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GABA‐Mediated Presynaptic Inhibition in Crayfish Primary Afferents by Non‐A, Non‐B GABA Receptors
Author(s) -
El Manira A.,
Clarac F.
Publication year - 1991
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1991.tb00055.x
Subject(s) - muscimol , gabaa receptor , neuroscience , picrotoxin , gabab receptor , neurotransmission , chemistry , bicuculline , biology , receptor , biochemistry
Abstract GABAergic presynaptic inhibition has been investigated in primary afferents using an in vitro preparation of the crayfish, Procambarus clarkii. Presynaptic terminals of a leg proprioceptor, the coxo‐basal (CB) chordotonal organ, were impaled in the neuorpil of the 5th thoracic ganglion. Pressure ejection of small volumes of the GABA A or GABA B receptor agonists, muscimol and 3‐aminopropylphosphinic acid (3‐APA), both induce depolarizing responses in the impaled CB sensory terminal. These depolarizations are not blocked by the specific GABA A and GABA B receptor antagonists, SR‐95531 and phaclofen, but they are abolished by picrotoxin. Both muscimol‐ and 3‐APA‐induced depolarizations are carried by an increase in conductance to Cl ‐ . The presynaptic increase in conductance to C1 ‐ by GABA receptor activation leads to a depression of sensory synaptic transmission through a shunting of the incoming spikes. Monosynaptic EPSPs elicited in motor neurons by CB sensory nerve stimulation are depressed by muscimol and 3‐APA. GABA‐mediated presynaptic modulation occurs in crayfish primary afferents which can adjust the gain of reflexes. These results show that GABA‐activated Cl ‐ channels can induce a modulation of synaptic transmission, but also that the distinction between GABA A and GABA B receptors, as in vertebrates, is not applicable to the crustacean primary afferents.