Functional glycine receptor maturation in the absence of glycinergic input in dopaminergic neurones of the rat substantia nigra

• Published in: The Journal of physiology 2002-08, Vol.542 (3), p.685-697
• Main Authors: Mangin, J. M., Guyon, A., Eugène, D., Paupardin‐Tritsch, D., Legendre, P.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn - growth & development; Animals, Newborn - metabolism; Cognitive Sciences; Dopamine - metabolism; Electric Conductivity; Glycine - physiology; Glycine Agents - pharmacology; In Vitro Techniques; Life Sciences; Male; Neurons - metabolism; Neurons and Cognition; Original; Rats; Rats, Wistar; Receptors, Glycine - metabolism; Receptors, Glycine - physiology; Strychnine - pharmacology; Substantia Nigra - cytology; Substantia Nigra - growth & development; Substantia Nigra - metabolism; Synaptic Transmission - drug effects; Taurine - physiology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2002.018978

The postnatal maturation pattern of glycine receptor channels (GlyRs) expressed by dopaminergic (DA) neurones of the rat substantia nigra pars compacta (SNc) was investigated using single-channel and whole-cell patch-clamp recordings in brain slices from rats aged 7–21 postnatal days (P). In neonatal rats (P7-P10), GlyRs exhibited a main conductance state of 100–110 pS with a mean open time of 16 ms. In juvenile rats (P19-P22), both the GlyR main conductance state (46-55 pS) and the mean open time (6.8 ms) were decreased. In neonatal rats, application of 30 μ m picrotoxin, which is known to block homomeric GlyRs, strongly reduced glycine-evoked responses, while it was much less effective in juvenile rats. These results suggest that these GlyRs correspond functionally to α 2 homomeric GlyRs in neonatal rats and α 1 /β heteromeric GlyRs in juvenile rats. A drastic but transient decrease in the glycine responsiveness of DA neurones occurred around P17 concomitant to the functional switch from the homomeric state to the heteromeric state. This age corresponds to a maturation phase for DA neurones. The application of 1 μ m gabazine blocked spontaneous or evoked inhibitory synaptic current, while the addition of 1 μ m strychnine had no effect, suggesting a lack of functional glycinergic synapses on DA neurones. Although it has been proposed that taurine is co-released with GABA at GABAergic synapses on DA neurones, in the present study the stimulation of GABAergic fibres failed to activate GlyRs. Blockade of taurine transporters and applications of high K + and hyposmotic solutions were also unable to induce any strychnine-sensitive current. We conclude that functional maturation of GlyRs can occur in the absence of any detectable GlyR activation in DA neurones of the SNc.