brain and behavior week 3
why you need sodium channels
axon wrapped in myelin, allows myelin to move without leaks along the way
like a pool w ripples
dense myelin sheath allows insulation to keep the charge from losing/dissipating across axon
increases conduction velocity significantly
10x conduction velocity because of the myelin sheath
axons without sheath (black border in picture) are diseases
axons with thin sheath (thin black border) are in recovery
What happens in the synapse when axon makes contact with dendrite?
*on picture, it’s when orange (pre synaptic neuron) meets blue (post synaptic neuron)
could be seen as soup
soup is diffusing from pre to post synaptic
could be seen as sparks
pre and post synaptic cell has tight contact or a channel, and direct zaps of current is allowing communication
otto loewi wanted to prove that communication between neurons is chemical
vagus nerve is part of parasympathetic nervous system (thus HR will go down)
heart 1 connect to electrical stimulate and HR went down
heart 2 not connected and HR went down too
meaning heart 2 be
explains that chemical synaptic transmission is slow
presynaptic axon
synaptic vesicle on left with black dots containing neurotransmitter, the chemical that will release and travel to the post synaptic cell
vesicle binds/fuses with membrane and its contents release into soupy environment between pre and post synaptic cell
synaptic cell contained inside pre synaptic cell
imagine a boat that docks, once it docks it’s almost like part of the dock, then allowing people to come off the boat
the binding of the vesicle to the membrane is aided by the cation CALCIUM (VERY IMPORTANT)
green ports in the picture are calcium channels allowing the vesicle to become one with the membrane
whatever is released will bind to the post synaptic cell
post synaptic dendrite
neurotransmitter released from pre to post synaptic membrane binds to receptors
receptors open ion channels (protein), aka transformational change
if NT is excitatory, sodium enters, allowing positive charge to depolarize membrane closer to threshold
generates EPSP - excitatory postsynaptic potential
graded polarization (increases incrementally, not just a shoot up in charge)
balances by adding positive to negative charge existing in the membrane
if NT is inhibitory, chlorine enters, allowing negative charge to hyperpolarize membrane further from threshold
generates IPSP - inhibitory postsynaptic potential
graded hyperpolarization - decreases incrementally, not drastic change of charge immediately)
becomes even more negative (already negative inside)
you cannot generate an action potential if chlorine comes in
different receptors have different functions
neurotransmitter released needs to be taken back up
pre synaptic cell has membrane that in pinched from the inside
when pinched, it takes the NT with it
then forms place for next synaptic vesicle to bind and fuse
3.2 (wed)
catch up lecture 4
catch up lecture 5 slide 9
electrophysiology used in labs across the world
coordination of excitation and inhibition
contracting muscles in leg, opposing muscles in the leg, information communicating to spinal cord (involuntary - your brain is not actively making the decision)
flexor and extensor, one pathway being excited, one pathway being inhibited, excitation pathway will win every time (think of a yo-yo)
neural circuit slide, each example performs specified functions due to their wiring patters of excitation and inhibition
FOCUS POINT
FAST NEUROTRANSMITTERS
glutamate
GABA
almost any drug you can think of works to inhibit or mimic glutamate or GABA
work to form object perception, speech, language, motor sequence initiation
SLOW NEUROMODULATORS
noradrenaline
serotonin
histamine
hypocretin
dopamine
essentially change state of the brain
biasing of perceptual content
^^^you need both slow and fast as they attend to specialized functions’
next slide shows binding of pre to post-synaptic cell involves glutamate and GABA, those are what is getting blocked when drugs are taken. that process is getting blocked.