Presynaptic inhibition by concanavalin A: are alpha-latrotoxin receptors involved in action potential-dependent transmitter release?

Abstract:

:Effects of concanavalin A on transmitter release were investigated in primary cultures of chick sympathetic neurons. The lectin reduced electrically evoked [3H]noradrenaline release by up to 30% with half-maximal inhibition at 0.16 microM. Concanavalin A also reduced the release triggered by extracellular Ca2+ in neurons depolarized by 25 mM K or rendered Ca2+-permeable by the ionophore A23187. The inhibitory action of concanavalin A on electrically evoked release was additive to that of the alpha2-adrenergic agonist UK 14,304. Inactivation of Gs and Gi/Go type G proteins by either cholera or pertussis toxin did not alter the inhibitory effect of the lectin. Concanavalin A failed to affect the resting membrane potential, action potential waveforms, or voltage-dependent K+ and Ca2+ currents. In contrast, the lectin efficiently blocked both the Ca2+-dependent and -independent alpha-latrotoxin-induced transmitter release, but only when applied before the toxin. The reduction of electrically evoked, as well as alpha-latrotoxin-evoked, release by concanavalin A was attenuated in the presence of glucose and abolished by methyl alpha-D-mannopyranoside. The dimeric derivative, succinyl-concanavalin A, was significantly less active than tetrameric concanavalin A. In bovine adrenal chromaffin cells, which displayed only weak secretory responses to alpha-latrotoxin, concanavalin A failed to alter K+-evoked catecholamine secretion. These results show that concanavalin A causes presynaptic inhibition in sympathetic neurons and indicate that cross-linking of alpha-latrotoxin receptors may reduce action potential-dependent transmitter release.

journal_name

J Neurochem

authors

Boehm S,Huck S

doi

10.1046/j.1471-4159.1998.71062421.x

subject

Has Abstract

pub_date

1998-12-01 00:00:00

pages

2421-30

issue

6

eissn

0022-3042

issn

1471-4159

journal_volume

71

pub_type

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