Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of the anti-serotonergic activity of carteolol and other beta-adrenoceptor blockers in their efficacy as anti-migraine agents has been examined in the membrane fraction of rat brain frontal cortex and pig choroid plexus, using radioligand binding methods. Carteolol and l-propranolol, which are suggested to have anti-migraine activity in man, were found to be active inhibitors of the binding of [125I]ICYP to 5-HT1B recognition sites and of [3H]-8-OH-DPAT to 5-HT1A recognition sites. Carteolol is devoid of activity at 5-HT1C and 5-HT2 recognition sites, whereas l-propranolol shows substantial affinity for these receptor subtypes. Atenolol, another beta-adrenoceptor blocker with anti-migraine activity, is devoid of activity at any of the 5-HT receptor subtypes examined. The possibility that carteolol and other beta-adrenoceptor antagonists exert their pharmacological effects through central 5-HT receptor subtypes is discussed in relation to the potential mechanism of the anti-migraine activity of carteolol.
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PMID:Interactions of carteolol and other beta-adrenoceptor blocking agents with serotonin receptor subtypes. 257 93

Migraine is a common, debilitating condition affecting up to 15% of the population. The ventroposteromedial nucleus of the thalamus relays trigeminal sensory input to the primary somatosensory cortex. In vivo electrophysiological recordings were made from the cell bodies of thalamocortical relay neurons in rats. We investigated whether microiontophoretic ejection of beta antagonists could inhibit thalamocortical activity in response to superior sagittal sinus (SSS) stimulation. We also studied 'postsynaptic' actions of these drugs through their modulatory actions on L-glutamate-evoked third order neuronal firing. Propranolol inhibited responses to SSS stimulation (P < 0.001) and L-glutamate ejection (P < 0.001). This was due to an action on beta receptors as it could be partially reversed by co-ejection of isoproterenol (SSS, P = 0.02; L-glutamate, P = 0.006). Serotonin (5-HT) receptor antagonism did not contribute to propranolol's action since the 5-HT1A receptor antagonist, (S)-WAY 100135 (P = 0.2), and the 5-HT1B/1D receptor antagonist, GR127935 (P = 0.6), did not affect L-glutamate-evoked neuronal firing. Atenolol inhibited both responses (SSS, P = 0.003; L-glutamate, P < 0.001). The beta2 antagonist ICI 118,551 had no effect (SSS, P = 0.9; L-glutamate, P = 0.4), nor did the beta2 agonist procaterol (SSS, P = 0.6; L-glutamate, P = 0.9). SR 59230A (beta3 antagonist) also produced no significant inhibition (SSS, P = 0.7; L-glutamate, P = 0.2), indicating an inhibitory role for beta1 antagonists only. beta Blockers therefore may exert some of their therapeutic effects in migraine through beta1 adrenoceptor antagonist actions in the thalamus. Thalamic involvement in migraine is attractive given the complex and widespread nature of the sensory disturbance.
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PMID:Propranolol modulates trigeminovascular responses in thalamic ventroposteromedial nucleus: a role in migraine? 1557 68