Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5- HT(H)), a slow depolarization (5-HT(D)) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HT(H) were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HT(H); the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K +](o). Barium (Ba 2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HT(H). The 5-HT(1A) receptor agonist (±)-8-hydroxy- dipropylamino-tetralin (8-OH-DPAT; 5-50 μM) hyperpolarized RVLM neurons. The 5-HT(1A) antagonist pindobind-5-HT(1A) (PBD; 1-3 μM) and the 5-HT 2/5-HT 1 receptor antagonist spiperone (1-10 μM) suppressed 5-HT(H) and the hyperpolarizing phase of biphasic responses; the 5-HT 2 receptor antagonist ketanserin (3 μM) was without significant effect 5-HT(D) were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HT(D). 5-HT(D) were reduced in an elevated [K +](o) (7.0 mM) solution and >60% in a low Na + (26 mM) solution and were not significantly changed in a low Cl - (6.7 mM) or Ca 2+-free/high Mg 2+ (10.9 mM) solution. The 5-HT 2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5- HT 2 antagonist ketanserin (1-10 μM) attenuated the 5-HT(D) and the depolarizing phase of biphasic responses, whereas the 5-HT(1A) receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HT(H) as well as the 5-HT(D). The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT(1A) and 5-HT 2 receptors, which are G-proteins coupled. 5-HT(H) may involve an increase of an inwardly rectifying K + conductance, and 5-HT(D) appear to be caused by a decrease of K + conductance and/or increase of nonselective cation conductance.
|Number of pages||9|
|Journal||Journal of Neurophysiology|
|Publication status||Published - Sep 1998|
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