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Inhibition by 5‐hydroxytryptamine and noradrenaline in substantia gelatinosa of guinea‐pig spinal trigeminal nucleus.
Author(s) -
Grudt T J,
Williams J T,
Travagli R A
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020716
Subject(s) - hyperpolarization (physics) , prazosin , inhibitory postsynaptic potential , postsynaptic potential , chemistry , idazoxan , depolarization , reversal potential , spinal trigeminal nucleus , bursting , neuroscience , autoreceptor , biophysics , agonist , receptor , antagonist , patch clamp , biology , stereochemistry , biochemistry , nociception , nuclear magnetic resonance spectroscopy
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.