Postsynaptic modulation of nucleus tractus solitarius neurons in response to Prostaglandin E2

Abstract

Prostaglandin E2 (PGE2), 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 PGE2 can alter the membrane properties of postsynaptic neurons within the nTS. Using whole‐cell patch‐clamp recording, we measured membrane voltage (VM) in response to injected current ramps in nTS neurons. We observed a decrease in maximum spike frequency after PGE2 application (19.6% decrease compared to control; n=3). The cells showed a decrease in both holding membrane potential (VH, 92.0% of control) as well as a decrease in the membrane potential threshold for spike firing (Vt, 92.6% of control). The chord resistance, Rchord = (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 PGE2 is able to modulate postsynaptic neurons within the nTS through an undetermined mechanism.