Pharmacology of amino acid receptors on vertebrate primary afferent nerve fibres

Abstract

1. 1. Structure-activity of primary afferent depolarising action (PAD) mediated by γ-aminobutyrate (GABA) analogues suggests a difference between subsynaptic receptors located at fibre terminations within the dorsal horn and axonal receptors which are distributed throughout non-synaptic regions. 2. 2. The interaction of the bicuculline-sensitive GABA receptor (GABA A) ionophore complex with barbiturates and benzodiazepines suggests that at least three binding sites are required to explain the independent GABA-mimetic, GABA-potentiating and picrotoxin-reversing effects of such agents. 3. 3. Difficulties with explanation of the depressant effects of baclofen on spinal transmission, in terms of the bicuculline-resistant GABA (GABA B) receptor hypothesis, are mentioned. 4. 4. Glutamate-induced PAD of low threshold afferents is mediated indirectly through release of potassium. However, such terminals possess receptors (possibly autoreceptors for l-glutamate), activated by (+)2-amino-4-phosphonobutyrate, which cause depression of transmitter release. 5. 5. Primary afferent C-fibres possess receptors which are selectively activated by kainate and which mediate picrotoxin-resistant PAD. Such receptors may be involved in the presynaptic conditioning of C-fibre transmitter release. 6. 6. The peripheral terminals of vestibular primary afferents, in amphibia, possess excitatory amino acid receptors which are probably activated by the transmitter released from hair cells.