Presynaptic effects of anandamide and WIN55,212-2 on glutamatergic nerve endings isolated from rat hippocampus

Cannizzaro, Carla; D’Amico, Monia; Preziosi, P; Martire, Maria

doi:10.1016/j.neuint.2005.10.009

Cited by 26 publications

(18 citation statements)

References 49 publications

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“…Despite the predominant influence of CB 1 receptors in hippocampal circuitry being exerted through the inhibition of GABA release, CB 1 receptors at glutamatergic presynaptic nerve terminals (Katona et al, 2006;Kawamura et al, 2006) also inhibit the K + -evoked release of glutamate (eg, Cannizzaro et al, 2006;D'Amico et al, 2004;Köfalvi et al, 2007). Importantly, the regulation of excitatory synaptic transmission is the most relevant role of the hippocampal A 1 receptors (Dunwiddie and Fredholm, 1989;Sebastião et al, 1990).…”

Section: Resultsmentioning

confidence: 99%

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

Sousa

Assaife-Lopes

Ribeiro

et al. 2010

Neuropsychopharmacol

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The cannabinoid CB 1 receptor-mediated modulation of g-aminobutyric acid (GABA) release from inhibitory interneurons is important for the integrity of hippocampal-dependent spatial memory. Although adenosine A 1 receptors have a central role in fine-tuning excitatory transmission in the hippocampus, A 1 receptors localized in GABAergic cells do not directly influence GABA release. CB 1 and A 1 receptors are the main targets for the effects of two of the most heavily consumed psychoactive substances worldwide: D 9 -tetrahydrocannabinol (THC, a CB 1 receptor agonist) and caffeine (an adenosine receptor antagonist). We first tested the hypothesis that an A 1 -CB 1 interaction influences GABA and glutamate release in the hippocampus. We found that A 1 receptor activation attenuated the CB 1 -mediated inhibition of GABA and glutamate release and this interaction was manifested at the level of G-protein activation. Using in vivo and in vitro approaches, we then investigated the functional implications of the adenosine-cannabinoid interplay that may arise following chronic caffeine consumption. Chronic administration of caffeine in mice (intraperitoneally, 3 mg/kg/day, for 15 days, 412 h before trials) led to an A 1 -mediated enhancement of the CB 1 -dependent acute disruptive effects of THC on a short-term spatial memory task, despite inducing a reduction in cortical and hippocampal CB 1 receptor number and an attenuation of CB 1 coupling with G protein. A 1 receptor levels were increased following chronic caffeine administration. This study shows that A 1 receptors exert a negative modulatory effect on CB 1 -mediated inhibition of GABA and glutamate release, and provides the first evidence of chronic caffeine-induced alterations on the cannabinoid system in the cortex and hippocampus, with functional implications in spatial memory.

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Section: Resultsmentioning

confidence: 99%

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

Sousa

Assaife-Lopes

Ribeiro

et al. 2010

Neuropsychopharmacol

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“…Lack of TRPV 1 R-triggered release of radiolabeled neurotransmitters from synaptosomal preparations (D'Amico et al, 2004;Köfalvi et al, 2005Köfalvi et al, , 2007Cannizzaro et al, 2006;Ferreira et al, 2009) can be a result of the age of the animals used and/or of the lack of temporal resolution of the technique itself, i.e. that a fast-desensitizing capsaicin effect (Baamonde et al, 2005) is diluted in the minute-scale sampling process.…”

Section: Capsaicin Increases the Frequency Of Post-synaptic Excitatormentioning

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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“…Several synthetic cannabinoids, such as HU210 (23,24) and WIN55,212-2 (24,25), have been confirmed as ligands of the CB 1 receptor. However, the effects of endogenous and synthetic cannabinoids differ (26).…”

Section: P Arkinson's Disease (Pd) Is a Common Neurodegenerativementioning

confidence: 99%

Cannabinoid Receptor Type 1 Protects Nigrostriatal Dopaminergic Neurons against MPTP Neurotoxicity by Inhibiting Microglial Activation

Chung

Bok

Huh

et al. 2011

The Journal of Immunology

111

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This study examined whether the cannabinoid receptor type 1 (CB1) receptor contributes to the survival of nigrostriatal dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease. MPTP induced significant loss of nigrostriatal DA neurons and microglial activation in the substantia nigra (SN), visualized with tyrosine hydroxylase or macrophage Ag complex-1 immunohistochemistry. Real-time PCR, ELISA, Western blotting, and immunohistochemistry disclosed upregulation of proinflammatory cytokines, activation of microglial NADPH oxidase, and subsequent reactive oxygen species production and oxidative damage of DNA and proteins in MPTP-treated SN, resulting in degeneration of DA neurons. Conversely, treatment with nonselective cannabinoid receptor agonists (WIN55,212-2 and HU210) led to increased survival of DA neurons in the SN, their fibers and dopamine levels in the striatum, and improved motor function. This neuroprotection by cannabinoids was accompanied by suppression of NADPH oxidase reactive oxygen species production and reduced expression of proinflammatory cytokines from activated microglia. Interestingly, cannabinoids protected DA neurons against 1-methyl-4-phenyl-pyridinium neurotoxicity in cocultures of mesencephalic neurons and microglia, but not in neuron-enriched mesencephalic cultures devoid of microglia. The observed neuroprotection and inhibition of microglial activation were reversed upon treatment with CB1 receptor selective antagonists AM251 and/or SR14,716A, confirming the involvement of the CB1 receptor. The present in vivo and in vitro findings clearly indicate that the CB1 receptor possesses anti-inflammatory properties and inhibits microglia-mediated oxidative stress. Our results collectively suggest that the cannabinoid system is beneficial for the treatment of Parkinson’s disease and other disorders associated with neuroinflammation and microglia-derived oxidative damage.

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Presynaptic effects of anandamide and WIN55,212-2 on glutamatergic nerve endings isolated from rat hippocampus

Cited by 26 publications

References 49 publications

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

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

Cannabinoid Receptor Type 1 Protects Nigrostriatal Dopaminergic Neurons against MPTP Neurotoxicity by Inhibiting Microglial Activation

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