Key result
Dorsal PAG CB1 activation triggers sympathoexcitatory and pressor responses attenuated by CB1 antagonism.
Why the study?
Endocannabinoids influence behavioral responses to stress, but their role in modulating sympathetic and cardiovascular responses via the periaqueductal gray was unclear.
Endocannabinoid CB1 signaling in rat dorsal PAG modulates sympathetic stress responses; hypothesis-generating for human autonomic-cardiovascular regulation.
Activation of the sympathetic nervous system is fundamental to the coordinated response to stress or danger. The midbrain periaqueductal gray (PAG) contains the neural substrate required to recruit the sympathetic nervous system and organize the physiological and behavioral responses required to respond to imposed challenges. Endocannabinoids have been shown to influence associated behavioral responses. The defense response was used in this study as a working model to examine endocannabinoid modulation of the sympathetic response to acute stress in the anesthetized rat. Microinjection of the cannabinoid 1 (CB1) receptor agonist anandamide into the defense pathway of the dorsal PAG could elicit an increase in renal sympathetic nerve activity and blood pressure, twitching of the whiskers, and movement of the limbs. The response was attenuated by prior microinjection of the CB1 receptor antagonist AM-281 at the same site. Electrical stimulation of the hypothalamic defense area could evoke similar sympathoexcitatory and pressor responses, which were significantly attenuated by microinjection of AM-281 into the dorsal PAG. These data indicate that endocannabinoids can modulate the sympathetic and cardiovascular components of the acute stress response via CB1 receptors at the level of the PAG.
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Caron Dean (2011) studied Acute stress. CB1 receptor agonist anandamide and antagonist AM-281 was evaluated on Renal sympathetic nerve activity and blood pressure. Microinjection of the CB1 agonist anandamide into the dorsal PAG elicited sympathoexcitatory and pressor responses, which were attenuated by the CB1 antagonist AM-281.
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