the membrane potential changes if the membrane's permeability to specific ions is altered (usually increased.

now the ion flows down its concentrations gradient = ion current

changes in membrane potential caused by ion flow through ion channels

Voltage gated channels open in response to membrane potential

2 types of channels for K+  those always opne and those closed in resting

Channel for N +  Always closed in resting cells   some does leak into cells though

Stimulus causes depolarization to threshold

voltage gate for Na+ channels open

electrochemical gradient inward =  + feedback loop

rapid reversal in membrane potential from -70 to +30 mV

Voltage gate for Na+ channels become inactivated

Voltage gate for K+ open

electrochemical gradient outward =feedback loop

restore original resting membrane potential

AP is produced by and increase in Na+permeability

After short delay, increase in K+ permeability

Depolarization and repolarization occur via diffusion and do not require active transport.

Once AP is completed Na+/K+ ATPase pump extrudes Na+ and recovers K+  (REQUIRES ATP)

All or none    Action Potential is all or none

When threshold reached  maximum potential change occurs

When RMP reaches threshold an AP is irreversibly fired

becasue positive feedback opens more and more Na+ channels

then the close and become inactivated until repolarized.

amplitude doesn not normally become more positive than +30

Stimulates more AP   but not bigger AP

more frequent

cannot produce AP of greater amplitude

the greater the stimulus the more APs that are produced

a weak stimulus actives a few axone with low threshold

stronger can activate more axons with higher threshold

Absolute refractory period where membrane is incapable of producing another AP

Relative refractory period  = VG ion channel shae alters

Vg K+ channels are open

Axon membrane can produce another action potential but requires stronger stimulus

Ability of neurone to transmit charge through cytoplasm

Axon cable properties are poor due to high internal resistance    also many charges leak out of axon through membrane

An Ap doesn not travel down the entire axon

Each AP is a stimulus to produce another AP in the next region of membrane with VG channels

Cable spread of depolarization with influx of Na+ depolarizes the adjacent region membrane, propagating the AP

Conduction rate is slow

Occurs in 1 directions, previous region is in its refractory period

Figure 7.19 will be on the test

know where the charges are

Myelin prevents movememt of Na+ and K+ through the membrane

Interruptions in myeline (nodes of Ranvier) contain VG Na+ and K+ channels

AP occurs only at the nodes

AP at 1 node depolarizes membrane to reach threshold at next node

like little steps along the way= slow

Saltatory conduction = leaps  = fast conduction

functinoal connection between neuron (presynaptic)

and another cell (postsynaptic - either another neuron or an effector cell ..esp. if gland)

Chemical and electric synapses

Synaptic transmission at chemical synapses is via neurotransmitters

Electrical synapses are rare in the nervous system

Impulses can be regenerated without interruption in adjacent cells

Depolarization flows from presynaptic to postsynaptic cell through channels = gap junctions

adjacent cells electrically couple through a channel

Formed by connexin proteins

found in smooth and cardiac muscles, brain and glial cells

Synaptic cleft separates  terminal  bouton of a presynaptic from post synaptic cell

Nts are in  synaptic vesicles

transmissin in 1 direction only

Axon of first (presynaptic) to second (postsynaptic) neuron

Vesicles fuse with bouton (presynaptic) membrane:  released by exocytosis

Amount of NT released depends on frequency of AP

APs travel down axon to depolarize bouton

open VG Ca++ channels in bouton

Ca++ enters bouton by electrochemical gradient

Ca++ binds to synaptotagmin (protein sensor)

Triggers exocytosis of synaptic vesicles;  release of NTs by exocytosis

Neurotransmitter Release

*will be on test*

action potentials reach the axon terminal

Ca++ enters axon terminal via voltage gated channels

Ca++ binds to sensor protein (snaptotagmin) in cytoplasm

Ca++ protein comples stimulates fusion and exocytosis of neurotransmitter

---neurotransmitter is released from the vesicle into synapse

Neurotransmitter difuses across cleft opening chemically-regulated ion channel

Depolarizing channels cause EPSP (excitatory postsynaptic potentials)

Hyperlarizing channels cause IPSP (inhibitory postsynaptic potentials)

These affect VG channels in post synaptic cell

EPSP and IPSP summate  If MP in postsynaptic cell reaches threshold at the axon hillock, a new AP is generated

axon hillock has many VG channels and is site where AP are normally initiated