Local activation of RCB1 suppresses burst firing of neurons in the reticular thalamic nucleus

The reticular thalamic nucleus (RTn) is the only thalamic nucleus that does not project to the cerebral cortex. Instead, it regulates the activity of the rest of the thalamo-cortical neurons through GABAergic projections, so that it is essential in filtering information from the thalamus to the cerebral cortex. The firing mode of RTn neurons is closely linked to sleep-wake cycles; when RTn neurons produce bursts firing, they induce burst firing of thalamo-cortical neurons and slow-wave sleep occurs with concomitant loss of consciousness; when neurons fire tonically, self-awareness occurs. On the other hand, despite the presence of CB1 receptors and mRNA that encodes such receptors, the effects of the electrical activity of the endocannabinoid system on RTn neurons has been poorly explored. In the present work, we show that local activation of RCB1 in RTn neurons through endogenous and synthetic cannabinoids preferentially produces an increase in the electrical activity of reticular neurons accompanied by a decrease in burst rate in anesthetized rodents. Figure A: effect of the local aplication of RCB1 agonist WIN 55,212-2 (20 pM) on the electrical activity of reticular thalamic neurons.