synapse Flashcards
action potential
rapid, large depolarisation from threshold mem potential
threshold potential more +ve > basal (RMP)
when does AP occur?
1) when external stimulus applied
2) info is transferred to neuron
steps to Action potential depolarisation
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)
electrochemical gradient
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
resting mem potential is usually +/-ve ??
more neg than threshold mem potential
mem must be depolarised –> threshold mem for AP signal to be evoked
forces acting on K that affects its movement
1) conc gradient favour EFFLUX of K (intracell –> extracell)
2) electrical gradient PULLS +ve K+ (extracell –> intracell)
2 gradients oppose each other
equilibrium potential
equilibrium potential (where OUT = INWARD gradients, no net movement of ion across mem
balanced at eg: -97mV, no net movement of K+
eqm potential eqn
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
mem potential
reflects conc and permeability of K, Na, other ions that are distributed across the mem
at rest, normal state movement
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)
alter K conc outside (incr extracell conc)
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
hypernatremia
still favour inflow of Na+ intracellularly
more positive rest mem potential
reach threshold easier, depolarisation easier as less stimulus needed to initiate AP
hypokalemia
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)
synaptic transmission
communication b. cells (b. neurons, nerves, muscles)
3 components:
1) presynaptic terminal
2) postsynaptic cell
3) synaptic cleft
2 types synaptic transmission
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
chemical synapse
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
neuromuscular junction definition
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
how depolarisation occurs at neuromuscular junction
1) transmitting (AP presynaptic)
2) receptive (Ach)
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)
release of Ca2+ in presynaptic axon
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
transmitters for diff synapse and their effects
Ach – excitatory at NMJ
glutamate – excitatory in CNS
GABA – inhibitory in CNS & NMJ
facilitate depolarisation at threshold mem potential
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
type of channels at membrane
ligand-gated channels (AP begins, NMJ to motor end plate)
voltage-gated channels (depol, repol)
sensation
conscious awareness of external stimuli (touch, pressure)
signal generated: external stimulus reach sensory cortex (along label line)
sensory receptor embedded in skin
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)
pacinian corpuscle
enclosed nerve ending has layers of connective tissue
1) receptive field: specific area of receptor that monitors non pain frequencies (vibration)
2) converts physical energy to signal
1* afferent
carry nerve impulses from receptors/ sense organs –> CNS
mechanoreceptor sensory receptors
sensitive to mechanical energy
touch, pressure (vibration), stretch, sound
nociceptor
free nerve ending, sensitive to tissue damage
noxious stimuli
eg: capsaicin (chemical) – Trpv1 receptor
chemoreceptor
sensitive to chemicals
O2, pH, various organic molecules – glucose
photoreceptor
responsive to light
photos of light
thermoreceptor
sensitive to hear and cold
varying degrees of heat
(> 44-45*C = noxious stimuli)
proprioceptor
sense position of body in space
types of 1* afferent
A: skeletal muscle within body
Ab: mechanoreceptor of skin
Ad: pain, temp
C: temp, pain itch
degree of myelination
A, Ab: largest diameter, thickest myelin
Ad: thinly myelinated
C: free nerve ending, unmyelinated
sensory transduction
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)
steps in sensory transduction
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
Trigger zone
axon hillock
sum of total signals (inhibitory & excitatory)
if > threshold = trigger AP
label lines
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
common somatosensory pathways
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
nociceptors (C, Ad 1* afferents)
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
external nociceptors
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)
intensity of stimulus incr when incr in
number of AP generated/ unit time
freq/ rate of AP from nociceptors activation
impaired sensory
loss of large diameter Ab fibers (less non-painful sensations)
absence of C/Ad fibers (loss of pain receptors)
what happens at efferent?
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)
depolarise
membrane depolarizes above the threshold voltage, and the influx of sodium ions
Repolarise, hyperpolarise
change in a cell’s membrane potential that makes it more negative.
inactivate Na, open K+ channels
generation of sensation signal
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
how action potential is relayed
myelinated > faster > unmyelinated
jumps over myelin sheath, nodes of ranvier is shorter distance than through nerve
AP in neuron
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
hyperexcitability in neurons
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)
control of seizure
1) enhance inhibitory synapse (limit AP firing, act on VG-Na+ channels)
2) hyperpolarisation (GABA, IPSP)
3) decr excitatory (glutamate, CNS)
contralateral pathway where for touch and pain?
□ Pain: spinothalamic/ anterolateral
* Touch: Dorsal column – cross at medulla
