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 microM) 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 GABAA‐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.
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