Effect of neramexane on ethanol dependence and reinforcement

Kotlińska, Jolanta; Biała, Grażyna; Rafalski, Piotr; Bocheński, Marcin; Danysz, Wojciech

doi:10.1016/j.ejphar.2004.09.036

Cited by 21 publications

(10 citation statements)

References 15 publications

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“…2000a). Ethanol (0.5 g/kg ip) produced CPP in rats after 15 daily pre‐treatments with the same dose (Biala & Kotlinska 1999; Kotlinska et al . 2004).…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 99%

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REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

2007

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Conditioned place preference (CPP) continues to be one of the most popular models to study the motivational effects of drugs and non-drug treatments in experimental animals. This is obvious from a steady year-to-year increase in the number of publications reporting the use this model. Since the compilation of the preceding review in 1998, more than 1000 new studies using place conditioning have been published, and the aim of the present review is to provide an overview of these recent publications. There are a number of trends and developments that are obvious in the literature of the last decade. First, as more and more knockout and transgenic animals become available, place conditioning is increasingly used to assess the motivational effects of drugs or non-drug rewards in genetically modified animals. Second, there is a still small but growing literature on the use of place conditioning to study the motivational aspects of pain, a field of pre-clinical research that has so far received little attention, because of the lack of appropriate animal models. Third, place conditioning continues to be widely used to study tolerance and sensitization to the rewarding effects of drugs induced by pre-treatment regimens. Fourth, extinction/reinstatement procedures in place conditioning are becoming increasingly popular. This interesting approach is thought to model certain aspects of relapse to addictive behavior and has previously almost exclusively been studied in drug self-administration paradigms. It has now also become established in the place conditioning literature and provides an additional and technically easy approach to this important phenomenon. The enormous number of studies to be covered in this review prevented in-depth discussion of many methodological, pharmacological or neurobiological aspects; to a large extent, the presentation of data had to be limited to a short and condensed summary of the most relevant findings.

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“…2000a). Ethanol (0.5 g/kg ip) produced CPP in rats after 15 daily pre‐treatments with the same dose (Biala & Kotlinska 1999; Kotlinska et al . 2004).…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 99%

“…Neither the glycinB‐site antagonist MRZ 2/570 (5 mg/kg ip) nor the non‐competitive NMDA receptor antagonist MRZ 2/579 (5 and 7 mg/kg ip) produced a place conditioning effect on their own (Popik et al . 1998; Kotlinska et al . 2004).…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 99%

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

2007

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“…In addition, neramexane as well as memantine effectively suppressed ethanol withdrawal induced seizures in alcohol dependent rats [12]. According to recent results by Kotlinska et al chronic administration of neramexane inhibits the development of ethanol dependence, reflected as a decrease in ethanol withdrawal-associated audiogenic seizures as well as the acquisition and expression of ethanol-induced place preference [108].…”

Section: Competitive and Channel Blocking Nmdar Antagonistsmentioning

confidence: 99%

Role of Altered Structure and Function of NMDA Receptors in Development of Alcohol Dependence

Nagy

Kolok²,

Boros³

et al. 2005

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Long-term alcohol exposure gives rise to development of physical dependence on alcohol in consequence of changes in certain neurotransmitter functions. Accumulating evidence suggests that the glutamatergic neurotransmitter system, especially the N-methyl-D-aspartate (NMDA) type of glutamate receptors is a particularly important site of ethanol's action, since ethanol is a potent inhibitor of the NMDA receptors (NMDARs) and prolonged ethanol exposition leads to a compensatory "upregulation" of NMDAR mediated functions supposedly contributing to the occurrence of ethanol tolerance, dependence as well as the acute and delayed signs of ethanol withdrawal.Recently, expression of different types of NMDAR subunits was found altered after long-term ethanol exposure. Especially, the expression of the NR2B and certain splice variant forms of the NR1 subunits were increased in primary neuronal cultures treated intermittently with ethanol. Since NMDA ion channels with such an altered subunit composition have increased permeability for calcium ions, increased agonist sensitivity, and relatively slow closing kinetics, the abovementioned alterations may underlie the enhanced NMDAR activation observed after long-term ethanol exposure. In accordance with these changes, the inhibitory potential of NR2B subunit-selective NMDAR antagonists is also increased, demonstrating excellent potency against alcohol withdrawal-induced in vitro cytotoxicity. Although in vivo data are few with these compounds, according to the effectiveness of the classic NMDAR antagonists in attenuation, not only the physical symptoms,but also some affective and motivational components of alcohol withdrawal, novel NR2B subunit selective NMDAR antagonists may offer a preferable alternative in the pharmacotherapy of alcohol dependence.

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“…Indeed, NMDAR antagonism in the VTA decreases systemic nicotine-induced dopamine release in the nucleus accumbens in rats [137,138] and NMDA antagonists and partial agonists, when co-administered with nicotine or cocaine, can block development of behavioral sensitization to subsequent drug challenge [139][140][141][142][143][144][145][146][147][148][149][150][151][152]. Thus, NMDAR antagonists may be able to block the transition from use to abuse or dependence of drugs or, more likely, may block the reward-related learning that occurs with early use of reinforcing drugs.…”

Section: Glycinergic Medications For Nicotine Dependence In Schizophrmentioning

confidence: 99%

Nicotinic and Glycinergic Medications for Disorders of Hedonic Regulation

Dyer¹,

Barr²,

Evins³

2007

LDDD

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Effect of neramexane on ethanol dependence and reinforcement

Cited by 21 publications

References 15 publications

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

Role of Altered Structure and Function of NMDA Receptors in Development of Alcohol Dependence

Nicotinic and Glycinergic Medications for Disorders of Hedonic Regulation

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