Topic: CB1 receptors

Oligodendrocytes produce central nervous system myelin and provide metabolic support to axons. Myelin formation and repair are energetically expensive and oligodendrocyte metabolic defects have been postulated as a cause of neurodegeneration. Endocannabinoids modulate neuronal and astroglial metabolism and attenuate inflammatory demyelination in multiple sclerosis (MS) through the activation of CB1 receptors (CB1Rs). Myelinating oligodendrocytes and precursor cells (OPCs) express CB1Rs that mediate protection from excitotoxicity and promote lineage progression but the metabolic implications of

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 t

The formation of new inhibitory synapses is essential to counterbalance a strong excitatory activity and maintain dendritic coordination between excitation and inhibition. We recently demonstrated that the activation of excitatory spines is followed by the production of endocannabinoids in dendrites, which mediates the formation of new inhibitory boutons via axonal CB1 receptors. Bouton formation was found to depend on an increase of the second messenger cyclic adenosine monophosphate (cAMP) and the activation of the downstream protein kinase A (PKA). We ask whether other neuromodulators are a