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Bart J Van der Schueren, Koen Van Laere, Nathalie Gérard, Guy Bormans, Jan N De Hoon
OBJECTIVE: To compare binding of the type 1 cannabinoid receptor (CB1R) between migraine patients and healthy volunteers. BACKGROUND: It has been suggested that endocannabinoid deficiency may play a role in the pathophysiology of migraine. Nonetheless, biochemical studies substantiating this idea remain scarce and are faced with methodological shortcomings partly because of the difficulty to perform measurements of endocannabinoids within the central nervous system itself...
March 2012: Headache
O Prospéro-García, K Guzmán, M Méndez-Diaz, A Herrera-Solís, A Ruiz-Contreras
INTRODUCTION: Sleep is a non-learned adaptive strategy that depends on the expression of several neurotransmitters and other molecules. The expression of some of these molecules depends on a number of different genes. Sleep disorders are associated with an inadequate expression of some molecules, which therefore indicates that these genes that code for these molecules participate in the regulation of normal sleep. AIM: To discuss the evidence on gene regulation over the occurrence of sleep and its architecture, as well as of sleep disorders, which supports the participation of specific genes...
February 16, 2009: Revista de Neurologia
Juan Guo, Stephen R Ikeda
Endocannabinoids may serve as retrograde messengers to inhibit neurotransmitter release during depolarization-induced suppression of inhibition (DSI) or excitation (DSE). We therefore tested whether endocannabinoids inhibit N-type voltage-dependent Ca2+ channels by activating G(i/o)-protein-coupled CB1 cannabinoid receptors (CB1R)--a possible mechanism underlying DSI/DSE. Three putative endocannabinoids [2-arachidonylglycerol (2-AG), 2-arachidonyl glycerol ether (2-AGE), and anandamide (AEA)] and the cannabimimetic aminoalkylindole WIN 55,212-2 (WIN) inhibited whole-cell Ca2+ currents in rat sympathetic neurons previously injected with cDNA encoding a human CB1R...
March 2004: Molecular Pharmacology
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