excitable membranes
description
Transcript of excitable membranes
excitablemembranes
action potential & propagation
Basic Neuroscience NBL 120 (2007)
ionic basis of APs
action potentials:
faithfully transmit information along the membrane (axon) of excitable cells
allow rapid communication between distant parts of a neuron
action potentials
the action potential is a regenerative electrochemical signal
two distinct voltage-gated ion channels are responsible for action potential generation
the action potential
3 main stages: resting
i.e. RMP
depolarization reversal of
membrane potential
repolarization return of membrane potential
to RMP
relationship between: membrane potential
ion equilibrium potentials
if the membrane becomes more permeable to one ion over other ions then the membrane potential will move towards the equilibrium potential for that ion (basis of AP).
membranepotential (mV)
EK
ENa
RMP
+67
-90-98
ECl
general rule
depolarization
rapid opening of Na-selective channels
entry of Na “down” its electrochemical gradient 1. membrane more permeable to Na than K 2. membrane potential moves towards Ena
3. because ENa is +ve the AP overshoots zero
4. At the peak of the AP Na is the primary ion determining the membrane potential
repolarization
closure (inactivation) of Na-selective channels slower opening of K-selective channels
1. membrane more permeable to K than Na2. membrane potential moves towards EK
the opening and closing of AP Na and K channels are controlled by changes in the membrane potential
voltage-gated ion channels
properties (e.g. time course) of voltage-gated channels are more easily examined using the voltage-clampholds or clamps the membrane constantmovement of ions (current) through the
channels is measured directly
voltage-clamp
relationship between: membrane potential ion equilibrium potentials
artificial manipulation of MP (voltage-clamp) - current will flow in the direction to move the MP towards the equilibrium potential of open ion channel
membranepotential (mV)
EK
ENa
RMP
+67
-90-98
ECl
general rule
voltage-clamp used to rapidly change the membrane potential over the same range as occurs during the AP2 current phases
rapid / transient inward current
slower outward steady current
AP current time course
the inward phase
carried by Na ions
selective agents block the 2 components
2 independent channels
all-or-none AP are not graded potentials
threshold in order for an AP to occur the membrane must be
depolarized beyond a threshold level inward Na overcomes resting outward K movement
electrical stimulation synaptic activation
what triggers an AP?
APs are regenerative
activation of Na channels is cyclical initial depolarizationopening of Na channelsNa entryetc..
accomodation
side-effects of inactivation
disease (e.g. paramyotonia congenita)
membrane capacitance properties
“bulk” solutions in and out are neutralthe transmembrane potential difference
exists within a narrow band just across the membrane capacitor:
separates / stores charge
time constant
changing the membrane voltage takes time charging a capacitor is not instantaneous
inject currentrecord voltage
axon
I
V
m= rmcm
how can AP rise so fast?
mrmcm
how electrical signals propagate
passive decay
length constant
length constant (passive process)
axon / dendritemembrane resistance (rm)
axial, or internal, resistance (ri)
diameter (d)
rm
ri (+ re) =
AP propagation
APs are conducted along excitable cell membranes away from their point of origine.g. down the axon
from cell soma to terminal
depolarization of the membrane during the AP is not restricted
to a single spot
the inward current carried by Na ions during the AP depolarizes adjacent portions of the membrane beyond threshold and the regenerative AP travels (in both directions) along the membrane
local circuits
following a single AP a second AP cannot be generated at the same site for some time (absolute versus relative)Na channels need to recover from inactivationopen K channels oppose inward Na movement
refractory period
local circuit propagation is slow (< 2 m/s) In motorneurons propagation is fast 100 m/s Schwann cell
envelop axons / layer of insulation increase resistance (Rm)(increase length constant) eliminate capacitance(time constant > 0)
Nodes of Ranvier discontinuity in myelin sheath (every few 200+ m)
myelination
saltatory conduction
APs are only generated at Nodes of Ranvier high density of Na / K channels
current flows rapidly between nodes little current leakage between nodes
AP “jumps” down fiber as successive nodal membrane capacitances are discharged
myelination disease
Charcot-Marie tooth disease progressive loss of PNS axons - weakness, atrophy
Node of RanvierSchwann cell
summary
RMP electrochemical gradients Nernst equation
AP initiation role of voltage-sensitive Na and K channels regenerative depolarization threshold and accommodation
passive properties time and length constants capacitance
AP propagation local circuits saltatory conduction