CB1-cannabinoid receptors are involved in the modulation of non-synaptic [3H]serotonin release from the rat hippocampus

Balázsa, Tamás; Bíró, Judit; Gullai, Nóra; Ledent, Catherine; Sperlágh, Beáta

doi:10.1016/j.neuint.2007.07.008

Cited by 29 publications

(16 citation statements)

References 47 publications

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“…Presynaptic metabotropic CB 1 cannabinoid receptors have long been known to modulate the release of amino acid and monoamine transmitters (Katona et al, 1999;Nakazi et al, 2000;Balázsa et al, 2008;Ferreira et al, 2012). The endocannabinoids, anandamide and NADA can activate the ionotropic TRPV 1 R besides the CB 1 R. Our aim was to investigate the little understood nature of presynaptic functional TRPV 1 Rs.…”

Section: Discussionmentioning

confidence: 99%

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Köles

Garção

Zádori

et al. 2013

Brain Research Bulletin

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Neocortical and striatal TRPV1 (vanilloid or capsaicin) receptors (TRPV1Rs) are excitatory ligand-gated ion channels, and are implicated in psychiatric disorders. However, the purported presynaptic neuromodulator role of TRPV1Rs in glutamatergic, serotonergic or dopaminergic terminals of the rodent forebrain remains little understood. With the help of patch-clamp electrophysiology and neurochemical approaches, we mapped the age-dependence of presynaptic TRPV1R function, and furthermore, we aimed at exploring whether the presence of CB1 cannabinoid receptors (CB1Rs) influences the function of the TRPV1Rs, as both receptor types share endogenous ligands. We found that the major factor which affects presynaptic TRPV1R function is age: by post-natal day 13, the amplitude of capsaicin-induced release of dopamine and glutamate is halved in the rat striatum, and two weeks later, capsaicin already loses its effect. However, TRPV1R receptor function is not enhanced by chemical or genetic ablation of the CB1Rs in dopaminergic, glutamatergic and serotonergic terminals of the mouse brain. Altogether, our data indicate a possible neurodevelopmental role for presynaptic TRPV1Rs in the rodent brain, but we found no cross-talk between TRPV1Rs and CB1Rs in the same nerve terminal. AbstractNeocortical and striatal TRPV 1 (vanilloid or capsaicin) receptors (TRPV 1 Rs) are excitatory ligandgated ion channels, and are implicated in psychiatric disorders. However, the purported presynaptic neuromodulator role of TRPV 1 Rs in glutamatergic, serotonergic or dopaminergic terminals of the rodent forebrain remains little understood. With the help of patch-clamp electrophysiology and neurochemical approaches, we mapped the age-dependence of presynaptic TRPV 1 R function, and furthermore, we aimed at exploring whether the presence of CB 1 cannabinoid receptors (CB 1 Rs) influences the function of the TRPV 1 Rs, as both receptor types share endogenous ligands.We found that the major factor which affects presynaptic TRPV 1 R function is age: by post-natal day 13, the amplitude of capsaicin-induced release of dopamine and glutamate is halved in the rat striatum, and two weeks later, capsaicin already loses its effect. However, TRPV 1 R receptor function is not enhanced by chemical or genetic ablation of the CB 1 Rs in dopaminergic, glutamatergic and serotonergic terminals of the mouse brain.Altogether, our data indicate a possible neurodevelopmental role for presynaptic TRPV 1 Rs in the rodent brain, but we found no cross-talk between TRPV 1 Rs and CB 1 Rs in the same nerve terminal.

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Section: Discussionmentioning

confidence: 99%

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Köles

Garção

Zádori

et al. 2013

Brain Research Bulletin

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“…The serotonergic system has been implicated in the regulation of impulse control, behavioural inhibition and effective decision making (Evenden 1999b;Clark et al 2004;Soubrié 1986), with reductions in serotonin (5-hydroxytryptamine, 5-HT) levels being associated with reduced inhibitory control and increases in impulsive behaviour (Clark et al 2009;Evenden 1999b). Cannabinoids have been shown to interact with 5-HT receptors (Kelaï et al 2006;Kimura et al 1998) and evidence from preclinical studies suggests the involvement of cannabinoid receptors (CB1) in the regulation of serotonergic responses (Lau and Schloss 2008;Mato et al 2007), whereby stimulation of CB1 receptors reduces (Balazsa et al 2008) and inhibits (Best and Regehr 2008;Nakazi et al 2000) 5-HT release. Administration of THC has been shown to decrease serotonergic activity in various brain regions in animal studies (Molina-Holgado et al 1993;Moranta et al 2004;Sagredo et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Reflection impulsivity in adolescent cannabis users: a comparison with alcohol-using and non-substance-using adolescents

et al. 2011

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Exposure to cannabis during adolescence is associated with increased risky and impulsive decision making, with users adopting strategies with higher levels of uncertainty and inefficient utilisation of information. The young cannabis users did show sensitivity to losses, suggesting that greater impulsivity early in their drug using career is more evident when there is a lack of negative consequences. This provides a window of opportunity for intervention before the onset of cannabis dependence.

