Hydrostatic pressure reduces synaptic efficiency by inhibiting transmitter release.
The amplitude of post-synaptic potentials at an identified synapse in the Aplysia central nervous system can be modulated by the application of hydrostatic pressure. Postsynaptically controlled functions, including responses to acetylcholine and the time course of decay of the synaptic responses, remain unaffected by compression. In contrast, frequency facilitation and posttetanic potentiation, which result from presynaptic processes, are altered by pressure in a manner similar to that of agents that block transmitter release. It is concluded that pressure reduces synaptic efficiency by interfering with certain presynaptic mechanisms associated with transmitter release.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000502:physiology; D004558:Electric Stimulation; D004566:Electrodes; D005071:Evoked Potentials / Q000187:drug effects; D005724:Ganglia / Q000502:physiology; D006874:Hydrostatic Pressure; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011312:Pressure; D013569:Synapses / Q000502:physiology*
D018377:Neurotransmitter Agents; D000109:Acetylcholine; D002118:Calcium