Lecture 3 (axon potential + channels) Flashcards
action potential (mv)
+30/+40mv
resting potential (mv)
-70mv
graded potential
proportional to the stimulation
action potential
all or nothing
temporal summation
stimulations across time (stimulation 2 adds to stimulation 1)
greater affect, ripple effect
spatial summation
stimulation across space (multiple stimulations at the same time)
creates larger ISPS or EPSP
types of summation
spatial (across space) and temporal (across time)
where to graded potentials integrate?
at the axon hillock
process of voltage gated Na+ channel (action potential)
1.) voltage gated ion channel opens (Na+ floods in)
2.) Strong depolarization (+40mv = EPSP)
3.) Gated ion channel closes
4.) Sodium potassium pump (3Na+ out, 2K+in) restore equilibrium
5.) absolute refractory (no firing)
6.) relative refractory (firing, but greater than usual stimulation -90mv)
7.) restore equilibrium (-70mv)
EPSP
Excitatory post-synaptic potential
IPSP
Inhibitory post-synaptic potential
factors that affect axon potentials
1.) threshold differences
2.) action potentials differ in shape
3.) rate of action potential discharge for the same amount of depolarization
4.) hebbian synapses
5.) temperature, time of day ect.
resting potential (balanced by:)
concentration gradient and the electrostatic gradient
concentration gradient
molecules diffuse from high to low pressure
osmotic pressure
K+ ions diffuse out of cell (can get back in through pump)
Other ions cannot get in as easily (selective permeability)
electrostatic gradient
different concentrations of electrical charges
K+ attracted to negative intracellular charge. CL- ions repelled by intracellular charge
nernst equation
equation for cell equilibrium
(only perfect but not quite)
leakage of K+ out, and Na+ comes into the cell
resting potential (how and at what mv?)
when the flow of K+ ions leaving the cell = flow of K+ ions coming in
through sodium potassium pump (3Na+ out, 2K+ in). Build up K+ in the cell. so K+ diffuse out. leads to negative charge, so K+ come back in.
-70mv
Excitatory synapse (what gated ion channels open?)
Na+ opens
K+ closes
Inhibitory synapses (what gated channels open?)
K+
Cl-
ways of opening gated ion channels (4 ways:)
1.) Chemical change in shape (ligand binds to a receptor) causing channel to open
2.) Gene-couple protein receptors (GPCR)
Second messenger action
3.) voltage change
4.) mechanical deformation (such as by touching things with your hands)
how do axons get over the “distance problem”?
Saltatory conduction (speeds up action potential!)
Regenerative potential
Saltatory conduction (steps)
Beads of myelin on the axon
Na+ channel opens on the nodes of Ranvier (depolarization)
action potential jumps from node to node
disease that affects saltatory conduction
multiple sclerosis
(Immune system generates antibodies that attack myelin)
** affects coordination and interpretation of sensory input
steps of action potential moving through pre-synaptic neuron:
1.) axon potential arrives at axon terminal
2.) depolarization causes Ca2+ gated ion channel to open
3.) Ca2+ vesicles fuse to the pre-synaptic membrane and rupture –releasing neurotransmitter into the cleft
4.) Crosses the cleft and binds to the post-synaptic membrane (specialized ligands)
5.) changes the excitatory level of the post-synaptic cell (may causes ISPS or EPSP)
mechanisms built into synapse that allow neurons to fire again: (2)
1.) Degration = enzymes that split and breakdown neurotransmitter
2.) Reuptake = neurotransmitter is reabsorb back into the axon terminal via transporters on the pre-synaptic neuron
Reuptake
neurotransmitter is reabsorb back into the axon terminal via transporters on the pre-synaptic neuron
Degradation
enzymes that split and breakdown neurotransmitter
Types of receptors: (two)
1.) Ligand Gated Ion Channel (Ionotropic)
*ligand bind to a receptor which causes the neuron shape to change (open gate/close gate)
2.) Metabotropic
G-CPR
*bind to a G protein out side of the cell, actives a second messenger inside the cell
Ligand Gated Ion Channel (Ionotropic)
ligand binds to a receptor
pore opens, ions flow through
causes change in membrane potential
metabotropic receptors
gene-couple protein receptors
ligand binds to gene-protein which actives second messenger inside the neuron
bigger changes:
*change in membrane charge
*alter energy use
* alter gene transcription
*slower, more amplified reactions (can open multiple pores at once)
Gap junction
Electrical synapse
*no modulation
* fast
*connexons
*restricted to local processing
- thought to be involved with epilepsy
