INHIBITION BY 5-HYDROXYTRYPTAMINE AND NORADRENALINE IN SUBSTANTIA-GELATINOSA OF GUINEA-PIG SPINAL TRIGEMINAL NUCLEUS
INHIBITION BY 5-HYDROXYTRYPTAMINE AND NORADRENALINE IN SUBSTANTIA-GELATINOSA OF GUINEA-PIG SPINAL TRIGEMINAL NUCLEUS
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DOI：
10.1113/jphysiol.1995.sp020716
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发表时间：
1995-05-15
影响因子：
5.5
通讯作者：
TRAVAGLI, RA
中科院分区：
文献类型：
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作者：
GRUDT, TJ;WILLIAMS, JT;TRAVAGLI, RA
1.取豚鼠三叉神经脊束核尾侧核尾侧脑片，进行全细胞和细胞内记录。5-羟色胺(5-HT)通过激活5-HT1a受体使70%的神经元超极化。这种作用可被5-氨基-色胺(5-CT)和(+/-)-2-dipropylamino-8-hydroxy-1，2，3，4-tetrahydronapthalene氢溴酸盐(8-OH-DPAT)所模拟，并被1-(2-methoxyphenyl)-4-[4-(2-phthalimido)-butyl]-piperazine氢溴酸盐(NaN190)和Pindobind-5-HT1a拮抗。9%的神经元被5-HT.3去极化。在约20%的记录中，5-羟色胺还诱发了由甘氨酸介导的重复性抑制性突触后电位。去甲肾上腺素(NA)使71%的神经元超极化。由于5-bromo-N-(4，5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine(UK14304)也引起超极化，而咪唑克生(1mU M)阻断NA和UK14304的超极化，这种作用是通过激活α(2)-肾上腺素受体介导的。苯肾上腺素使部分神经元去极化，这种去极化可被哌唑嗪阻断，提示这一作用是通过激活α(1)-肾上腺素能受体介导的。NA还在约20%的记录中诱发了GABA(A)介导的抑制性突触后电位。突触活性的增加可被苯肾上腺素模拟，并被哌唑嗪阻断。这些结果表明，5-羟色胺和去甲肾上腺素抑制神经元的机制至少有两种：(I)在许多细胞中，5-羟色胺和去甲肾上腺素都通过增加钾电导来介导超极化；(Ii)5-羟色胺和去甲肾上腺素也激活含GABA和甘氨酸的中间神经元，在不同的细胞群中引起IPSP。
1. Whole-cell and intracellular recordings were made from neurons in slices of guinea-pig spinal trigeminal nucleus pars caudalis.2. 5-Hydroxytryptamine (5-HT) hyperpolarized 70% of neurons by activating 5-HT1A receptors. The effect was mimicked by 5-carboxamidotryptamine (5-CT) and (+/-)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronapthalene hydrobromide (8-OH-DPAT) and antagonized by 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)-butyl]-piperazine hydrobromide (NAN 190) and pindobind-5-HT1A. Nine per cent of the neurons were depolarized by 5-HT.3. In about 20% of recordings, 5-HT also evoked repetitive inhibitory postsynaptic potentials that were mediated by glycine.4. Noradrenaline (NA) hyperpolarized 71% of neurons. This effect was mediated by activation of alpha(2)-adrenoceptors, since 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK14304) also caused a hyperpolarization and idazoxan (1 mu M) blocked the hyperpolarization to both NA and UK14304. Phenylephrine depolarized a subset of neurons and this depolarization was blocked by prazosin, suggesting an action mediated by activation of alpha(1)-adrenoceptors.5. NA also evoked repetitive GABA(A)-mediated inhibitory postsynaptic potentials in about 20% of recordings. The increase in synaptic activity was mimicked by phenylephrine and blocked by prazosin.6. These results indicate that there are at least two mechanisms through which 5-HT and NA inhibit neurons: (i) in many cells both 5-HT and NA mediate a hyperpolarization through an increase of a potassium conductance; (ii) 5-HT and NA also activated GABA- and glycine-containing interneurons to cause IPSPs in separate groups of cells.