17beta-estradiol attenuates excitatory neurotransmission and enhances the excitability of rat parabrachial neurons in vitro.
The steroid hormone 17beta-estradiol and its respective receptors have been found in several cardiovascular nuclei in the central nervous system including the parabrachial nucleus. In a previous study, we provided evidence that 17beta-estradiol attenuated an outward potassium conductance in parabrachial neurons of male rats, using an in vitro slice preparation. In this study we sought to enhance the comprehensive information provided previously on estradiol's postsynaptic effects in the parabrachial nucleus by directly examining whether 17beta-estradiol application will modulate excitatory synaptic neurotransmission. Using a pontine slice preparation and whole-cell patch-clamp recording, bath application of either 17beta-estradiol (20-100 muM) or BSA-17beta-estradiol (50 muM) decreased the amplitude of evoked excitatory postsynaptic currents (from 30-60% of control) recorded from neurons in the parabrachial nucleus. The paired pulse ratio was not significantly affected and suggests a post-synaptic site of action. The inhibitory effect on the synaptic current was relatively long-lasting (non-reversible) and was blocked by the selective estrogen receptor antagonist, ICI 182,780. Furthermore, 17beta-estradiol reduced the maximum current elicited by a ramp protocol, increased the input resistance measured between resting membrane potential and action potential threshold and caused an increase in the firing frequency of the cells under current-clamp. In summary, 17beta-estradiol caused 3 effects: first, a depolarization; second, a reduction in evoked excitatory postsynaptic potentials; and third, an enhancement of action potential firing frequency in neurons of the parabrachial nucleus. These observations are consistent with our previous findings and support a role for estrogen in modulating neurotransmission in this nucleus.
Fatehi
Mohammad
M
Department of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Canada.
Zidichouski
Jeffrey A
JA
Kombian
Samuel B
SB
Saleh
Tarek M
TM
D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000378:metabolism; D017776:Autonomic Pathways / Q000187:drug effects / Q000378:metabolism; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects* / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D011149:Pons / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology
D004958:Estradiol