THE CANNABINOID 1 RECEPTOR ANTAGONIST AM251 ALTERS THE KYOTORPHIN EFFECT ON DENSITY OF CB1 IMMUNOPOSITIVE NEURONS IN THE AMYGDALA

The endocannabinoid system is a modulatory system that has been strongly associated with the regulation of functions as learning and memory, pain perception and sensory physiology. Studies of the endocannabinoid system support its importance for multiple aspects of brain function. It is known that cannabinoid CB1 receptors are particularly concentrated in limbic structures such as the hippocampus and amygdala. There is also considerable evidence describing the common feature of opioid and cannabinoid receptor systems. Opioid-modulating peptides have been widely proved as the modulators of opioid functions. Literature data and our previous investigations show that the short-chain opioid-like neuropeptide/neuromodulator kyotorphin (KTP) binds to a specific receptor and plays a role in pain regulation, thermoregulation, and exploratory behaviour. It also alters the pattern of NADPH-d-reactive neurons in the hypothalamic paraventricular nucleus and striatum of Wistar rats. To our knowledge, no attention has been directed to the interaction between KTP and cannabinoid systems. Therefore, the objectives of the present study were twofold: 1) to investigate the effect of KTP on density of CB1 immunopositive neurons in the amygdala of male Wistar rats; 2) to examine whether this effect is prevented by CB1 receptor antagonist AM251. Our results revealed that density of CB1 receptors was significantly increased in rats treated with KTP compared to the control. This effect was completely abolished by administration of AM251, which indicated the involvement of neuropeptide in the endocannabinoid signalling.