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Burst Firing in Gonadotrophin‐Releasing Hormone Neurones does not Require Ionotrophic GABA or Glutamate Receptor Activation
Author(s) -
Lee K.,
Liu X.,
Herbison A. E.
Publication year - 2012
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2012.02360.x
Subject(s) - cnqx , bursting , bicuculline , ampa receptor , glutamate receptor , picrotoxin , chemistry , endocrinology , nmda receptor , dnqx , medicine , kainate receptor , gonadotropin releasing hormone , neuroscience , receptor , gabaa receptor , biology , hormone , luteinizing hormone , biochemistry
Burst firing is a feature of many neuroendocrine cell types, including the hypothalamic gonadotrophin‐releasing hormone ( G n RH ) neurones that control fertility. The role of intrinsic and extrinsic influences in generating G n RH 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 G n RH neurones in sagittal brain slices prepared from adult male mice. Blockade of AMPA and NMDA glutamate receptors with a cocktail of CNQX and AP 5 was found to have no effects on burst firing in G n RH 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 G n RH neurones. To examine the importance of both glutamate and GABA ionotrophic signalling, a cocktail including picrotoxin, CNQX and AP 5 was used but, again, this was found to have no effects on G n RH 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 Gn RH neurones was undertaken and found to have no impact on burst firing. Taken together, these observations indicate that bursting in G n RH neurones is not dependent upon acute ionotrophic GABA and glutamate signalling and suggest that extrinsic inputs to G n RH neurones acting through AMPA , NMDA and GABA A receptors are unlikely to be required for burst initiation in these cells.