Facilitation and depression of synaptic transmission in amphibian sympathetic ganglia.

Abstract:

:There have been few reports concerning facilitation and depression in sympathetic ganglia9,17,40. In the present investigation, pairs of excitatory postsynaptic potentials (EPSPs) were recorded intracellularly from bullfrog paravertebral sympathetic ganglia for an analysis of the site and mechanism responsible for the phenomena of facilitation and depression of ganglionic transmission. The ratio of the amplitude of the second of a depression of ganglionic transmission. The ratio of the amplitude of the second of a pair of EPSPs divided by the first was compared to the time interval between each pair of EPSPs divided by the first was compared to the time interval between each pulse. These ratios demonstrated two phases: an earlier phase of facilitation (20-500 msec pulse intervals) and a later phase of depression (500 msec-10 sec). Additional parameters-rate of rise of synaptic potentials (dV/dt), synaptic currents (EPSCs), and synaptic conductances (Gtr)-were determined and all confirmed the results obtained with EPSPs. Furthermore, the degree of facilitation or depression could be modulated by altering the extracellular concentration of calcium. On the other hand, comparison of the amplitude of pairs of presynaptic terminal spikes did not show any variability over similar stimulus intervals, nor were the amplitudes of miniature EPSPs significantly different before or after an evoked EPSP. Therefore, the processes of facilitation and depression of ganglionic transmission occur as a result of normal nerve terminal activity. The processes are occurring simultaneously, such that one or the other may predominate depending upon the interval between pulses, as well as the relative concentration of extracellular calcium.

journal_name

Brain Res

journal_title

Brain research

authors

Tashiro N,Gallagher JP,Nishi S

doi

10.1016/0006-8993(76)90840-4

subject

Has Abstract

pub_date

1976-12-10 00:00:00

pages

45-62

issue

1

eissn

0006-8993

issn

1872-6240

pii

0006-8993(76)90840-4

journal_volume

118

pub_type

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