The Expression Pattern of TRPV1 in Brain

Menigoz, Aurélie; Boudes, Mathieu

doi:10.1523/jneurosci.2589-11.2011

Cited by 46 publications

(29 citation statements)

References 21 publications

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“…In this regard, it has been reported that TRPV1-dependent thermoregulation is due to modulation of receptors outside the blood-brain barrier, more precisely those tonically activated in the viscera (Gavva et al, 2007). Our results on the effect of (Hori, 1984;Hori et al, 1988), the exact localization of TRPV1 receptors within the rodent and human hypothalamus is still debated (Menigoz and Boudes, 2011). Reportedly, peripheral TRPV1 receptors tonically suppress cold defenses by inhibiting thermogenesis and skin vasoconstriction (Gavva, 2008).…”

Section: Discussionmentioning

confidence: 72%

Ischemic Neuroprotection by TRPV1 Receptor-Induced Hypothermia

Muzzi

Felici

Cavone

et al. 2012

J Cereb Blood Flow Metab

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Although treatment of stroke patients with mild hypothermia is a promising therapeutic approach, chemicals inducing prompt and safe reduction of body temperature are an unmet need. We measured the effects of the transient receptor potential vanilloid-1 (TRPV1) agonist rinvanil on thermoregulation and ischemic brain injury in mice. Intraperitoneal or intracerebroventricular injection of rinvanil induces mild hypothermia that is prevented by the receptor antagonist capsazepine. Both intraischemic and postischemic treatments provide permanent neuroprotection in animals subjected to transient middle cerebral artery occlusion (MCAo), an effect lost in mice artificially kept normothermic. Data indicate that TRPV1 receptor agonists are promising candidates for hypothermic treatment of stroke.

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Section: Discussionmentioning

confidence: 72%

Ischemic Neuroprotection by TRPV1 Receptor-Induced Hypothermia

Muzzi

Felici

Cavone

et al. 2012

J Cereb Blood Flow Metab

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“…TRPV1 receptors are distributed throughout the body, including the brain, spinal cord (Kim et al, 2012) and peripheral nervous system (Menigoz and Boudes, 2011; Roberts et al, 2004; Szallasi et al, 1995) where they play a vital role in hyperalgesia. Because TRPV1 ligands are crucial to the enhancement of nociception in many models of hyperalgesia (Chung et al, 2011; Fujii et al, 2008; Roberts et al, 2011; Szabo et al, 2005), we questioned whether TRPV1 receptor-expressing neuronal populations mediate stress-induced musculoskeletal hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

Forced swim-induced musculoskeletal hyperalgesia is mediated by CRF2 receptors but not by TRPV1 receptors

et al. 2013

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The exacerbation of musculoskeletal pain by stress in humans is modeled by the musculoskeletal hyperalgesia in rodents following a forced swim. We hypothesized that stress-sensitive corticotropin releasing factor (CRF) receptors and transient receptor vanilloid 1 (TRPV1) receptors are responsible for the swim stress-induced musculoskeletal hyperalgesia. We confirmed that a cold swim (26°C) caused a transient, morphine-sensitive decrease in grip force responses reflecting musculoskeletal hyperalgesia in mice. Pretreatment with the CRF2 receptor antagonist astressin 2B, but not the CRF1 receptor antagonist NBI-35965, attenuated this hyperalgesia. Desensitizing the TRPV1 receptor centrally or peripherally using desensitizing doses of resiniferatoxin (RTX) failed to prevent the musculoskeletal hyperalgesia produced by cold swim. SB-366791, a TRPV1 antagonist, also failed to influence swim-induced hyperalgesia. Together these data indicate that swim stress-induced musculoskeletal hyperalgesia is mediated, in part, by CRF2 receptors but is independent of the TRPV1 receptor.

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“…2), and cannabinoids have been shown to increase salt and fluid retention by upregulating sodium and potassium ATPase activity in these cells (Sampaio et al, 2014). While some studies have shown TRPV1 in the hypothalamus (Menigoz & Boudes, 2011), their association with endocannabinoids and their role in osmoregulation remain unclear. One study suggests that TRPV1 is expressed in vasopressin neurons, but the TRPV1 is truncated and lacks the carboxy terminus, which is thought to make it responsive to changes in osmolarity, but insensitive to the TRPV1 agonist capsaicin (Sudbury, Ciura, Sharif-Naeini, & Bourque, 2010).…”

Section: Receptor Distribution In Osmoregulatory Tissuesmentioning

confidence: 99%