Inhibitory effect of 17beta-estradiol in the parabrachial nucleus is mediated by GABA
1Department 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
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.
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