neurons Flashcards
neuron dendrites function
receive electrical input
neuron cell body function
passively conducts electrical signals
neuron axon hillock/initial segment/trigger zone function
initiates action potentials
neuron axon function
propagates action potentials
neuron axon terminal function
releases chemical signals across synapse
how much more negative are neuron cytosol compared to extracellular fluid
50 to 70mV more negative
how are intracellular potentials measured today?
1.)microelectrode recording technique
2.) patch clamp technique
what affects Resting Membrane Potential (RMP)
1.) unequal concentrations of ions inside and outside of cell resulting in electrochemical gradient
2.) unequal membrane permeability to these ions
two main types of ion channels in neurons
leak channels - open at rest (many K+, fewer Na+ leak channels)
gated channels - closed at rest, (voltage, mechanical, ligand stimuli)
1:40 is the ratio of….
ratio of sodium to potassium leak channels/ratio of membrane permeability of sodium to potassium ions
nernst equation calculates…
-equilibrium potential for one type of ion
-considers only concentration of ion inside and outside of cell
equilibrium potential for K+ and Na+
K+ = -80mV
Na+ = +60mV
nernst equation application to neurons and glial cells
-only applies when membrane is permeable only to one ion
-applicable to glial cells because they’re only permeable to K+ so RMP is -80mV
-NOT applicable to neurons as they’re permeable to more than one ion type
goldmans equation calculates…
resting membrane potential (-65mV)
considers concentration gradient AND relative permeability of resting membrane to K+ and Na+ ions
factors in nernst equation
ion concentration extracellular and intracellular
faradays
gas constant
temperature
valence of ion
threshold value required to generate AP
approx -55mV
4 phases of action potentials
stimulus, fast depolarisation, repolarisation, after hyperpolarisation
absolute vs relative refractory period
absolute during fast depolarisation and repolarisation - no stimulus can cause another AP
relative during the end of repolarisation and after hyperpolarisation - stimulus can only cause another AP if larger than the original threshold
fast depolarisation caused by
stimulus reaching threshold activates voltage-gated Na+ channels letting sodium into the cell (relative permeability of Na+ to K+ now 20:1 so more permeable to Na+)
repolarisation caused by
quick inactivation of Na+ voltage gated channels and activation of voltage gated K+ channels
after hyperpolarisation caused by
membrane permeability of K+ to Na+ really large 100:1
Na+ voltage gated channel mechanism during repolarisation and after hyperpolarisation
repolarisation when Na+ gated channel INACTIVATES due to inactivation gate shuts (ball and chain)
after hyperpolarisation (back at RMP) when Na+ gated channel AT REST due to activation gate shut and inactivation gate open
what causes passive current to dissipate
leak channels
receptor potential
graded depolarisation
end plate/neuromuscular junction
motorneuron with axon forming synpase on muscle fibre
end plate potential is always
suprathreshold meaning an action potential is always triggered
factors determining synaptic action
1.) type of neurotransmitter/ neuromodulator
2.) type 3.) and amount of receptor
long term potentiation vs long term depression
LTP = stimulating multiple times leads to more receptors expressed
LTD = stimulating multiple times leads to less receptors expressed
why can only neurons and muscle fibres SUDDENLY change their membrane potential
because of voltage gated ion channels allowing them to be excitatory
