| Hwang, L.L. and Dun N.J. |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=80 ------>confirm_bywho=wslee ------>insert_bywho=llhwang ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=1041 ------>medlineContent= ------>unit=000 ------>insert_date=20000626 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=J. Neurophysiol. ------>paper_name=5-hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro. ------>confirm_date=20020507 ------>tch_id=089017 ------>pmid=9744919 ------>page1=1033 ------>fullAbstract=Whole cell patch recordings were made from rostral ventrolateral medullar (RVLM) neurons of brain-stem 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 microM)-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 microM) hyperpolarized RVLM neurons. The 5-HT1A antagonist pindobind-5-HT1A (PBD; 1-3 microM) and the 5-HT2/5-HT1 receptor antagonist spiperone (1-10 microM) suppressed 5-HTH and the hyperpolarizing phase of biphasic responses; the 5-HT2 receptor antagonist ketanserin (3 microM) 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 Ca(2+)-free/high Mg2+ (10.9 mM) solution. The 5-HT2 receptor agonist alpha-methyl-5-HT (50 microM) depolarized RVLM neurons, and the 5-HT2 antagonist ketanserin (1-10 microM) attenuated the 5-HTD and the depolarizing phase of biphasic responses, whereas the 5-HT1A receptor antagonist PBD (2 microM) 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. ------>tmu_sno=None ------>sno=2097 ------>authors2=None ------>authors3=None ------>authors4=None ------>authors5=None ------>authors6=None ------>authors6_c=None ------>authors=Hwang, L.L. and Dun N.J. ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho= ------>publish_year=1998 ------>submit_flag= ------>publish_month=None |