17β-estradiol attenuates excitatory neurotransmission and enhances the excitability of rat parabrachial neurons in vitro

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DOIResolve DOI: http://doi.org/10.1002/jnr.20959
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TypeArticle
Journal titleJournal of Neuroscience Research
Volume84
IssueJune 3
Pages666674; # of pages: 9
Subjectautonomic; patch-clamp electrophysiology; excitatory postsynaptic currents; estrogen
AbstractThe steroid hormone 17β-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 17β-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 17β-estradiol application will modulate excitatory synaptic neurotransmission. Using a pontine slice preparation and whole-cell patch-clamp recording, bath application of either 17β-estradiol (20–100 μM) or BSA-17β-estradiol (50 μM) 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, 17β-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, 17β-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.
Publication date
PublisherWiley
Copyright noticeThe material in this document is covered by the provisions of the Copyright Act, by Canadian laws, policies, regulations and international agreements. Such provisions serve to identify the information source and, in specific instances, to prohibit reproduction of materials without written permission
LanguageEnglish
AffiliationNational Research Council Canada; NRC Institute for Nutrisciences and Health
Access conditionavailable
unlimited
public
Peer reviewedYes
NPARC number9132444
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Record identifiera9a0255b-548f-4909-ab1c-c45de8968169
Record created2009-10-03
Record modified2016-05-09
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