Persistent downregulation of hippocampal CREB mRNA parallels a Y‐maze deficit in adolescent rats following semi‐chronic amphetamine administration

Featherby, Travis; Buuse, Maarten van den; Lubman, Dan I.; Lawrence, Andrew J

doi:10.1038/bjp.2008.126

Cited by 24 publications

(21 citation statements)

References 59 publications

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“…The reduction in grooming responses observed in the juvenile rats is consistent with a number of other reports documenting behavioural subsensitivity in response to psychostimulant drugs in younger animals (Bolanos et al, 1998, Featherby et al, 2008, Banerjee et al, 2009, Zakharova et al, 2009a). The underlying mechanisms contributing to this subsensitivity have remained elusive, and are further complicated by evidence showing that adolescents exhibit enhanced, and not diminished, dopamine release following amphetamine or cocaine administration (Laviola et al, 2001, Walker and Kuhn, 2008) and increased sensitivity to dopamine transporter blockade by cocaine (Bolanos et al, 1998).…”

Section: Discussionsupporting

confidence: 90%

Reduced striatal dopamine D1–D2 receptor heteromer expression and behavioural subsensitivity in juvenile rats

et al. 2012

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In adult rat striatum the dopamine D1-D2 receptor heteromer is expressed selectively in a subset of medium spiny neurons (MSNs) that coexpress the dopamine D1 and D2 receptors (D1R and D2R) as well as dynorphin (DYN) and enkephalin (ENK), with higher coexpression in nucleus accumbens (NAc) and much lower in the caudate putamen (CP). In the present study we showed that in neonatal striatal cultured neurons >90% exhibited the D1R/D2R-DYN/ENK phenotype. Similarly, in the striatum of juvenile rats (age 26-28 days) coexpression of D1R and D2R was also coincident with expression of both DYN and ENK. Quantification of the number of striatal MSNs exhibiting coexpression of D1R and D2R in juvenile rats revealed significantly lower coexpression in NAc shell, but not core, and CP than in adult rats. However, within MSNs that coexpressed D1R and D2R, the propensity to form the D1-D2 receptor heteromer did not differ between age groups. Consistent with reduced coexpression of the D1R and D2R, juvenile rats exhibited subsensitivity to D1-D2 receptor heteromer-induced grooming following activation by SKF 83959. Given the proposed role of D1R/D2R-coexpressing MSNs in the regulation of thalamic output, and the recent discovery that these MSNs exhibit both inhibitory and excitatory capabilities, these findings suggest that the functional regulation of neurotransmission by the dopamine D1-D2 receptor heteromer within the juvenile striatum may be significantly different than in the adult.

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Section: Discussionsupporting

confidence: 90%

Reduced striatal dopamine D1–D2 receptor heteromer expression and behavioural subsensitivity in juvenile rats

et al. 2012

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“…Accordingly, new experimental therapeutics provide correlation between reduction of neuroinflammation and improved cognitive impairment in Alzheimer's disease [45]. Interestingly, behavioral changes associated with amphetamine treatment during adolescence are cognitive deficits [31]. Our data demonstrate that periadolescent amphetamine treatment has modest consequences in WT mice in the Y-maze test but causes a transient disruption of the working memory in the Y-maze in MK−/− mice.…”

Section: Discussionmentioning

confidence: 80%

“…These processes have been related to the cognitive deficits caused by amphetamines abuse in humans [6]. Thus, we next tested the possibility that endogenous MK modulates the cognitive effects caused by a 10-day amphetamine treatment during adolescence, a stage especially vulnerable to the cognitive deficits induced by these drugs [23, 31]. Six days after the last amphetamine (or saline) administration, we assessed for the first time the behavior of six-week-old mice from both genotypes on the Y-maze (Figure 6).…”

Section: Resultsmentioning

confidence: 99%

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

Vicente-Rodríguez

Fernández-Calle

Gramage

et al. 2016

Mediators of Inflammation

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Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine. To test this hypothesis, we studied astrogliosis and microglial response induced by amphetamine (10 mg/kg i.p. four times, every 2 h) in different brain areas of MK−/− mice and wild type (WT) mice. We found that amphetamine-induced microgliosis and astrocytosis are enhanced in the striatum of MK−/− mice in a region-specific manner. Surprisingly, LPS-induced astrogliosis in the striatum was blocked in MK−/− mice. Since striatal neuroinflammation induced by amphetamine-type stimulants correlates with the cognitive deficits induced by these drugs, we also tested the long-term effects of periadolescent amphetamine treatment (3 mg/kg i.p. daily for 10 days) in a memory task in MK−/− and WT mice. Significant deficits in the Y-maze test were only observed in amphetamine-pretreated MK−/− mice. The data demonstrate for the first time that MK is a novel modulator of neuroinflammation depending on the inflammatory stimulus and the brain area considered. The data indicate that MK limits amphetamine-induced striatal neuroinflammation. In addition, our data demonstrate that periadolescent amphetamine treatment in mice results in transient disruption of learning and memory processes in absence of endogenous MK.

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“…The Y-maze is a working memory task that is cortically- and hippocampally-mediated (Dillon et al, 2008; Featherby et al, 2008; Wagner et al, 2007). Performance in the Y-maze was significantly influenced by reproductive function [ F (1,44) = 5.25, p < 0.05].…”

Section: Resultsmentioning

confidence: 99%

II. Cognitive performance of middle-aged female rats is influenced by capacity to metabolize progesterone in the prefrontal cortex and hippocampus

2011

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Cognitive decline can occur with aging; however, some individuals experience less cognitive decline than do others. Secretion of ovarian hormones is reduced post-menopause and may contribute to cognitive function. The extent to which hormonal effects may be parsed out from other age-related factors to influence cognition is of interest. Middle aged (12-month-old) female rats that were retired breeders were categorized as maintaining or declining reproductive function based upon their estrous cyclicity (regular 4-5 day cycles), fertility (> 60 % successful pregnancy) and fecundity (> 10 pups/litter). Performance in object recognition, Y-maze, water maze, inhibitory avoidance, and contextual/cued fear conditioning was evaluated. Estradiol, progesterone (P4), dihydroprogesterone, and 5α-pregnan-3α-ol-20-one (3α,5α-THP) were assessed in medial prefrontal cortex (mPFC) and hippocampus: corticosterone was assessed in plasma. Rats maintaining reproductive function performed significantly better on the object recognition, Y-maze, water maze, inhibitory avoidance, and cued fear conditioning tasks, than did rats with declining reproductive function. Steroid concentrations varied greatly within groups. Higher levels of P4 in mPFC and hippocampus were associated with better Y-maze performance. In mPFC, higher levels of P4 were associated with poorer inhibitory avoidance performance: greater levels of 3α,5α-THP were associated with better object memory. Neither estradiol, nor corticosterone, levels significantly contributed to cognitive performance. Thus, the capacity for cortico-limbic P4 utilization may influence cognitive performance in aging.

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Persistent downregulation of hippocampal CREB mRNA parallels a Y‐maze deficit in adolescent rats following semi‐chronic amphetamine administration

Cited by 24 publications

References 59 publications

Reduced striatal dopamine D1–D2 receptor heteromer expression and behavioural subsensitivity in juvenile rats

Reduced striatal dopamine D1–D2 receptor heteromer expression and behavioural subsensitivity in juvenile rats

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

II. Cognitive performance of middle-aged female rats is influenced by capacity to metabolize progesterone in the prefrontal cortex and hippocampus

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