Hippocampal cannabinoid-1 receptor upregulation upon endothelin-B receptor deficiency: a neuroprotective substitution effect?

Endothelin (ETB)-receptors mediate anti-apoptotic actions. Lack of functional ETB-receptors leads to increased neuronal apoptosis in the hippocampus. The increased apoptosis must be compensated by other mechanisms, however, as ETB-deficient rats display normal overall brain morphology.

Neuromorphological background of cannabis addiction.

The expression of central cannabinoid (CB1) receptors in tyrosine hydroxylase (TH) containing neurones was demonstrated. Co-localisation was present in different brain areas responsible for reward-related mechanisms. The immunohistochemical investigations have shown that co-localisation is present in parts of mesolimbic-mesocortical dopaminergic system like nucleus accumbens (Nacb), ventral tegmental area (VTA), in the striatum, pyriform cortex, respectively.