neural communication & plasticity Flashcards
nissl stain vs golgi stain
nissl: stains all cell bodies
golgi: stains a %, shows dendrites more clearly
brain layer 1
molecular layer
brain layer 2
outer granular layer
brain layer 3
outer pyramidal layer
brain layer 4
inner granular layer
brain layer 5
inner pyramidal layer
brain layer 6
multiform layer
central sulcus (forward & behind)
forward: action
behind: perception
broadman’s cortical map
began to map certain functions to certain brain areas
afferent
info to brain
efferent
info from brain
dorsal roots
afferent
sensory info
ventral roots
efferent
movement info
Wilhelm von Waldeyer defined what?
defined a neuron as communication cell in NS
named: dendrite & axon
charles sherrington’s discovery ( 3 reasons supporting)
synapse exists b/c:
1. degeneration was discrete, not continuous
2. reflexes were slowed down by a junction
3. something makes reflex conduction unidirectional
1897: cajal & sherrington
synapse!!
(only theoretical)
george oliver & henry dale
naturally occurring substances mimic nerve stimulation
chemical?
loewi (vagusstoff)
stimulation of one heart activates the other heart in a connected chamber (inhibitory effect observed)
therefore: chemical
how many neural impulses is there a second? chemical synapse
1000-2000
have neurotransmitters changed over time?
primitive animals had the same neurotransmitters as we do now
it is the WAY the NT’s act that changes via evolution
what can you infer about a NT’s function from their chemical structure?
nothing!
cajal’s discovery (relating to synaptic plasticity)
discovered “growth cones”
how fixed is the NS?
how many inputs can one neuron have?
50,000
why was hippocampus studied? (& hippocampus deficit)
studied to further understand synaptic connections (in rat brains)
deficit = memory
CA3 -> CA1 experiment
stimulate pathway one (CA3 -> CA1)
pathway 1: stronger epsp post-tetanus
pathway 2: same epsp post-tetanus
therefore -> more stimulation = strengthens a pathway
long term potentiation
frequent use of one synapse strengthens the synapse long-term
(this can have no affect on adjacent neurons OR it can have little affect on adjacent)
LTP: specitivity
only one synapse strengthened
How? NMDA channels are opened only active synapses, confining LTP to these sites.
LTP: associativity
adjacent synapses strengthened as well
How? strong neighbouring inputs depolarise & remove Mg2+ block
how does LTP occur?
depolarisation inside (state of LTP) = Ca2+ influx via NMDA receptors
Ca2+ = production of more receptors via CAMKII & CKP = stronger synapse
NMDA receptors
internal depolarisation = more positive inside = repels Mg2+ away
