Matos F F, Urban C, Yocca F D
Department of Neuropharmacology, Bristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, CT, USA.
J Neural Transm (Vienna). 1996;103(1-2):173-90. doi: 10.1007/BF01292626.
Somatodendritic and terminal release of serotonin (5-HT) was investigated by simultaneously measuring extracellular concentrations of 5-HT, 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) in the dorsal raphé and ventral hippocampus in freely moving rats. Perfusion of tetrodotoxin (TTX, 1 microM and 10 microM) into the dorsal raphé simultaneously decreased dorsal raphé and hippocampal 5-HT release. However, following TTX perfusion into the hippocampus (10 microM), hippocampal 5-HT release was profoundly reduced but dorsal raphé 5-HT remained unchanged. Systemic injections with 5-HT1A agonist, buspirone (1.0-5.0 mg/kg, i.p.) decreased 5-HT and 5-HIAA and increased HVA concentrations in the dorsal raphé and in the hippocampus. The decreases in the raphé and hippocampal 5-HT induced by systemic buspirone were antagonized in rats pretreated with 1.0 mM (-) pindolol, locally perfused into the dorsal raphé. Local dorsal raphé perfusion of (-) pindolol alone (0.01-1.0 mM) increased dorsal raphé 5-HT and concomitantly induced a small increase in hippocampal 5-HT. Buspirone perfusion into the dorsal raphé did not change (10 nM, 100 nM), or produced a small increase (1.0 mM) in raphé 5-HT, without changing hippocampal 5-HT. These data provide evidence that 5-HT release in the dorsal raphé is dependent on the opening of fast activated sodium channels and that dorsal raphé 5-HT1A receptors control somatodendritic and hippocampal 5-HT release
通过同时测量自由活动大鼠背侧中缝核和腹侧海马中5-羟色胺（5-HT）、5-羟吲哚-3-乙酸（5-HIAA）和高香草酸（HVA）的细胞外浓度，研究了5-HT的树突体和终末释放。向背侧中缝核灌注河豚毒素（TTX，1微摩尔和10微摩尔）可同时降低背侧中缝核和海马中的5-HT释放。然而，向海马灌注TTX（10微摩尔）后，海马中的5-HT释放显著减少，但背侧中缝核中的5-HT保持不变。全身注射5-HT1A激动剂丁螺环酮（1.0 - 5.0毫克/千克，腹腔注射）可降低背侧中缝核和海马中5-HT和5-HIAA的浓度，并增加HVA的浓度。在用1.0毫摩尔（-）吲哚洛尔预处理并局部灌注到背侧中缝核的大鼠中，全身注射丁螺环酮诱导的中缝核和海马中5-HT的降低被拮抗。单独向背侧中缝核局部灌注（-）吲哚洛尔（0.01 - 1.0毫摩尔）可增加背侧中缝核中的5-HT，并同时使海马中的5-HT略有增加。向背侧中缝核灌注丁螺环酮（10纳摩尔、100纳摩尔）对中缝核中的5-HT没有影响，或使其略有增加（1.0毫摩尔），而海马中的5-HT没有变化。这些数据表明，背侧中缝核中的5-HT释放依赖于快速激活的钠通道的开放，并且背侧中缝核中的5-HT1A受体控制树突体和海马中的5-HT释放
