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J Neurophysiol 80: 1033-1041, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 3 September 1998, pp. 1033-1041
Copyright ©1998 The American Physiological Society

5-Hydroxytryptamine Responses in Immature Rat Rostral Ventrolateral Medulla Neurons In Vitro

L. L. Hwang and N. J. Dun

Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo, Ohio 43614

Hwang, L. L. and N. J. Dun. 5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro. J. Neurophysiol. 80: 1033-1041, 1998. 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-HTH), a slow depolarization (5-HTD) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 µM)-containing solution. 5-HTH were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HTH; the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K+]o. Barium (Ba2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HTH. The 5-HT1A receptor agonist (±)-8-hydroxy-dipropylamino-tetralin (8-OH-DPAT; 5-50 µM) hyperpolarized RVLM neurons. The 5-HT1A antagonist pindobind-5-HT1A (PBD; 1-3 µM) and the 5-HT2/5-HT1 receptor antagonist spiperone (1-10 µM) suppressed 5-HTH and the hyperpolarizing phase of biphasic responses; the 5-HT2 receptor antagonist ketanserin (3 µM) was without significant effect. 5-HTD 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-HTD. 5-HTD 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 Ca2+-free/high Mg2+ (10.9 mM) solution. The 5-HT2 receptor agonist alpha -methyl-5-HT (50 µM) depolarized RVLM neurons, and the 5-HT2 antagonist ketanserin (1-10 µM) attenuated the 5-HTD and the depolarizing phase of biphasic responses, whereas the 5-HT1A receptor antagonist PBD (2 µM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-beta -S in patch solution significantly reduced the 5-HTH as well as the 5-HTD. The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT1A and 5-HT2 receptors, which are G-proteins coupled. 5-HTH may involve an increase of an inwardly rectifying K+ conductance, and 5-HTD appear to be caused by a decrease of K+ conductance and/or increase of nonselective cation conductance.




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