Endo K, Morita K, Uchiyama Y, Takada K, Tsujimoto A, Dohi T
Department of Oral and Maxillofacial Surgery, Hiroshima University School of Dentistry, Japan.
Jpn J Pharmacol. 1993 Jul;62(3):325-8. doi: 10.1254/jjp.62.325.
Influences of drug-induced manipulations of central serotonergic function on lidocaine- and pentylenetetrazol (PTZ)-induced convulsions were examined in mice. Agents that suppressed serotonergic transmission increased, whereas drugs that facilitated serotonin (5-HT) function decreased the incidence of lidocaine-induced convulsions. These treatments had similar influences on the incidence of PTZ-induced convulsions. Lidocaine (10(-5)-10(-3) M) reduced the stimulation evoked [3H]5-HT release from cortical slices, followed with an increased spontaneous [3H] overflow at higher concentrations. These results may suggest that brain 5-HT neurons are causally involved as inhibitory neurons in lidocaine-induced convulsions as in the case of PTZ-induced convulsions.
在小鼠中研究了药物诱导的中枢5-羟色胺能功能操纵对利多卡因和戊四氮（PTZ）诱导惊厥的影响。抑制5-羟色胺能传递的药物会增加利多卡因诱导惊厥的发生率，而促进5-羟色胺（5-HT）功能的药物则会降低其发生率。这些处理对PTZ诱导惊厥的发生率有类似影响。利多卡因（10^-5 - 10^-3 M）可减少皮质切片刺激诱发的[3H]5-HT释放，而在较高浓度时自发性[3H]溢出增加。这些结果可能表明，脑5-HT神经元作为抑制性神经元，如同在PTZ诱导惊厥的情况一样，在利多卡因诱导惊厥中也起着因果作用。
