Behavioral Neuroscience - Action Potential

Action potential * All mental activity * nervous sys consists of neurons which carry info * neuro info is carried as electrical currents * between neurons info is carried as NTs
To start action potential * when threshold is reached at axon hillock voltage dependent gates Na+ gates (ion channels) open at massive amounts * voltage dependent: ion channel that opens or closes according to the value of the membrane potential * strong influx (inward flow) of Na+ * electrostatic and concentration gradient drive Na+ inside of neuron * influx is so strong that a reversal in polarity occurs * inside becomes +40, outside becomes negative (different from postsynaptic potential)
Peak of action potential * electrical gradients are reversed; now both gradients are now in the same direction * K pushed out by electrical gradient b/c outside is more negative than inside and concentration gradient b/c actual concentration grad doesn’t change much * At this point – NA+ channels are closed * Rapid efflux (outward flow of K+ ) * So much rushes out, that there is an overshoot of the original \n polarity (-80mv inside)
Overshoot period is called the relative refractory period \n (Afterpotentials ) * Hard to get cell to re-fire at this time
Resting potential restored by natural diffusion and NA+/K+ pump (transporter)
Pumps NA+ out, and K+ into the neuron
Protein found in the membrane that extrudes sodium ions from and transports potassium ions into the cell
for myelinated neurons process re-occurs at each node of Ranvier (saltatory conduction)
Saltatory conduction: conduction of action potential by \n myelinated axons. * The action potential appears to jump from \n one node of Ranvier to the next

Exocytosis * When AP reaches axon terminal/terminal buttons, Ca 2+ channels open (voltage-dependent) * AP activates heteroreceptors (found in axon terminals) which open Ca 2+ channels * b/c of gradients, Ca2+ enters the cell * activates enzymes that propel vesicles along microtubules running down TB (even removes blocking proteins!) * Vesicles merge with presynaptic membrane , drop NT into synapse, and diffuse across to activate receptors on next locations * if neuron = produces IPSP/EPSP, if muscle/gland = inhibit/excite * this process = exocytosis
several specialized long-chain proteins called SNARES mediate exocytosis * serve as tethers: those attached to vesicles are called v-SNARES, while those attached to the presynaptic membrane = t-SNARES (t for target)
when v-SNARES on the vesicle attach to t-SNARES the vesicle is said to be docked ready to be released
another protein attached to the vesicle called synaptotagmin, serves as Ca 2+ sensors
when the AP arrives at axon terminal, incoming Ca ion binds and activates synaptotagmin which then triggers the final fusion (t and v connect.
Final stage --- clearing out synapse * Reuptake: the entry of NTs just liberated by a terminal button back through its membrane, thus terminating the postsynaptic potential * NT is packaged and brought back into th pre-synaptic neuron * Enzymatic breakdown: the destruction of a neurotransmitter by an enzyme after its release * ex. the destruction of acetylcholine by acetylcholinesterase * NTs reduced to inactive molecules; they diffuse away * Autoreceptors: receptors on the axon terminal that become active when large number of NT present * inhibits release of additional neurotransmitters * nothing to do w/ AP
Synapse
Most drugs (medical/recreational) influence what happens in the synapse
Drugs can have 2 effects
agonist - increases activity of an NT
antagonist - decrease the lvl of a NT
many most substances can both act as an agonist for one neurotransmitter and an antagonist for another