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Exercise decreases the spiking response to excitation of a subpopulation of 2nd‐order aortic baroreceptor neurons in the nucleus tractus solitarii (NTS) of spontaneously hypertensive rats (SHRs)
Author(s) -
Bechtold Andrea G,
Zhang YiMing,
AccorsiMendonca Daniela,
Chen ChaoYin,
Bonham Ann C
Publication year - 2007
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.21.5.a463-c
Subject(s) - baroreceptor , baroreflex , inhibitory postsynaptic potential , medicine , depolarization , endocrinology , electrophysiology , cardiology , neuroscience , heart rate , blood pressure , biology
A single bout of exercise decreases blood pressure (post‐exercise hypotension; PEH) and baroreflex gain in hypertensive subjects, effects which could help to manage hypertension as an adjunct to traditional therapy. Our recent findings showing that exercise decreases inhibitory synaptic inputs onto NTS baroreceptor neurons led us to test the hypothesis that exercise decreases the spiking response to excitation of NTS baroreceptor neurons. Spiking response to excitation (1 s depolarizing current injections) was assessed using whole‐cell patch clamp recordings from brainstem slices containing anatomically identified 2nd‐order baroreceptor NTS neurons in SHRs following 40 min of treadmill running (PEH). Neurons were categorized as rapid spiking (RS; delay < 20 ms) or delayed spiking (DS; delay > 100 ms) based on the onset of the spiking response to excitation following a hyperpolarizing pre‐pulse. In RS neurons, but not DS neurons (SHAM n=9; PEH n=15), the firing response was significantly decreased (p<0.01) in PEH (n=33) compared to SHAM (n=43) rats and the action potential afterhyperpolarization was reduced (PEH=−12.1± 2 mV; SHAM=−21.9 ± 1.9 mV; p<0.05). Attenuated responsiveness of RS neurons following exercise may contribute to reduced baroreflex gain during PEH. Thus, neuroplasticity at the first central synapses in the central baroreflex network may play a major role in PEH. (Support: HL‐67183)