated/ unit time

freq/ rate of AP from nociceptors activation

43
Q

impaired sensory

A

loss of large diameter Ab fibers (less non-painful sensations)

absence of C/Ad fibers (loss of pain receptors)

44
Q

what happens at efferent?

A

neurons in CNS will generate another signal

efferent distinct by location

usually in ventral horn of spinal cord (controls movement).

doral arm (mostly cell bodies on sensory neurons)

45
Q

depolarise

A

membrane depolarizes above the threshold voltage, and the influx of sodium ions

46
Q

Repolarise, hyperpolarise

A

change in a cell’s membrane potential that makes it more negative.

inactivate Na, open K+ channels

47
Q

generation of sensation signal

A

1) receptors transduce external stimuli to electrical charge

2) electrical charge depolarises = action potential ***

3) relay action potential to CNS, processed in cortex to understand the sensation

48
Q

how action potential is relayed

A

myelinated > faster > unmyelinated

jumps over myelin sheath, nodes of ranvier is shorter distance than through nerve

49
Q

AP in neuron

A

requires excitatory neurotransmitter (efferent converts to electrical energy)

transfer signals from 1 neuron –> another
evokes synaptic potential (EPSP, IPSP –> evokes AP)

  • An EPSP has a reversal potential more positive than the action potential threshold = DEPOL
  • an IPSP has a reversal potential more negative than threshold = HYPERPOL
50
Q

hyperexcitability in neurons

A

eg rhythmic firing of large pop of neurons ==> SEIZURE ===> epilepsy (multiple, unprovoked)

  • abnormal activity in small areas of cortex –> trigger for seizures –> spread to other synaptically connected region

uncontrolled movement (jerking)

51
Q

control of seizure

A

1) enhance inhibitory synapse (limit AP firing, act on VG-Na+ channels)

2) hyperpolarisation (GABA, IPSP)

3) decr excitatory (glutamate, CNS)

52
Q

contralateral pathway where for touch and pain?

A

□ Pain: spinothalamic/ anterolateral
* Touch: Dorsal column – cross at medulla