Involvement of CB 1 and TRPV1 receptors located in the ventral medial prefrontal cortex in the modulation of stress coping behavior

Sartim, Ariandra Guerini; Moreira, Fabrício A.; Joca, Sâmia Regiane Lourenço

doi:10.1016/j.neuroscience.2016.10.031

Cited by 29 publications

(15 citation statements)

References 46 publications

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“…Activation of TRPV1 by differential ligands or in differential conditions (physiological or pathological) might exert distinct effects on NMDA receptors. This is accordance with the reports that both TRPV1 agonists and antagonists show the antidepressant effects partly through the inhibition of NMDA receptors (Abdelhamid et al, 2014; Amiri et al, 2016; Manna and Umathe, 2012; Sartim et al, 2017). …”

Section: Discussionsupporting

confidence: 93%

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Huang

Cheng

Tan

et al. 2017

Experimental Neurology

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Capsaicin, the ingredient responsible for the pungent taste of hot chili peppers, is widely used in the study and management of pain. Recently, its neuroprotective effect has been described in multiple studies. Herein, we investigated the underlying mechanisms for the neuroprotective effect of capsaicin. Direct injection of capsaicin (1 or 3 nmol) into the peri-infarct area reduced the infarct volume and improved neurological behavioral scoring and motor coordination function in the middle cerebral artery occlusion (MCAO)/reperfusion model in rats. The time window of the protective effect of capsaicin was within 1 h after reperfusion, when excitotoxicity is the main reason of cell death. In cultured cortical neurons, administration of capsaicin attenuated glutamate-induced excitotoxic injury. With respect to the mechanisms of the neuroprotective effect of capsaicin, reduced calcium influx after glutamate stimulation was observed following capsaicin pretreatment in cortical neurons. Trpv1 knockout abolished the inhibitory effect of capsaicin on glutamate-induced calcium influx and subsequent neuronal death. Reduced expression of GluN1 and GluN2B, subunits of NMDA receptor, was examined after capsaicin treatment in cortical neurons. In summary, our studies reveal that the neuroprotective effect of capsaicin in cortical neurons is TRPV1-dependent and down-regulation of the expression and function of NMDA receptors contributes to the protection afforded by capsaicin.

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Section: Discussionsupporting

confidence: 93%

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Huang

Cheng

Tan

et al. 2017

Experimental Neurology

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“…For instance, this compound produces anxiolytic-like effects in mice tested in the open arms (Micale et al, 2009; John and Currie, 2012). Moreover, AA-5-HT also reduces depression-like behaviors without changing locomotor activity (Navarria et al, 2014; Sartim et al, 2017). It is worthy to note that to our knowledge, the current report provides for the very first time direct evidence about the effects of AA-5-HT in sleep modulation.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, different doses of AA-5-HT (0–0.5 nmol) administered into the basolateral amygdala prior to elevated plus maze testing increased time spent into the open arms (John and Currie, 2012). In addition, it has been shown that AA-5-HT induces anticonvulsant effects (Micale et al, 2009; Vilela et al, 2014), reduces depression-like behavior (Navarria et al, 2014; Kirkedal et al, 2016) and promotes recovery from stress (Sartim et al, 2017). Despite this accumulating body of evidence regarding the neurobiological role of AA-5-HT, no evidence is available on whether this compound might modulate the sleep-wake cycle.…”

Section: Introductionmentioning

confidence: 99%

Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

Murillo-Rodrı́guez

Marzo

Machado

et al. 2017

Front. Mol. Neurosci.

