Depolarizing responses to glycine, β‐alanine and muscimol in isolated optic nerve and cuneate nucleus

Abstract

1Concentration-dependent depolarizations were evoked by glycine and P-alanine 5 x 10-4 -10-2M and by the y-aminobutyric acid (GABA) analogue, muscimol 10-6 -10O4M. 2 The maximal response to glycine was several-fold higher than that to muscimol on optic nerve but the reverse was found on the dorsal funiculus fibres in the cuneate nucleus. P-Alanine evoked a similar maximal response to glycine on optic nerve but a considerably higher maximum than glycine in the cuneate nucleus. 3 Strychnine was 19.5 times more potent as a glycine antagonist (pA2 = 6.58) than as a muscimol antagonist. Bicuculline was 156 times more potent as a muscimol antagonist than as a glycine antagonist. Other antagonists of muscimol, i.e. tubocurarine, picrotoxin and leptazol, and potentiators of muscimol, i.e. pentobarbitone and flurazepam, had little or no effect on responses to glycine.4 Responses to P-alanine had pharmacological properties compatible with a mixed action on both GABA and glycine receptors. 5 The rat isolated optic nerve appears to be a useful preparation for studying the pharmacology of the neuronal glycine receptor plus chloride ionophore complex.

Enhancement of homomeric glycine receptor function by longchain alcohols and anaesthetics

“…Indeed, several electrophysiological studies showed that clinical concentrations of halothane and enflurane potentiate the glycine-induced Cl-currents in dissociated neurones from the nucleus tractus solitarius of the rat (Wakamori et al, 1991). In addition, Harrison et al (1993) (Machu & Harris, 1994 (Simmonds, 1983). In our study, etomidate and ketamine were completely ineffective on glycine receptor function, while alphaxalone and pentobarbitone produced a modest potentiation of homomeric al glycine receptor function.…”

Glycine stimulates striatal dopamine release in conscious rats

“…For instance, glycine could inhibit inhibitory interneurones in the striatum; inhibit inhibitory heteroreceptors on dopaminergic terminals; de-inactivate local calcium channels by membrane hypopolarization (Llinas et al, 1983); or increase transmembrane Cl-conductance in nearby axons (Simmonds, 1983;Raiteri et al, 1990), thereby producing receptor-mediated depolarization rather than hyperpolarization.…”

Conduction block and glial injury induced in developing central white matter by glycine, GABA, noradrenalin, or nicotine, studied in isolated neonatal rat optic nerve

“…Neonatal optic nerve nicotinic acetylcholine receptor (nAChR) activation has a similar effect upon action potential conduction (Zhang et al, 2004), and the actions of both GABA-A and nAChR activation are largely reversible. β-Adrenoreceptor or serotonin receptor activation also reversibly effects axon excitability in this preparation (Honmou and Young 1995;Saruhashi et al, 1997), while glycine receptor activation has a powerful depolarizing effect upon the membrane potential of neonatal optic nerve axons (Simmonds 1983). The significance of the expression of neurotransmitter receptors other than those for glutamate in developing central white matter for injury has not been examined and previous studies have concentrated upon brief periods of receptor activation.…”