Abstract

Electrical or chemical stimulation of some structures of the midbrain tectum, such as the dorsal periaqueductal gray matter, deep layers of the superior colliculus and inferior colliculus induce fear and flight behavior. These structures constitute the main neural substrates commanding defensive behavior in brainstem. Many neurotransmitters are implicated in the modulation of aversion at the mesencephalic level. The aim of this work is to investigate the involvement of opioid mechanisms in modulation of defensive behavior in dorsal mesencephalon. Male Wistar rats were fixed in a stereotaxic frame and a chemitrode was implanted into the midbrain, targeted to the central nucleus of the inferior colliculus. In the present study, the effects of peripheral and central administration of naloxone, naltrexone or naloxonazine on aversive thresholds (freezing and escape reactions) elicited by electrical stimulation of the midbrain tectum were determined. Peripherally and centrally administered naloxone caused a significant increase in the freezing and flight thresholds elicited by electrical stimulation of the aversive substrates of the inferior colliculus. These effects were confirmed by peripheral and central administration of naltrexone and by microinjections of naloxonazine in inferior colliculus. These findings suggest that endogenous opioids are involved in the modulation of the aversive behavior elicited by midbrain tectum stimulation. Since microinjections of naloxonazine in the central nucleus of the inferior colliculus caused a significant increase in the aversive thresholds elicited by electrical stimulation of this structure, it is possible that micro1 opioid receptor located in this nucleus may be critically implicated in this neural circuitry.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.