Existence of capsaicin-sensitive glutamatergic terminals in rat hypothalamus

Sasamura, Takashi; Sasaki, Miwa; Tohda, Chihiro; Kuraishi, Yasushi

doi:10.1097/00001756-199806220-00025

Cited by 147 publications

(121 citation statements)

References 13 publications

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“…From the observation that TRPV1 and tyrosine hydroxylase expression are colocalized in the substantia nigra, it was suggested that vanilloid-sensitive neurons are monoaminergic in this region (Mezey et al, 2000). Expression of TRPV1 receptors on glutamatergic terminals is also likely as their activation produces glutamate release in the rat hypothalamus (Sasamura et al, 1998), substantia nigra (Marinelli et al, 2003), and substantia gelatinosa (Yue et al, 2004). Further work has demonstrated that activation of TRPV1 receptors in the ventral tegmental area causes dopamine release in the nucleus accumbens, which may be due to increased glutamatergic transmission onto dopaminergic neurons (Marinelli et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Long

Malone

Taylor

2005

Neuropsychopharmacol

151

102

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Cannabidiol, a nonpsychoactive constituent of the Cannabis sativa plant, has been reported to act as an agonist of the vanilloid 1 channel in the transient receptor potential family (TRPV1) and also to inhibit the hydrolysis and cellular uptake of the endogenous cannabinoid anandamide. Cannabidiol has also been reported to have potential as an antipsychotic. We investigated the effect of cannabidiol on sensorimotor gating deficits in mice induced by the noncompetitive NMDA receptor antagonist, MK-801. Sensorimotor gating is deficient in psychotic disorders such as schizophrenia and may be reliably measured by prepulse inhibition (PPI) of the startle response in rodents and humans. MK-801 (0.3-1 mg/kg i.p.) dose dependently disrupted PPI while cannabidiol (1-15 mg/kg i.p.), when administered with vehicle, had no effect on PPI. Cannabidiol (5 mg/kg i.p.) successfully reversed disruptions in PPI induced by MK-801 (1 mg/kg i.p.), as did the atypical antipsychotic clozapine (4 mg/kg i.p.). Pretreatment with capsazepine (20 mg/kg i.p.) prevented the reversal of MK-801-induced disruption of PPI by cannabidiol, providing preliminary evidence that TRPV1 receptors are involved in the reversal of MK-801-induced sensorimotor gating deficits by cannabidiol.

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Section: Discussionmentioning

confidence: 99%

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Long

Malone

Taylor

2005

Neuropsychopharmacol

151

102

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“…The TRPV1 receptor is localized in neuron cell bodies and dendrites, astrocytes and perivascular structures within the brain. (Liapi and Wood, 2005;Mezey et al, 2000;Roberts et al, 2004;Sasamura et al, 1998). At subcellular level TRPV1…”

Section: Expression Of Trpv1 In the Brainmentioning

confidence: 99%

“…Capsaicin evokes glutamate release from slices of hypothalamus and lumbar dorsal horn, but not cerebellum. Such capsaicin action has shown to be Ca 2+ dependent and inhibited by the TRPV1 receptor antagonist, capsazepine, thus suggesting that TRPV1 receptor may be expressed on glutamatergic neurons in the hypothalamus (Sasamura et al, 1998) …”

Section: Expression Of Trpv1 In the Brainmentioning

confidence: 99%

Role of TRPV1 receptors in descending modulation of pain

Palazzo

Rossi

Maione

2008

Molecular and Cellular Endocrinology

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Transient receptor potential vanilloid type 1 (TRPV1) receptor is a ligand-gated non selective cation channel activated by heat (>43°), low pH and endogenous lipid molecules such as anandamide, Narachydonoyl-dopamine, N-acyl-dopamines and products of lipoxygenases (12-and 15-(S)-HPETE) termed endovanilloids. Apart from peripheral primary afferent neurons and dorsal root ganglia, TRPV1 receptor is expressed throughout the brain. Recent evidence show that TRPV1 receptor stimulation by endocannabinoids or by capsaicin within the periaqueductal grey (PAG) leads to analgesia and this effect is associated with glutamate increase and the activation of OFF cell population in the rostral ventromedial medulla (RVM). Activation of the antinociceptive descending pathway via TPRV1 receptor stimulation in the PAG may be a novel strategy for producing analgesia. This review will summarize the more recent insights into the role of TRPV1 receptor within the antinociceptive descending pathway and its possible exploitation as a target for novel pain-killer agents.

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“…Besides the control of synaptic transmission in the brain (Sasamura et al, 1998;Doyle et al, 2002;Marinelli et al, 2002Marinelli et al, , 2003, the TRPV1 channels are also known to be involved in mediating nociceptive and stressful processes in the peripheral nervous system (O'Neil and Brown, 2003).…”

Section: Introductionmentioning

confidence: 99%

Activation of TRPV1 in the VTA Excites Dopaminergic Neurons and Increases Chemical- and Noxious-Induced Dopamine Release in the Nucleus Accumbens

Marinelli

Pascucci

Bernardi

et al. 2004

Neuropsychopharmacol

128

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Dopamine (DA)-containing neurons of the ventral tegmental area (VTA) provide dopaminergic input to the nucleus accumbens and to the prefrontal cortex within the mesolimbic pathway. In the present study, we combined electrophysiological recordings and microdialysis techniques to investigate the function of transient receptor potential vanilloid 1 (TRPV1) channel in the VTA. In brain slices, application of the TRPV1 receptor agonist capsaicin increased the firing rate of rat dopamine neurons and in a proportion of tested cells (44%) it also induced a bursting behavior. The effects of capsaicin were concentration dependent. The increase in neuronal firing was dependent on enhanced glutamatergic transmission since it was blocked by the superfusion of the ionotropic glutamate antagonists, CNQX and AP5. Interestingly, microinjection of capsaicin into the VTA and noxious tail stimulation transiently enhanced dopamine release into the nucleus accumbens. Both the in vitro and in vivo effects were mediated by TRPV1 activation in the VTA since they were reduced by co-perfusion of the selective TRPV1 receptor antagonist iodoresineferatoxin. Our data suggest a novel role for TRPV1 channels in the mesencephalon of rat, namely activation of the DA system following a peripheral noxious stimulation.

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Existence of capsaicin-sensitive glutamatergic terminals in rat hypothalamus

Cited by 147 publications

References 13 publications

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Role of TRPV1 receptors in descending modulation of pain

Activation of TRPV1 in the VTA Excites Dopaminergic Neurons and Increases Chemical- and Noxious-Induced Dopamine Release in the Nucleus Accumbens

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