title: Inhibitory effect of 17beta-estradiol in the parabrachial nucleus is mediated by GABA.
abstract: In the present investigation, electrophysiological recordings of thalamic relay neurons were used to investigate the role of estrogen as a modulator of visceral afferent information through the PBN to forebrain structures. Experiments were done in anaesthetized (sodium thiobutabarbitol; 100 mg/kg) male and ovariectomized female rats supplemented for 7 days prior with either 17beta-estradiol (OVX-E(2)) or saline (OVX-S). A portion of the right cervical vagus was isolated for the electrical activation (0.8 Hz, 2 ms duration) of visceral afferents. The evoked single and multi-unit activity was recorded via a recording electrode in the ventrobasal thalamus. Exogenous microinjection of 17beta-estradiol (0.1, 0.25 and 0.5 microM; 200 nl) into the parabrachial nucleus (PBN) produced a significant, dose-dependent attenuation in the magnitude of visceral afferent activation-evoked responses of neurons recorded in the thalamus in both male and OVX-E(2) groups. No effect on evoked thalamic activity was observed following injection of estrogen into the PBN of OVX-S animals. Co-injection of estrogen with the GABA(A) receptor antagonist, bicuculine (0.1 microM; 200 nl) but not phaclofen (GABA(B); 0.1, 0.5 or 1 microM; 200 nl) resulted in an increase in the evoked thalamic response in males (55+/-11%) and OVX-E(2) female (68+/-15%) rats. These studies suggest that estrogen inhibits neurotransmission in the PBN via an interaction with the GABA(A) receptor to modulate the flow of visceral information to the thalamus.
authors.affiliation: Department of Anatomy and Physiology, Atlantic Veterinary College, University of Prince Edward Island, PEI Health Research Institute, Charlottetown, P.E.I., Canada C1A 4P3. tsaleh@upei.ca
authors.forename: T M
authors.initials: TM
authors.lastname: Saleh
authors.forename: M C
authors.initials: MC
authors.lastname: Saleh
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001418:Baclofen / Q000031:analogs & derivatives* / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D000077267:Fulvestrant; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010052:Ovariectomy; D011149:Pons / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011960:Receptors, Estrogen / Q000037:antagonists & inhibitors / Q000378:metabolism; D011963:Receptors, GABA-A / Q000378:metabolism; D018080:Receptors, GABA-B / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014630:Vagus Nerve / Q000187:drug effects / Q000378:metabolism; D020651:Ventral Thalamic Nuclei / Q000187:drug effects / Q000378:metabolism; D017833:Visceral Afferents / Q000187:drug effects / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D004965:Estrogen Antagonists; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D011960:Receptors, Estrogen; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; C052329:phaclofen; D000077267:Fulvestrant; D004958:Estradiol; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; D001640:Bicuculline