Lecture DetailsEdit

David Reser; Week 2 MED1022; Physiology

Lecture ContentEdit

There can be chemical and electrical synapses. There can be feedback mechanisms; feed forward mechanisms to amplify signals; and lateral inhibition to have an effect on other surrounding neurons to decrease action potentials. Graded potentials can occur and summate either temporally or spatially. Synapses can be axo-dendritic, axo-somatic (on cell body, or soma) or axo-axonic. Whether a downstream neuron fires an action potential after recieving an input from the presynaptic cell depends on the type, location and amplitude of the postsynaptic potential and past firing history.

Preservation about the history of neuronal activity can employ some/all of the following mechanisms- facilitation of transmitter release, increasing current flow through ion channels, increasing the area of the postsynaptic density, increasing transmitter receptor population, changes in spine density. Changes in synaptic activity can be reflected in the structure of the presynaptic and postsynaptic membranes and the morphology of the dendritic spine itself.

Long term potentiation is where repeated postsynaptic depolarisation will increase response size from a stimulus, leading to a larger influence of that synapse. NMDA dependent LTP involves glutamate activate ion channel receptors usually blocked by Mg. With strong membrane depolarisation in the presence of permissive cofactors Mg is removed and Ca ions flow through the channel. Due to the intracellular actions of Ca, the increased signal can be maintained for months.

Cortical architecture (1 molecular layer; 2 external granular layer; 3 external pyramidal layer; 4 internal granular layer; 5 internal pyramidal layer; 6 multiform layer) yields numerous sites for plastic modification of synaptic strength to give rise to a flexible and modifiable network. Purkinje cell is the greatest site of convergence in the CNS.

Medium spiny neurons combine information from cortical neurons and dopaminergic input from substantia nigra to modulate the output of cells in the globus palladius or SNpr. GP and SNpr project in turn to the thalamus, which projects to the cortex.