title: Burst firing in gonadotrophin-releasing hormone neurones does not require ionotrophic GABA or glutamate receptor activation.
abstract: Burst firing is a feature of many neuroendocrine cell types, including the hypothalamic gonadotrophin-releasing hormone (GnRH) neurones that control fertility. The role of intrinsic and extrinsic influences in generating GnRH neurone burst firing is presently unclear. In the present study, we investigated the role of fast amino acid transmission in burst firing by examining the effects of receptor antagonists on bursting displayed by green fluorescent protein GnRH neurones in sagittal brain slices prepared from adult male mice. Blockade of AMPA and NMDA glutamate receptors with a cocktail of CNQX and AP5 was found to have no effects on burst firing in GnRH neurones. The frequency of bursts, dynamics of individual bursts, or percentage of firing clustered in bursts was not altered. Similarly, GABA(A)  receptor antagonists bicuculline and picrotoxin had no effects upon burst firing in GnRH neurones. To examine the importance of both glutamate and GABA ionotrophic signalling, a cocktail including picrotoxin, CNQX and AP5 was used but, again, this was found to have no effects on GnRH neurone burst firing. To further question the impact of endogenous amino acid release on burst firing, electrical activation of anteroventral periventricular nuclei GABA/glutamate inputs to GnRH neurones was undertaken and found to have no impact on burst firing. Taken together, these observations indicate that bursting in GnRH neurones is not dependent upon acute ionotrophic GABA and glutamate signalling and suggest that extrinsic inputs to GnRH neurones acting through AMPA, NMDA and GABA(A)  receptors are unlikely to be required for burst initiation in these cells.
authors: Centre for Neuroendocrinology and Department of Physiology, University of Otago, Dunedin, New Zealand.
authors: K
authors: K
authors: Lee
authors: X
authors: X
authors: Liu
authors: A E
authors: AE
authors: Herbison
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D058787:GABA-A Receptor Antagonists; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D016202:N-Methylaspartate / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009924:Organ Culture Techniques; D011963:Receptors, GABA-A / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D058468:Receptors, Ionotropic Glutamate / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D055366:Synaptic Potentials / Q000187:drug effects / Q000235:genetics* / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D058468:Receptors, Ionotropic Glutamate; D007987:Gonadotropin-Releasing Hormone; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid