Antagonism at metabotropic glutamate 5 receptors inhibits nicotine- and cocaine-taking behaviours and prevents nicotine-triggered relapse to nicotine-seeking. Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas. Interestingly, the increase in VTA glutamate levels in cocaine-experienced animals was also observed after self-administration of saline, suggesting that VTA glutamate release may be linked to expectation of cocaine and induced by cocaine-associated cues Wise, Effects of drugs of abuse on glutamate levels in specific brain regions. Effects of MS on chronic ethanol consumption and GLT1 modulation of glutamate levels in male alcohol-preferring rats. The effects of piracetam on heroin-induced CPP and neuronal apoptosis in rats. Metabotropic glutamate receptor 7 modulates the rewarding effects of cocaine in rats:
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Overall, one can conclude that AMPA receptors contribute to both the reinforcing and motivational effects of cocaine via a PKA-mediated pathway. Rewards increase motivation to perform or repeat tasks and can be broadly classified as natural and drug rewards Schultz, A comparison of the effects of electrical stimulation of the lateral and ventromedial hypothalamus on the activity of neurons in the ventral tegmental area and substantia nigra. Activation of the cystine-glutamate exchanger, using N -acetylcysteine, increases extrasynaptic glutamate levels. Oral ethanol self-administration in the rat: In fact, in humans, the processing of rewards differs between adults and adolescents Fareri et al. Taken together, these data suggest that NAcc glutamate levels can be modulated by cues predicting availability or unavailability of cocaine.
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Dopaminergic terminals in the nucleus accumbens but not the dorsal striatum corelease glutamate. Roles and regulation of glutamate transporters in the central nervous system. Taken together, it appears that knockout of mGlu5 receptors increases sensitivity to alcohol. Blockade of glutamatergic neurotransmission via metabotropic receptors in the VTA also attenuated the rewarding effects of drugs of abuse. In summary, these findings suggest that efficient clearance of synaptic glutamate helps in reducing the rewarding effects of cocaine and alcohol. Extrasynaptic targeting of NMDA receptors following D1 dopamine receptor activation and cocaine self-administration.
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However, the specific role of the different glutamatergic inputs to the VTA dopaminergic neurons in the rewarding effects of drugs of abuse needs to be further explored. The role of mGlu8 receptors in the rewarding effects of other drugs of abuse has not yet been explored. Further, we will discuss effects of pharmacological manipulation of glutamate transmission in the VTA and NAcc on drug reward. In the subsequent section, we will discuss the effects of blocking glutamatergic transmission using pharmacological compounds on behavioral measures of drug reward. Although the effects of ibudilast on the rewarding effects of heroin have not been evaluated, ibudilast attenuated morphine-induced CPP, and increase in NAcc dopamine after morphine administration Hutchinson et al.
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