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The endocannabinoid system comprises several molecular entities such as endogenous ligands [anandamide (AEA) and 2-arachidonoylglycerol (2-AG)], receptors (CB1 and CB2), enzymes such as [fatty acid amide hydrolase (FAHH) and monoacylglycerol lipase (MAGL)], as well as the anandamide membrane transporter. Although the role of this complex neurobiological system in the sleep–wake cycle modulation has been studied, the contribution of the blocker of FAAH/transient receptor potential cation channel subfamily V member 1 (TRPV1), N-arachidonoyl-serotonin (AA-5-HT) in sleep has not been investigated. Thus, in the present study, varying doses of AA-5-HT (5, 10, or 20 mg/Kg, i.p.) injected at the beginning of the lights-on period of rats, caused no statistical changes in sleep patterns. However, similar pharmacological treatment given to animals at the beginning of the dark period decreased wakefulness (W) and increased slow wave sleep (SWS) as well as rapid eye movement sleep (REMS). Power spectra analysis of states of vigilance showed that injection of AA-5-HT during the lights-off period diminished alpha spectrum across alertness in a dose-dependent fashion. In opposition, delta power spectra was enhanced as well as theta spectrum, during SWS and REMS, respectively. Moreover, the highest dose of AA-5-HT decreased wake-related contents of neurotransmitters such as dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT) whereas the levels of adenosine (AD) were enhanced. In addition, the sleep-inducing properties of AA-5-HT were confirmed since this compound blocked the increase in W caused by stimulants such as cannabidiol (CBD) or modafinil (MOD) during the lights-on period. Additionally, administration of AA-5-HT also prevented the enhancement in contents of DA, NE, EP, 5-HT and AD after CBD of MOD injection. Lastly, the role of AA-5-HT in sleep homeostasis was tested in animals that received either CBD or MOD after total sleep deprivation (TSD). The injection of CBD or MOD increased alertness during sleep rebound period after TSD. However, AA-5-HT blocked this effect by allowing animals to display an enhancement in sleep across sleep rebound period. Overall, our findings provide evidence that AA-5-HT is an important modulator of sleep, sleep homeostasis and neurotransmitter contents.

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“…Wang, Treadway, Covey, Cheer, and Lupica (2017) found that cocaine is capable of mobilizing 2-AG content in the VTA to increase the frequency of DA transients in the NAc. Moreover, eCB signaling has also been heavily explored in the context of stress-associated behaviors (Sartim, Moreira, & Joca, 2017). Namely, eCB tone in the amygdala has been demonstrated to play a pivotal role in regu-lating the hypothalamic–pituitary–adrenal (HPA), whose activation is largely responsible for the stress response (Hill et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Fatty acid binding protein deletion prevents stress‐induced preference for cocaine and dampens stress‐induced corticosterone levels

Hamilton¹,

Marion²,

Figueiredo³

et al. 2018

Synapse

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Genetic and pharmacological manipulation of endocannabinoid (eCB) signaling has previously been shown to have an important role on the rewarding properties of drugs of abuse, including cocaine. Recently, fatty acid binding proteins (FABPs) have been proposed as intracellular transporters of the endocannabinoid anandamide (AEA) as well as other bioactive lipids to their catabolic enzyme, fatty acid amide hydrolase (FAAH). The role of these transporters in modulating the brains reward system has yet to be investigated. This study examined the effects of genetic deletion of FABP 5/7 on cocaine preference, as assessed by the Conditioned Place Preference (CPP) paradigm. Male and female wild type (WT) and FABP 5/7 KO mice showed similar acquisition of cocaine CPP, with no differences found in overall locomotor activity. In addition, while male and female WT mice showed stress-induced CPP for cocaine, male and female FABP 5/7 KO mice failed to show a stress-induced preference for the cocaine-paired chamber. Additionally, serum corticosterone levels were analyzed to explore any potential differences in stress response that may be responsible for the lack of stress-induced preference for cocaine. Serum samples were obtained in animals under basal conditions as well as following a 30-min tube restraint stress. Male and female FABP 5/7 KO mice showed reduced corticosterone levels under stress compared to their WT counterparts. The reduction in corticosterone response under stress may mediate that lack of a stress-induced preference for cocaine in the FABP 5/7 KO mice. Thus, the role of FABPs may play an important role in drug-seeking behavior under stressful conditions.

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Involvement of CB 1 and TRPV1 receptors located in the ventral medial prefrontal cortex in the modulation of stress coping behavior

Cited by 29 publications

References 46 publications

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

Fatty acid binding protein deletion prevents stress‐induced preference for cocaine and dampens stress‐induced corticosterone levels

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