Structural plasticity associated with exposure to drugs of abuse

Robinson, Terry E.; Kolb, Bryan

doi:10.1016/j.neuropharm.2004.06.025

Cited by 993 publications

(878 citation statements)

References 105 publications

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“…In both the case of the NAC and hippocampus, the alcohol-induced increases in dendritic spine head size was accompanied by increased synaptic targeting of NMDA receptors and clustering with PSD-95, as well as an enlargement in PSD-95-associated F-actin clusters [214][215][216]. Taken together, these data support the hypothesis that chronic drug exposure engages homeostatic responses that alter the dendritic processing of glutamate, and other neurochemical signals, ultimately affecting synaptic efficacy within key brain regions regulating the addictive properties of drugs of abuse [123,184,185,216].…”

Section: Potential Role For Homers In Drug-induced Alterations In Strsupporting

confidence: 59%

“…Mounting evidence supports the theory that the addicted state results from a drug-induced usurpation of the cellular and molecular mechanisms underlying other forms of synaptic plasticity (e.g., learning and memory) within the neural circuits underlying motivation and psychomotor activation [c.f., 184,185]. Moreover, the chronic nature of addiction suggests that drug-induced structural plasticity within these neural circuits endures for months, if not years, following cessation of drug administration [184,185].…”

Section: Potential Role For Homers In Drug-induced Alterations In Strmentioning

confidence: 99%

“…Moreover, the chronic nature of addiction suggests that drug-induced structural plasticity within these neural circuits endures for months, if not years, following cessation of drug administration [184,185]. Indeed there exists now considerable data supporting persistent effects of various drugs of abuse upon neuronal morphology, particularly in the structural plasticity of dendritic spines of neurons within the PFC and NAC.…”

Section: Potential Role For Homers In Drug-induced Alterations In Strmentioning

confidence: 99%

“…Like repeated drug administration (see above), repeated exposure to stressors induces morphological abnormalities within glutamatergic pyramidal neurons within the cortex of laboratory animals [e.g., 184,221,[296][297][298]. Both psychological and physiological stressors can elevate corticoaccumbens glutamate levels [299][300][301] and repeated maternal stress elicits "cocainelike" alterations in basal and cocaine-stimulated glutamate release within the NAC of adult offspring in conjunction with a "pre-sensitized" cocaine behavioral phenotype [295].…”

Section: Stressor-induced Regulation Of Homers: Implications For Addimentioning

confidence: 99%

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Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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Drug addiction is a chronic, relapsing disorder, characterized by an uncontrollable motivation to seek and use drugs. Converging clinical and preclinical observations implicate pathologies within the corticolimbic glutamate system in the genetic predisposition to, and the development of, an addicted phenotype. Such observations pose cellular factors regulating glutamate transmission as likely molecular candidates in the etiology of addiction. Members of the Homer family of proteins regulate signal transduction through, and the trafficking of, glutamate receptors, as well as maintain and regulate extracellular glutamate levels in corticolimbic brain regions. This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.

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Section: Potential Role For Homers In Drug-induced Alterations In Strsupporting

confidence: 59%

Section: Potential Role For Homers In Drug-induced Alterations In Strmentioning

confidence: 99%

Section: Potential Role For Homers In Drug-induced Alterations In Strmentioning

confidence: 99%

Section: Stressor-induced Regulation Of Homers: Implications For Addimentioning

confidence: 99%

See 2 more Smart Citations

Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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“…Together with evidence demonstrating the disruption of the prefrontal modulation of accumbens neurons following repeated psychostimulant exposure (Goto and Grace, 2005), the present findings suggest that repeated AMPH-exposure disrupts such telencephalic innervation of basal forebrain cholinergic neurons and thus, prefrontal ACh release. A range of neuronal mechanisms could be responsible for such a disruption, including abnormalities in glutamatergic and dopaminergic neurotransmission in prefrontal and mesolimbic regions (Giorgetti et al, 2001;Lu and Wolf, 1999;Peterson et al, 2006;Prasad et al, 1995) as well as structural reorganization of prefrontal and mesolimbic neurons (Crombag et al, 2005;Robinson and Kolb, 2004).…”

Section: Discussionmentioning

confidence: 99%

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Kozak

Martı́nez

Young

et al. 2007

Neuropsychopharmacol

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Impairments in attentional functions and capacities represent core aspects of the cognitive symptoms of schizophrenia. Attentional performance has been demonstrated to depend on the integrity and activity of cortical cholinergic inputs. The neurobiological, behavioral, and cognitive effects of repeated exposure to psychostimulants model important aspects of schizophrenia. In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH. In non-performing rats, pretreatment with AMPH did not affect the increases in ACh release produced by AMPH-challenges. In contrast, attentional task performanceassociated increases in ACh release were attenuated in AMPH-pretreated and AMPH-challenged rats. This effect of repeated AMPH exposure on ACh release was already present before task-onset, suggesting that the loss of cognitive control that characterized these animals' performance was a result of cholinergic dysregulation. The findings indicate that the demonstration of repeated AMPH-induced dysregulation of the prefrontal cholinergic input system depends on interactions between the effects of repeated AMPH exposure and cognitive performance-associated recruitment of this neuronal system. Repeated AMPH-induced disruption of prefrontal cholinergic activity and attentional performance represents a useful model to investigate the cholinergic mechanisms contributing to the cognitive impairments of schizophrenia.

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CNS Stimulants

Nichols

2010

Burger's Medicinal Chemistry and Drug Discovery

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This chapter briefly describes the development, structure–activity relationships, and mechanism of action for the important psychostimulants such as amphetamines, methylphenidate, and cocaine. Derived from natural products known for centuries, at low doses these drugs lead to increased arousal, improved performance on tasks of vigilance and alertness, and a sense of self‐confidence and well being. High doses can produce feelings of elation or euphoria, and result in profound abuse liability. This chapter reviews the current and future use of psychostimulants, as well as other drugs that cause CNS arousal, albeit by different mechanisms.

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Structural plasticity associated with exposure to drugs of abuse

Cited by 993 publications

References 105 publications

Homers regulate drug-induced neuroplasticity: Implications for addiction

Homers regulate drug-induced neuroplasticity: Implications for addiction

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

CNS Stimulants

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