Signalling 2 Flashcards
nerve impulse definition
wave of depolarisation of the membrane of the axon
where are the ions distributed at resting potential
approx. 70mV
^[Na+] outside the cell
^[K+] inside the cell
^[Cl-] outside the cell
process of action potential
DEPOLARISATION
1- Na+ channels open
2- Na+ flows into cell
process of AP
REPOLARISATION
3- depolarisation causes K+ v.g. channels to open
4- Na+ channels close
5- K+ flows out of the cell
process of AP
HYPERPOLARISATION
6- K+ channels are slow-closing, so the membrane overshoots and becomes hyperpolarised
~90mV
process of AP
RETURN TO REST
Na+ channels reset
Na+/K+ pump
what causes the wave of depolarisation to be unidirectional
refractory period
short period of time immediately following an AP when a new AP cannot be initiated in the same area of the membrane
absolute refractory period
when Na+ channels are closed and cannot be activated
relative refractory period
Na+ channels could reopen, but the membrane is hyperpolarised and so a larger stimulation is required to reach the threshold value (-55mV) for continuation of the AP
AP stimulation
1- ligand binds to ligand-gated channels, causing them to open (or mechanically-gated)
2- Na+ moves down conc. gradient, through channels, into cell
3- number of Na+ moving in depends on strength of signal
4- if membrane potential = -55mV, v.g. Na+ channels open and there is an influx of Na+ (temporary deceleration of rate)
how does an AP start
multiple inputs from multiple dendrites
- Excitatory Pre-Synaptic Potentials (EPSPs)
- Inhibitory Pre-Synaptic Potentials
(IPSPs)
- vary in magnitude (‘graded’)
summation of changes in membrane potential
- EPSPs increase chance of AP initiation; IPSPs decreases chance
if overall membrane potential reaches threshold voltage, the v.g. Na_+ channels open and AP is initiated
summation
spatial - inputs from different areas - e.g. from different dendrites
temporal - input occurs multiple times from the same areas/ dendrite
- repeated inputs in a short time period
how does summation affect APs
generated more or less FREQUENTLY
reflex arc
stimulus -> receptor -> sensory neuron -> CNS -> relay neuron -> CNA -> motor neuron -> effector -> response
NT general info
chemical signals
different NTs associated with different NS functions (e.g. memory, movement)
excitatory or inhibitory (promote or inhibit formation of AP in receiving neuron)
many drugs act on NT signalling
NT chemical classification
amino-acids + derivatives
- e.g. glutamate - main excitatory NT in CNS
- e.g. GABA - main inhibitory NT in CNS
Catecholamines (monoamines)
- derived from Tyr
- e.g. dopamine, serotonin
Acetylcholine
- derived from choline
- NMJ
Peptides
- e.g. Substance P, endorphins
what is the GABA-A receptor
an ion-channel-receptor (ionotropic)
Cl- ion channel
GABA-A receptor process
GABA released from presynaptic neuron into synapse, which then binds to the GABA-A receptor on post-synaptic membrane
1- binding of ligand (GABA) to receptor
2- causes conformational change that opens ion channel (‘ligand-gated’)
3- Ion moves through channel along conc. gradient
4- Hyperpolarisation -> harder to reach threshold voltage for AP
Benzodiazepines, ethanol, some anaesthetics: potentiate GABA activation of GABA-AR
- more inhibition of APs - sedative action
ACh at NMJ
nAChR = Na+ channel receptor
1- ACh binds
2- allows Na+ entry
3- Na+ influx (DEPOLARISATION) of muscle CM
4- depolarisation initiates contraction
Acetylcholinesterase in cleft removes ACh
Myasthenia gravis (muscle weakness)
autoimmune antibodies attack ACh receptors at NMJ
treatment: AChE inhibitors used to enhance NMJ transmission
signalling via GAP junctions
connexin proteins form connection with channel
ions carry charge from one cell to another
e.g. electrical synapses between neurons (most are chemical)
- cardiac myocytes
cardiac myocytes
heartbeat: electrical impulse travelling across heart tissue causes contraction of cardiac muscle
specialised cells with neuron-like properties spread charge throughout hear (e.g. Purkinje fibres)
