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Brain Advance Access published online on December 1, 2004
Brain, doi:10.1093/brain/awh298
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Received June 1, 2004
Revised July 26, 2004
Accepted July 28, 2004

Article

Propranolol modulates trigeminovascular responses in thalamic ventroposteromedial nucleus: a role in migraine?

Kevin G. Shields 1 and Peter J. Goadsby 1*

1 Headache Group, Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK

* To whom correspondence should be addressed.
Peter J. Goadsby, E-mail: peterg{at}ion.ucl.ac.uk


  Abstract

Summary 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 {beta}2 antagonist ICI 118,551 had no effect (SSS, P = 0.9; L-glutamate, P = 0.4), nor did the {beta}2 agonist procaterol (SSS, P = 0.6; L-glutamate, P = 0.9). SR 59230A ({beta}3 antagonist) also produced no significant inhibition (SSS, P = 0.7; L-glutamate, P = 0.2), indicating an inhibitory role for {beta}1 antagonists only. {beta} Blockers therefore may exert some of their therapeutic effects in migraine through {beta}1 adrenoceptor antagonist actions in the thalamus. Thalamic involvement in migraine is attractive given the complex and widespread nature of the sensory disturbance.

Keywords: thalamus; migraine; {beta} blockers; trigeminovascular.
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