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Na+ channels
Voltage gated @ axon,
Mechanical (ligand) @ dendrites
K+ channels
Voltage gated
Ca++ Channels
Voltage gated @ axon terminals
Cl-
Chemically gated
Nernst Equation
Eq(ion) = 61/z log[ion(out)/ion(in)]
Gate types
*Voltage
* ligand-gated (extracellular/Intracellular ligand)
*Mechanically gated
Graded and Action Potential comparison
Action Potential
Action Potential Complete graph,
Memorize the YELLOW Na
Violet K+
AP inactivation, Absolute refractory period.

INFLOW of Na ions.
Myelin Sheath

Nodes of ranvier

Saltatory Conduction
it’s a lipid, that surrounds. It acts as an insulator

*Farther the myelination (bigger nodes of ranvier) the faster the transmission of action potential.

Jump down axons as Na+ channels are in nodes.
Inactivation property
Property that is responsible for one way direction is
Graded potentials (Additional info)
can BOTH depolarize or hyperpolarize the cell

found in dendrite and axon

The way the neuron works is that what you want is graded potentials coming all over the dendritic bodies and adding up to the axon and eventually being able to meet the threshold in the axon hillock.
Excitation Secretion couploing
the conversion of electrical signal to chemical (and back again).

If Ca enters hte pre synaptic terminal, it will depolarize the terminal and cause AP.

It will then stimulate NT vesicles to migrate down the synapse and perform excitatosis to release NT in synapse.
(Excitation-Secretion Coupling)
Neurocrines:
7 major classes:
1. acetylcholine
2. amines
3. amino acids
4. purines (ATP, AMP)
5. gases (NO
6. peptides
7. lipids (eicosanoids
cannabinoid R)
Major Neurcrines

1. Acetylcholine (ACh)
2. Norephinephrine
3. Dopamine
4. Serotonin
5. Histamine
Major Neucrines (part 2)
Amino Acid
1. Glutamate
2. GABA
3. Glycine
Purines
4. Adenosine
Gases
5. Nitric Oxide (NO)
Acetylcholinesterase
chops the ACh, then
choline byproduct is transported back into the axon terminal and used to make more ACh.
Turning off Synaptic Response
1. returned to Axon terminal for reuse, or transported into glial cells.
2. Enzymes inactivation
3. NT can diffuse out of synaptic cleft
Action potential (Stimulus strength)
converted to FREQUENCY, the bigger the stimulus strength, the more trains of Action potential will occur,

*But all with same amplitude, just different in number
Type of NT receptor dictates creation of EPSP or IPSP

Ca2+

Cl- (from GABA)
- Ca2+ = exocytosis of synaptic vesicle -

-Cl- = hyperpolarizes the cell, making it harder to activate.
Ionotropic –

metabotrophic --
=when ions channels open., fast, short lived

= Triggers a secondary response inside the cell. Slow, but usually long life.
Divergent pathways

Convergent pathways
Integration = neuron to neuron
communication

Pre synaptic

Post Synaptic
Synaptic Plasticity

NMDA-R & hippocampus
critical to memory
and learning
in hippocampus

#6 Is paracrine
regulation