Lecture 7: Neuronal Plasticity I : Molecular Mechanisms Flashcards
Neural Plasticity
the ability of the brain cells(neurons, glia, astrocytes) to adapt in terms of genetics, structure, physiology and behavior
forms of neural plasticity
synaptic : short/long term, strengthen/weaken
Long term potentiation/depression
behavioral: Aplysia gill withdrawal reflex
habitation- you constantly being exposed to a stimuli and you get tired off it (ex. listening to a song for the first time)
Hebbs theory of changes underlying learning and memory in 3 stages:
(1) Synaptic changes(strengthening)
(2) formation of a “cell assembly”( a group of neurons working together)
(3) formation of a “phase sequence” ( A group of neurons firing together)
synaptic plasticity
change in synaptic strength
alterations in the presynaptic terminal
amount of neurotransmitters/neuromodulators released as well as the expression of calcium channels
alterations in the postsynaptic side
amount of receptors expressed (up regulation or down regulation)
The maintenance of LTP is due to the
The induction of LTP relies on
insertion of more AMPA receptors into the postsynaptic membrane
the activation of NMDA receptors
LTP
the insertion of AMPA receptors on the postsynaptic side increases the strength of the synaptic potential(more Na+ ions can eneter the cell)
CREB
cAMP response element binding protein
LTP activates BLANK which phosphorylate targets
protein kinases
LTD activates BLANK that cleaves phosphate groups from these targets molecules
a Ca2+ dependent phosphatase
evidence in support of this is that phosphatase inhibitors block LTD
LTD is associated with
loss of synaptic AMPA receptors
cocaine exposure caused a
larger response to AMPA but not NMDA