Modification of d-amphetamine-induced responses by baclofen in rats

Phillis, Benjamin D.; Ong, Jennifer; White, Jason M.; Bonnielle, Claudia

doi:10.1007/s002130000562

Cited by 27 publications

(10 citation statements)

References 25 publications

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“…For example, baclofen reduced behavioral activation induced by acute alcohol injections (Broadbent and Harless, 1999;Chester and Cunningham, 1999) and reduced ethanol intake (Colombo et al, 2003), particularly in limited access paradigms (Anstrom et al, 2003) and in dependent rats (Walker and Koob, 2007). The suppression of alcohol self-administration by baclofen is consistent with other preclinical literature in which the drug reduced self-administration of cocaine (Campbell et al, 1999), amphetamines (Phillis et al, 2001), heroin (Xi and Stein, 1999), and nicotine (Corrigall et al, 2001). Because baclofen inhibits dopaminergic neurons (Erhardt et al, 2002;Olpe et al, 1977) and inhibits cocaine selfadministration after intrategmental injections (Brebner et al, 2000), it is possible that baclofen's effects on self-administration are mediated by its inhibition of dopaminergic activity.…”

Section: Discussionsupporting

confidence: 83%

Baclofen Blocks Expression and Sensitization of Anxiety‐Like Behavior in an Animal Model of Repeated Stress and Ethanol Withdrawal

Knapp

Overstreet

Breese

2007

Alcoholism Clin & Exp Res

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Section: Discussionsupporting

confidence: 83%

Baclofen Blocks Expression and Sensitization of Anxiety‐Like Behavior in an Animal Model of Repeated Stress and Ethanol Withdrawal

Knapp

Overstreet

Breese

2007

Alcoholism Clin & Exp Res

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“…The data collected in the present study are also consonant with several findings indicating that pretreatment with baclofen or GS39783 suppressed hyperlocomotion induced in rats and mice by acute injection of other drugs of abuse, including alcohol (Quintanilla et al, 2008; Holstein et al, 2009), cocaine (Kalivas et al, 1990; Lhuillier et al, 2007), morphine (Woo et al, 2001; Leite-Morris et al, 2002), and d -amphetamine (Kalivas et al, 1990; Phillis et al, 2001). Together, these data suggest that activation of the GABA B receptor may suppress the stimulant, euphorigenic-like properties of different drugs of abuse, underlining – once more – the therapeutic, anti -addictive potential of baclofen and GABA B PAMs.…”

Section: Discussionmentioning

confidence: 99%

Activation of the GABAB Receptor Prevents Nicotine-Induced Locomotor Stimulation in Mice

Lobina¹,

Carai²,

Froestl³

et al. 2011

Front. Psychiatry

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Recent studies demonstrated that activation of the GABAB receptor, either by means of orthosteric agonists or positive allosteric modulators (PAMs), inhibited different nicotine-related behaviors, including intravenous self-administration and conditioned place preference, in rodents. The present study investigated whether the anti-nicotine effects of the GABAB receptor agonist, baclofen, and GABAB PAMs, CGP7930, and GS39783, extend to nicotine stimulant effects. To this end, CD1 mice were initially treated with baclofen (0, 1.25, and 2.5 mg/kg, i.p.), CGP7930 (0, 25, and 50 mg/kg, i.g.), or GS39783 (0, 25, and 50 mg/kg, i.g.), then treated with nicotine (0 and 0.05 mg/kg, s.c.), and finally exposed to an automated apparatus for recording of locomotor activity. Pretreatment with doses of baclofen, CGP7930, or GS39783 that did not alter locomotor activity when given with nicotine vehicle fully prevented hyperlocomotion induced by 0.05 mg/kg nicotine. These data extend to nicotine stimulant effects the capacity of baclofen and GABAB PAMs to block the reinforcing, motivational, and rewarding properties of nicotine. These data strengthen the hypothesis that activation of the GABAB receptor may represent a potentially useful, anti-smoking therapeutic strategy.

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“…A possible mechanism behind this may be that baclofen stabilizes dopamine neuron firing in the midbrain (Erhardt et al, 1998(Erhardt et al, , 2002. In support of this, baclofen has proven effective against the disruption of PPI by metamphetamine (Arai et al, 2008), D-amphetamineinduced hypermotility and disruption of successive discrimination (Ahlenius et al, 1975;Phillis et al, 2001;Zhou et al, 2004). Although the hyperactivity caused by common psychotomimetics such as D-amphetamine, traditionally has been attributed to stimulation of the mesocorticolimbic dopamine system, this may not be true for NMDA receptor antagonists such as PCP where the effects on locomotion are temporally dissociated from changes in dopamine levels (Adams and Moghaddam, 1998).…”

Section: Effects Of Baclofenmentioning

confidence: 94%

Prefrontal GABAB Receptor Activation Attenuates Phencyclidine-Induced Impairments of Prepulse Inhibition: Involvement of Nitric Oxide

Fejgin

Pålsson

Wass

et al. 2009

Neuropsychopharmacol

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Recent theories propose that both GABA and glutamate signaling are compromised in patients with schizophrenia. These deficits can be observed in several brain regions including the prefrontal cortex (PFC), an area extensively linked to the cognitive dysfunction in this disease and notably affected by NMDA receptor antagonists such as phencyclidine (PCP). We have previously demonstrated that inhibition of the nitric oxide (NO) pathways in the brain, particularly in the PFC, prevents a wide range of PCP-induced behavioral deficits including disruption of prepulse inhibition (PPI). This study investigated the role of GABA(B) receptor signaling and NO in the effects of PCP on PPI. Mice received systemic or prefrontal injections of the GABA(B) receptor agonist baclofen (2.5-5 mg/kg and 1 mM) before PCP treatment (5 mg/kg) and were thereafter tested for PPI. GABA/NO interactions were studied by combining baclofen and the NO synthase inhibitor L-NAME (20 mg/kg) in subthreshold doses. The role of GABA(B) receptors for NO production in vivo was assessed using NO-sensors implanted into the rat PFC. PCP-induced PPI deficits were attenuated in an additive manner by systemic baclofen treatment, whereas prefrontal microinjections of baclofen completely blocked the effects of PCP, without affecting PPI per se. The combination of baclofen and L-NAME was more effective in preventing the effects of PCP than any compound by itself. Additionally, baclofen decreased NO release in the PFC in a dose-related manner. This study proposes a role for GABA(B) receptor signaling in the effects of PCP, with altered NO levels as a downstream consequence. Thus, prefrontal NO signaling mirrors an altered level of cortical inhibition that may be of importance for information processing deficits in schizophrenia.

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Modification of d-amphetamine-induced responses by baclofen in rats

Cited by 27 publications

References 25 publications

Baclofen Blocks Expression and Sensitization of Anxiety‐Like Behavior in an Animal Model of Repeated Stress and Ethanol Withdrawal

Baclofen Blocks Expression and Sensitization of Anxiety‐Like Behavior in an Animal Model of Repeated Stress and Ethanol Withdrawal

Activation of the GABAB Receptor Prevents Nicotine-Induced Locomotor Stimulation in Mice

Prefrontal GABAB Receptor Activation Attenuates Phencyclidine-Induced Impairments of Prepulse Inhibition: Involvement of Nitric Oxide

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