Postnatal maturation of GABA(A) and GABA(C) receptor function in the mammalian superior colliculus.
In the stratum griseum superficiale (SGS) of the mammalian superior colliculus, GABA(C) receptors seem to control the excitability of projection neurons by selective inactivation of local GABAergic interneurons. As the onset of visual responses to SC begins well after birth in the rat, it is possible to study developmental changes in GABAergic mechanisms that are linked to the onset of visual information processing. In order to analyse postnatal changes in inhibitory mechanisms that involve GABA receptor function, we used extracellular field potential (FP) recordings and single cell patch-clamp techniques in slices from postnatal day 4 (P4) to P32 and examined the effects of GABA and muscimol on electrically evoked SGS cell activity. While GABA(A) receptor activation affected FP amplitudes throughout postnatal development, GABA(C) receptor activation did not significantly change FP amplitudes until the third postnatal week. Results from patch-clamping single cells, however, clearly demonstrate that GABA(C) receptors are already functional at P4--similar to GABA(A) receptors. Throughout postnatal development, activation of GABA(C) receptors leads to a strong inhibition of inhibitory postsynaptic activity, indicating that GABA(C) receptors are expressed by inhibitory interneurons. Furthermore, the proportion of neurons that show decreased excitatory postsynaptic activity during GABA(C) receptor activation correlates with the proportion of GABAergic interneurons in SGS. Our patch-clamp results indicate that the functional expression of GABA(C) receptors by GABAergic interneurons does not change significantly during postnatal development. However, our measurements of FP amplitudes indicate that the maturation of the efferent connections of these GABAergic neurons within SGS during the third postnatal week strongly changes GABA(C) receptor function.
Boller
M
M
Allgemeine Zoologie & Neurobiologie, Ruhr-Universität Bochum, D-44780 Bochum, Germany.
Schmidt
M
M
D000375:Aging / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D004305:Dose-Response Relationship, Drug; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D007395:Interneurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009118:Muscimol / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D018408:Patch-Clamp Techniques; D051381:Rats; D020318:Rats, Long-Evans; D018079:Receptors, GABA / Q000187:drug effects / Q000378:metabolism*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism*; D013477:Superior Colliculi / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism* / Q000494:pharmacology
D018755:GABA Agonists; D018756:GABA Antagonists; C087200:GABA-C receptor; D018079:Receptors, GABA; D011963:Receptors, GABA-A; D009118:Muscimol; D005680:gamma-Aminobutyric Acid