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“…Indeed, in intact animals, the motor suppressive effects of cannabinoid agonists have been linked to stimulation of CB 1 receptors located on glutamatergic cortico-striatal terminals (Monory et al 2007), which in turn inhibits GLU release (Huang et al 2001). Finally, we cannot exclude that WIN might modulate other neurotransmitter/neuromodulator systems regulating basal ganglia function, such as acetylcholine, serotonin, nitric oxide and GABA (Malone and Taylor 1999; Kofalvi et al 2005; Bambico et al 2007; Narushima et al 2007; Sergeeva et al 2007; Balazsa et al 2008). In particular, physical manifestations of AIMs have been linked with enhanced GABA overflow in the output nuclei of the basal ganglia (Mela et al 2007) and stimulation of CB 1 receptors may affect the excitability of striatal medium spiny neurons by acting at GABAergic interneurons in the striatum (Narushima et al 2007) where they are highly expressed (Uchigashima et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Neurochemical changes in the striatum of dyskinetic rats after administration of the cannabinoid agonist WIN55,212-2

Morgese

Cassano

Gaetani

et al. 2009

Neurochemistry International

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Chronic use of levodopa, the most effective treatment for Parkinson's disease, causes abnormal involuntary movements named dyskinesias, which are linked to maladaptive changes in plasticity and disturbances of dopamine and glutamate neurotransmission in the basal ganglia. Dyskinesias can be modeled in rats with unilateral 6-hydroxydopamine lesions by repeated administration of low doses of levodopa (6 mg/kg, s.c.). Previous studies from our lab showed that sub-chronic treatment with the cannabinoid agonist WIN55,212-2 attenuates levodopa-induced dyskinesias at doses that do not interfere with physiological motor function. To investigate the neurochemical changes underlying WIN55,212-2 anti-dyskinetic effects, we used in vivo microdialysis to monitor extracellular dopamine and glutamate in the dorsal striatum of the both hemisphere of freely-moving 6-hydroxydopamine-treated, SHAM-operated and intact rats receiving levodopa acutely or chronically (11 days), and studied how sub-chronic WIN55,212-2 (1 injection × 3 days, 20 min before levodopa) affected these neurochemical outputs.Our data indicate that: 1) the 6-hydroxydopamine lesion decreases dopamine turnover in the denervated striatum; 2) levodopa injection reduces extracellular glutamate in the side ipsilateral to the lesion of dyskinetic rats; 3) sub-chronic WIN55,212-2 prevents levodopa-induced glutamate volume transmission unbalances across the two hemispheres; 4) levodopa-induced dyskinesias are inversely correlated with glutamate levels in the denervated striatum. These data indicate that the anti-dyskinetic properties of WIN55,212-2 are accompanied by changes of dopamine and glutamate outputs in the two brain hemispheres of 6-hydroxydopamine-treated rats.Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of nigrostriatal neurons. Although the dopamine (DA) precursor levodopa represents the golden standard for PD therapy, its long-term use causes disabling abnormal involuntary movements (AIMs) known as dyskinesias. In rodents, levodopa-induced dyskinesias can be mimicked by chronic administration of low doses of levodopa following nigrostriatal denervation by unilateral injection of the neurotoxin 6-hydroxydopamine (6-OHDA). ThisCorresponding author: Tommaso Cassano, PhD, Department of Biomedical Sciences, University of Foggia, Foggia, Italy, 71100, Phone: +39 0881 588042, Fax: +39 0881 588037, E-mail: tommaso.cassano@unifg.it. * These authors contributed equally to the present study Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Lundblad et al. 2002) and displ...

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CB1-cannabinoid receptors are involved in the modulation of non-synaptic [3H]serotonin release from the rat hippocampus

Cited by 29 publications

References 47 publications

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Reflection impulsivity in adolescent cannabis users: a comparison with alcohol-using and non-substance-using adolescents

Neurochemical changes in the striatum of dyskinetic rats after administration of the cannabinoid agonist WIN55,212-2

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