University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

405

Pages:

4
Author:

Mariam A.

Process of learning    Habituation: decrease in response to a stimulus after repeated presentations (non-associative learning). o Aplysia californica has a reflex with its gills. o Continually stimulating this reflex will cause it to stop. Sensitisation: repeated administrations of a stimulus results in the progressive amplification of a response (non-associative learning). o Stimulating tail of aplysia californica causes increase in neurotransmitter release from sensory neuron to motor neuron. o ESPS of sensory neuron will be bigger. Long-term potentiation: long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously. Long term potentiation (LTP)  Intense (“tetanic”) stimulation of axons leading from the entorhinal cortex to the dentate gyrus (the “perforant path”) causes long-term increase in the magnitude of postsynaptic potentials in the dentate gyrus cells.  LTP can be produced in many areas of the brain and can last for several months.  Associative LTP: o In field CA1 of the hippocampus (and elsewhere). o Results from stimulating two inputs to the CA1 pyramidal cells. o Appears to obey the Hebb rule – when a weak and strong input are stimulated simultaneously, the weak input is strengthened. NMDA receptor  Synaptic strengthening seems to occur when molecule of neurotransmitter bind to a receptor on a dendritic spine that is already depolarised.  Thus, two factors are required: o Release of neurotransmitter. o Postsynaptic depolarisation.  NMDA receptor is a glutamate receptor with some peculiar properties; it is both electrically gated and chemically gated.  Whenever CA1 pyramidal neurons fires, all of its dendritic spines become briefly depolarised; if this is followed by a weak synapse during backwash of depolarisation, it will be strengthened.  Mechanism of action – getting the Ca2+ into postsynaptic neuron: o In resting state, Ca2+ channel of the NMDA receptor is blocked by Mg2+. o Even with glutamate binding, the Mg2+ still binds to the Ca2+ channel. o However, when glutamate binding is coupled with depolarisation of the postsynaptic neuron, Mg2+ is extruded and hence allows Ca2+ to enter.  Inhibition can be caused by: o EGTA: binds to Ca2+ and renders them biologically inert. o AP5: blocks NMDA receptors, and thus prevents LTP in CA1 of the hippocampus. AMPA receptor  Hypothetical model describes the insertion of new AMPA receptors into the postsynaptic membrane of dendritic spines after LTP.  Mechanism of action: o When Ca2+ enters the postsynaptic membrane, it phosphorylates and activates calmodulin kinase II. o Linking proteins attach on to the activated CaM-KII on one side, with their other side attaching on to AMPA receptors brought to the synaptic membrane in vesicles.  Addition of new AMPA receptors results in larger postsynaptic potentials when the terminal button releases glutamate.