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Postsynaptic modulation of nucleus tractus solitarius neurons in response to Prostaglandin E2
Author(s) -
Gresham Ken,
Mayer Catherine,
Martin Richard J,
Wilson Christopher G
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1088.2
Subject(s) - postsynaptic potential , chemistry , excitatory postsynaptic potential , membrane potential , patch clamp , postsynaptic current , prostaglandin e2 , current clamp , neurotransmission , glutamate receptor , inhibitory postsynaptic potential , neuroscience , biophysics , electrophysiology , endocrinology , biology , receptor , biochemistry
Prostaglandin E 2 (PGE 2 ), produced in response to proinflammatory cytokines, can alter synaptic activity within the nucleus tractus solitarius (nTS) by altering glutamate release from vagal afferent terminals. Modulation of activity within the nTS alters signaling to other regions of the brainstem, including the regions responsible for respiratory rhythm generation. We hypothesized that PGE 2 can alter the membrane properties of postsynaptic neurons within the nTS. Using whole‐cell patch‐clamp recording, we measured membrane voltage (V M ) in response to injected current ramps in nTS neurons. We observed a decrease in maximum spike frequency after PGE 2 application (19.6% decrease compared to control; n=3). The cells showed a decrease in both holding membrane potential (V H , 92.0% of control) as well as a decrease in the membrane potential threshold for spike firing (V t , 92.6% of control). The chord resistance, R chord = (Vh – Vt)/It , where It is the threshold current that elicits action potentials in the ramp protocol, showed a variable response in the three neurons recorded. Our data suggests that PGE 2 is able to modulate postsynaptic neurons within the nTS through an undetermined mechanism.