Differential Effects of Nicotine and Complex Housing on Subsequent Experience-Dependent Structural Plasticity in the Nucleus Accumbens.

Hamilton, Derek A.; Kolb, Bryan

doi:10.1037/0735-7044.119.2.355

Cited by 58 publications

(38 citation statements)

References 46 publications

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“…DA depletion resulting from 6-OHDA lesions also reduces spine density in the medial PFC [102]. These findings can be contrasted with the increases in medial PFC and NAc spine density, but not parietal cortex, observed by following chronic stimulant [91,103,104] or PCP exposure [105], the latter of which represents one of the major approaches to modeling schizophrenia symptoms in rodents.…”

Section: Non-human Animal Investigations Provide Neural Interpretatiocontrasting

confidence: 51%

“…Because dendritic spines are the primary cites of excitatory synapses, they also indicate possible changes in neural activity elicited via axodendritic connections. Exposure to drugs and other forms of experience induce persistent modifications in dendritic morphology and spine density [86,[88][89][90][91], that can be linked to specific behavioral, cognitive, and functional consequences [65,86,92]. Dendritic morphology and spine density are also thought to be related to functional consequences of neurological disorders [93].…”

Section: Non-human Animal Investigations Provide Neural Interpretatiomentioning

confidence: 99%

See 1 more Smart Citation

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

Abbott¹,

Jaramillo²,

Wilcox³

et al. 2013

Current Medicinal Chemistry

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The evidence that antipsychotics improve brain function and reduce symptoms in schizophrenia is unmistakable, but how antipsychotics change brain function is poorly understood, especially within neuronal systems. In this review, we investigated the hypothesized normalization of the functional magnetic resonance imaging (fMRI) blood oxygen level dependent signal in the context of antipsychotic treatment. First, we conducted a systematic PubMed search to identify eight fMRI investigations that met the following inclusion criteria: case-control, longitudinal design; pre-and post-treatment contrasts with a healthy comparison group; and antipsychotic-free or antipsychoticnaïve patients with schizophrenia at the start of the investigation. We hypothesized that aberrant activation patterns or connectivity between patients with schizophrenia and healthy comparisons at the first imaging assessment would no longer be apparent or "normalize" at the second imaging assessment. The included studies differed by analysis method and fMRI task but demonstrated normalization of fMRI activation or connectivity during the treatment interval. Second, we reviewed putative mechanisms from animal studies that support normalization of the BOLD signal in schizophrenia. We provided several neuronal-based interpretations of these changes of the BOLD signal that may be attributable to long-term antipsychotic administration.

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Section: Non-human Animal Investigations Provide Neural Interpretatiocontrasting

confidence: 51%

Section: Non-human Animal Investigations Provide Neural Interpretatiomentioning

confidence: 99%

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

Abbott¹,

Jaramillo²,

Wilcox³

et al. 2013

Current Medicinal Chemistry

View full text Add to dashboard Cite

show abstract

“…Drug abuse studies have focused on learning and memory processes (O'Brien et al, 1992;Berke and Hyman, 2000;Wise, 2000;Robinson and Kolb, 2004;Wolf et al, 2004;Hamilton and Kolb, 2005;Liu et al, 2005). Changes occur within dopaminergic brain regions that are similar to those found in learning and memory studies, such as long-term potentiation and depression (LTP and LTD, respectively) (Bonci and Malenka, 1999;Thomas et al, 2000;Liu et al, 2005;Wolf et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Repeated cocaine effects on learning, memory and extinction in the pond snail Lymnaea stagnalis

Carter

Lukowiak

Schenk

et al. 2006

Journal of Experimental Biology

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SUMMARY The persistence of drug addiction suggests that drugs of abuse enhance learning and/or impair extinction of the drug memory. We studied the effects of repeated cocaine on learning, memory and reinstatement in the pond snail, Lymnaea stagnalis. Respiratory behavior can be operantly conditioned and extinguished in Lymnaea, and this behavior is dependent on a critical dopamine neuron. We tested the hypothesis that repeated cocaine exposure promotes learning and memory or attenuates the ability to extinguish the memory of respiratory behavior that relies on this dopaminergic neuron. Rotating disk electrode voltammetry revealed a Km and Vmax of dopamine uptake in snail brain of 0.9 μmol l-1 and 558 pmol s-1 g-1 respectively, and the IC50 of cocaine for dopamine was approximately 0.03 μmol l-1. For operant conditioning, snails were given 5 days of 1 h day-1 immersion in water (control) or 0.1 μmol l-1cocaine, which was the lowest dose that maximally inhibited dopamine uptake,and snails were trained 3 days later. No changes were found between the two groups for learning or memory of the operant behavior. However, snails treated with 0.1 μmol l-1 cocaine demonstrated impairment of extinction memory during reinstatement of the behavior compared with controls. Our findings suggest that repeated exposure to cocaine modifies the interaction between the original memory trace and active inhibition of this trace through extinction training. An understanding of these basic processes in a simple model system may have important implications for treatment strategies in cocaine addiction.

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“…An understanding of how these drugs initiate enhanced learning and memory is valuable from two perspectives: first, such drugs could be useful as cognitive enhancers in humans with memory impairments, and second, amphetamines as drugs of abuse are believed to produce persistent memory by inducing a type of pathological memory (Berke and Hyman, 2000;Hamilton and Kolb, 2005;Huang et al, 2009;Liu et al, 2005;O'Brien et al, 1992;Robinson and Kolb, 2004;Thomas et al, 2008;Wise, 2000;Wolf et al, 2004). Most of the focus on psychostimulants has been on the ability of amphetamines to enhance formation of several different forms of memory (Blaiss and Janak, 2006;Blaiss and Janak, 2007;Fenu and Di Chiara, 2003;Janak and Martinez, 1992;McGaugh, 2000;Oscos et al, 1988;Packard and Teather, 1998;Simon and Setlow, 2006;Wiig et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine enhances memory of operantly conditioned respiratory behavior in the snail Lymnaea stagnalis

Kennedy

Houmes

Wyrick

et al. 2010

Journal of Experimental Biology

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SUMMARYAmphetamines have been used as cognitive enhancers to promote learning and memory. Amphetamines are also drugs of abuse that may promote the initiation of strong memories that ultimately lead to addiction. To understand how methamphetamine (Meth) may be augmenting learning and memory, we chose a relatively simple system, the pond snail, Lymnaea stagnalis. We studied the effects of Meth exposure on the long-term memory (LTM), extinction and reinstatement of operantly conditioned aerial respiratory behavior in Lymnaea. We first determined doses of Meth that would acutely alter respiratory behavior. Next, we measured the impact of training snails in Meth solution or water (control group) using a training procedure that produces LTM (>6h) in control conditions. Meth exposure impaired the expression of LTM 21h after two training sessions, but this appeared to be a context-dependent effect only. However, snails exposed to 3.3mmoll -1 Meth during training had a decreased rate of extinction of the operantly conditioned memory. We then tested whether this decreased ability of snails to extinguish memory was due to enhanced LTM or impaired extinction of that memory. Snails were operantly conditioned in water and exposed to Meth 16h after their last trial but 4-5h prior to extinction. Meth produced an increase rather than a decrease in extinction rate. Thus, Meth impaired extinction only when snails were exposed to Meth during training. Last, we tested the effect of Meth on the ability to form LTM using a single training procedure that is suboptimal for LTM formation. Control snails did not demonstrate LTM, as expected, but pre-exposure of snails to 3.3mmoll -1 Meth 24h prior to the single training session produced LTM 24h later, indicating that Meth pre-exposure primed snails for LTM formation. Taken together, our studies suggest that LTM is strengthened by Meth such that extinction training is less effective. Lymnaea provides a simple and useful model system to dissect the cellular and/or molecular mechanisms of how Meth may initiate the formation of stronger memories.

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Differential Effects of Nicotine and Complex Housing on Subsequent Experience-Dependent Structural Plasticity in the Nucleus Accumbens.

Cited by 58 publications

References 46 publications

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

Repeated cocaine effects on learning, memory and extinction in the pond snail Lymnaea stagnalis

Methamphetamine enhances memory of operantly conditioned respiratory behavior in the snail Lymnaea stagnalis

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