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Cannabinoids in the amygdala-parabrachial circuit, and the regulation of pain

Grant number: 19/12439-3
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): October 01, 2019
Effective date (End): September 30, 2020
Field of knowledge:Humanities - Psychology - Physiological Psychology
Principal researcher:Christie Ramos Andrade Leite Panissi
Grantee:Gleice Kelli Ribeiro da Silva Cardoso
Supervisor abroad: Asaf Keller
Home Institution: Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto (FFCLRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: University of Maryland, Baltimore (UMB), United States  
Associated to the scholarship:18/06877-5 - Systemic treatment with canabidiol in a neuropathic pain model: evaluation of the sensorial-discriminative and emotional-motivacional components pain sensitivity, BP.DR

Abstract

The neuropathic pain, it develops as a consequence of an injury or disease that affects somatosensory pathways in the peripheral or central nervous system and accompanies many systemic diseases. Among the neurochemical systems of pain modulation, the cannabinoid system is an important endogenous system that participates in the circuit of pain sensitivity, functioning parallel to the opioid system and playing crucial roles in the development and resolution of pain states, as well as affective and cognitive aspects of pain. Nociceptive signals originating from the periphery are transported to the brain via specific afferent and ascending pathways. The spino- (trigemino-) parabrachio-amygdaloid pathway is one of the main mediator pathways of specific ascending neuron signals from nociception to the central amygdala, a limbic structure involved in emotional responses associated with the aversive signal, including the emotional aspects of pain. Evidence has implicated the amygdala in pain modulation, and it appears that the amygdala is critically involved in both pain enhancement (hyperalgesia) and pain reduction (hypoalgesia or analgesia). The capsular part of the central amygdala (CeC) is called the "nociceptive amygdala," since it receives nociceptive information from various pathways, including the monosynaptic entry of the lateral parabrachial nucleus (LPB), a major target of ascending neurons in the spinal cord and dorsal horn. Thus, based on the literature, we will investigate the hypothesis that the CB1 receptor presynaptically regulates the release of GABA from amygdala stimuli in parabrachial neurons to suppress pain in a chronic pain model (infra-orbital nerve constriction). we intend to understand the mechanisms that would be involved in modulation of neuropathic pain and related to endocannabinoid neurotransmission in the amygdala inhibitory projection to the parabrachial nucleus. (AU)

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