Neuroplasticity

neuroplaxia

local myelin damage, axon remains intact

Causes of axonal injury

Stretch, crush, shear, laceration

axonotmesis

continuity of axon is lost → wallerian degeneration

may or may not include damage to layers of nerve

neurotmesis

complete transection of nerve

surgery necessary

causes of CNS axon injury

trauma, decreased blood flow, neurogenerative disease

downstream effect

CNS damage triggers necrosis and apoptotic cell death of several axons

neurogenesis

creation of CNS neuronal growth

low level of glial that can proliferate thru life

what 2 areas show potential for neurogenesis?

olfactory bulb and hippocampus

neuroplasticity

ability of nervous system to respond to intrinsic stimuli by reorganizing its structure, function, and connections

chemical mechanism

immediate to short term changes to chemical synapses

increased NT released into synaptic cleft

structural mechanism

long term changes to neuronal structure

modify exisiting postsynaptic receptors

create new postsynaptic receptors

increased dendritic growth and terminal axons

functional mechanism

long term changes to neuronal function

cortical remapping

process in which existing cortical map is affected and ultimately changed by a stimulus

“neurons that fire together, wire together”

habituation

simplest form

decrease in response to repeated, benign stimulus

short term habituation

changes pre synaptically (decrease release of excitatory NTs

effects are transient

<30 mins

long term habituation

changes post synaptically

decrease receptors on postsynaptic receptors

>30 mins

experience dependent plasticity

selective stabilization of certain synapses and removal of others in response to experience

leads to persistent, long lasting changes to stabilized synapses to improve overall neural networks

long term potentiation

process by which the synaptic connections between neurons become stronger by frequent activation

high intensity stimulation

AMPA receptors

permeable to Na+

ligand receptors, open in response to glutamate linking with receptor

NMDA receptors

permeable to Na+ and Ca2+

contain Mg2+ blockade in channel

long term depression

conversion of active synapses into silent ones

low intensity, prolonged stimulation