Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior in rats: Additional evidence

Lisboa, Sabrina F.; Borges, Anna A.; Nejo, Priscila; Fassini, Aline; Guimarães, Francisco Silveira; Resstel, Leonardo Barbosa Moraes

doi:10.1016/j.pnpbp.2015.01.005

Cited by 36 publications

(29 citation statements)

References 58 publications

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“…In contrast, pharmacological and genetic deletion of CB 1 Rs in rodents are generally known to have anxiogenic effects (Blasio et al 2013;Patel & Hillard 2006) and produce a behavioral and neural phenotype indicative of chronic stress exposure, including heightened emotional behavior (Haller et al 2002;Maccarrone et al 2002;Martin et al 2002;Urigüen et al 2004), HPA axis dysregulation (Barna et al 2004;Cota et al 2007) and shorter, less complex pyramidal neurons in the medial PFC (Hill et al 2011;Lee et al 2014c). Correspondingly, CB 1 R agonists directly infused into the hippocampus and medial PFC are known to exert anxiolytic effects (Lisboa et al 2015). However, there are known inconsistent results reported in the literature (e.g.…”

Section: Adult Corticolimbic Ecb Signaling Regulates Adult Unconditiomentioning

confidence: 99%

Developmental regulation of fear learning and anxiety behavior by endocannabinoids

Lee¹,

Hill

Lee

2015

Genes Brain and Behavior

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The developing brain undergoes substantial maturation into adulthood and the development of specific neural structures occurs on differing timelines. Transient imbalances between developmental trajectories of corticolimbic structures, which are known to contribute to regulation over fear learning and anxiety, can leave an individual susceptible to mental illness, particularly anxiety disorders. There is a substantial body of literature indicating that the endocannabinoid system critically regulates stress responsivity and emotional behavior throughout the life span, making this system a novel therapeutic target for stress- and anxiety-related disorders. During early life and adolescence, corticolimbic endocannabinoid signaling changes dynamically and coincides with different sensitive periods of fear learning, suggesting that endocannabinoid signaling underlies age-specific fear learning responses. Moreover, perturbations to these normative fluctuations in corticolimbic endocannabinoid signaling, such as stress or cannabinoid exposure, could serve as a neural substrate contributing to alterations to the normative developmental trajectory of neural structures governing emotional behavior and fear learning. In this review, we first introduce the components of the endocannabinoid system and discuss clinical and rodent models demonstrating endocannabinoid regulation of fear learning and anxiety in adulthood. Next, we highlight distinct fear learning and regulation profiles throughout development and discuss the ontogeny of the endocannabinoid system in the central nervous system, and models of pharmacological augmentation of endocannabinoid signaling during development in the context of fear learning and anxiety.

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Section: Adult Corticolimbic Ecb Signaling Regulates Adult Unconditiomentioning

confidence: 99%

Developmental regulation of fear learning and anxiety behavior by endocannabinoids

Lee¹,

Hill

Lee

2015

Genes Brain and Behavior

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“…Another study suggested that sustained conditioned responses in PrL correlated with fear extinction failure [39]. Endocannabinoids have been shown to regulate PrL activity by activating cannabinoid type 1 (CB1) receptors and anxiety-like behaviors in rats [40]. Furthermore, CB1 receptors are part of neuronal mitochondria membranes, where they regulate respiration and energy metabolism [41].…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine Treatment Rescues Energy Metabolism Pathway Alterations in a Posttraumatic Stress Disorder Mouse Model

Kao

Henes

et al. 2016

Complex Psychiatry

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Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock-induced PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo ¹⁵N metabolic labeling combined with mass spectrometry in the prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala, central nucleus of the amygdala and CA1 of the hippocampus between shocked and nonshocked (control) mice, with and without fluoxetine treatment. In silico pathway analyses revealed an upregulation of the citric acid cycle pathway in PrL, and downregulation in ACC and nucleus accumbens (NAc). Chronic fluoxetine treatment prevented decreased citric acid cycle activity in NAc and ACC and ameliorated conditioned fear response in shocked mice. Our results shed light on the role of energy metabolism in PTSD pathogenesis and suggest potential therapy through mitochondrial targeting.

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“…De forma similar, foi observada que a inibição seletiva reversível do CPFMv no MCC atenuou as respostas comportamental e autonômica durante a re-exposição ao contexto aversivo (Resstel et al, 2006a;Lisboa et al, 2010b). (Aguiar et al, 2009;Lisboa et al, 2015) e reduzem a REC no MCC (Lisboa et al, 2010a;. Entretanto não se sabe ao certo quais mecanimos estariam envolvidos nessas respostas mediadas pelos receptores CB1 e TRPV1 no CPFMv, mas acredita-se que a neurotransmissão glutamatérgica possa representar uma das possibilidades, uma vez que esta transmissão modula a REC no CPFMv .…”

Section: Introductionunclassified

“…Foi demonstrado que o antagonista de receptores CB1 e o agonista de receptores TRPV1 no CPFMv aumentam a REC durante a reexposição ao contexto aversivo, sendo esta resposta dependente de ativação de receptores NMDA de glutamato e produção de NO através da nNOS. Entretanto, enquanto a resposta evocada pelo antagonista CB1 envolve difusão do NO na Trabalhos do grupo com CPFMv demonstraram que o efeito tipo-ansiolítico no LCE mediado pelos eCBs nesta estrutura é via ativação dos receptores CB1 locais(Lisboa et al, 2015). No MCC também já foi demonstrado esta mesma relação do receptor CB1 mediando as respostas tipo-ansiolíticas dos eCBs(Lisboa et al, 2010a).…”

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Os receptores CB1 e TRPV1 da porção ventral do córtex pré-frontal medial modulam a resposta emocional condicionada: participação das neurotransmissões colinérgica, glutamatérgica e nitrérgica

Uliana¹

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Portanto, podemos sugerir que a re-exposição ao contexto aversivo aumenta os níveis de ACh no CPFMv e, assim, ativa receptores M3 que, por sua vez, induzem a produção de eCBs, possivelmente AEA, e NO. O NO atuaria présinapticamente aumentando a liberação de glutamato, e a AEA ativaria receptores TRPV1 pós-sinápticos que ativaria mecanismos de estresse nitrosativo decorrentes da produção do NO.

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Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior in rats: Additional evidence

Cited by 36 publications

References 58 publications

Developmental regulation of fear learning and anxiety behavior by endocannabinoids

Developmental regulation of fear learning and anxiety behavior by endocannabinoids

Fluoxetine Treatment Rescues Energy Metabolism Pathway Alterations in a Posttraumatic Stress Disorder Mouse Model

Os receptores CB1 e TRPV1 da porção ventral do córtex pré-frontal medial modulam a resposta emocional condicionada: participação das neurotransmissões colinérgica, glutamatérgica e nitrérgica

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