Postnatal development of D 1 dopamine receptors in the medial prefrontal cortex, striatum and nucleus accumbens of normal and neonatal 6-hydroxydopamine treated rats: a quantitative autoradiographic analysis

Leslie, Catherine Amoroso; Robertson, Matthew; Cutler, Andrew J.; Bennett, James P.

doi:10.1016/0165-3806(91)90195-o

Cited by 116 publications

(93 citation statements)

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“…Expression was characteristically higher in young animals relative to older animals, regardless of genotype [main effect of age F (1,27) ϭ 10.1, P ϭ 0.004; F (1,33) ϭ 88.4, P Ͻ 0.001] (17,18), and fold change calculations indicated adult arg Ϫ/Ϫ mice experienced greater age-related pruning of D1 and D2 than wt mice (t 16 ϭ Ϫ3.1, P ϭ 0.007; t 22 ϭ Ϫ3.5, P ϭ 0.002) (Fig. 1C).…”

Section: Prefrontal Postsynaptic Density Protein 95 and Dopamine Recementioning

confidence: 99%

Loss of dendrite stabilization by the Abl-related gene (Arg) kinase regulates behavioral flexibility and sensitivity to cocaine

Gourley

Koleske

Taylor

2009

Proc. Natl. Acad. Sci. U.S.A.

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Adolescence is characterized by increased vulnerability to developing neuropsychiatric disorders and involves a period of prefrontal cortical dendritic refinement and synaptic pruning that culminates in cytoskeletal stabilization in adulthood. The Abl-related gene (Arg) acts through p190RhoGAP to inhibit the RhoA GTPase and stabilize cortical dendritic arbors beginning in adolescence. Cortical axons, dendrites, and synapses develop normally in Argdeficient (arg ؊/؊ ) mice, but adult dendrites destabilize and regress; thus, arg ؊/؊ mice present a model of adolescent-onset dendritic simplification. We show that arg ؊/؊ mice are impaired in a reversal task and that deficits are grossly exacerbated by low-dose cocaine administration. Although ventral prefrontal dopamine D2 receptor levels predict ''perseverative'' error counts in wild-type mice, no such relationship is found in arg ؊/؊ mice. Moreover, arg ؊/؊ mice are insensitive to the disruptive effects of the D2/D3 antagonist haloperidol in reversal but show normal sensitivity to its locomotor-depressant actions. Arg deficiency and orbitofrontal cortical Arg inhibition via STI-571 infusion also enhance the psychomotor stimulant actions of cocaine. These findings provide evidence that stabilization of dendritic structure beginning in adolescence is critical for the development of adaptive and flexible behavior after cocaine exposure.A dolescence is a critical period of maturation for corticostriatal neurocircuitry and is characterized by increased risk taking, novelty seeking, and vulnerability to addictive drugs that, with repeated use, are associated with cognitive dysfunction in adulthood (1-3). In utero cocaine exposure has limited effects on cognitive performance in adult rodents (4-6), but adolescent and adult cocaine use is associated with poor inhibitory control, inflexible behavior, and drug-related compulsivity. Here, we use an animal model of late-onset dendritic simplification to test the hypothesis that the transition from dendritic refinement and synaptic pruning processes that occur in the adolescent prefrontal cortex (PFC), to the dendrite stabilization processes occurring in the adult PFC, is a period of vulnerability to cocaine.Numerous proteins regulate cortical dendrite development; to date, however, only a few have been implicated in cytoskeletal stability in adolescence and adulthood, serving primarily to antagonize inherent cytoskeletal retraction machinery. For example, activation of the master cytoskeletal regulator, RhoA (Rho), induces neurite retraction, a process required for pruning and refining neuronal connections during development. Rho activation in mature neurons, however, leads to synapse loss and dendritic regression in a wide variety of experimental systems (7-9). Recent studies have identified a Rho inhibitory pathway involving integrin adhesion receptors, the Abl family tyrosine kinase, Arg, and the Rho inhibitor, p190RhoGAP, that acts in dendritic spines of late adolescent mice to maintain synapses and promote dendrite stabi...

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Section: Prefrontal Postsynaptic Density Protein 95 and Dopamine Recementioning

confidence: 99%

Loss of dendrite stabilization by the Abl-related gene (Arg) kinase regulates behavioral flexibility and sensitivity to cocaine

Gourley

Koleske

Taylor

2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Among the numerous alterations seen in mesocorticolimbic brain regions during adolescence are regionally specific ontogenetic alterations in patterns of DA production and utilization, with estimates of DA synthesis and turnover in PFC being higher early in adolescence than later in adolescence and in adulthood, whereas DA synthesis and/or turnover estimates in nucleus accumbens and striatum conversely are lower earlier than late in adolescence (e.g., Teicher et al, 1993;Andersen et al, 1997, although see also Leslie et al, 1991). Stressors would likely exacerbate the shift in DA balance toward even greater mesocortical than mesolimbic/striatal DA activity during early adolescence, given the greater sensitivity of the mesocortical DA projection system to activation by stressors (Dunn, 1988).…”

Section: The Neuroscience Of Adolescencementioning

confidence: 99%

Assessment of adolescent neurotoxicity: Rationale and methodological considerations

Spear

2007

Neurotoxicology and Teratology

103

106

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This introduction to the special issue of Neurotoxicology and Teratology on "Risk of neurobehavioral toxicity in adolescence" begins by broadly considering the ontogeny and phylogeny of adolescence, and the potential value of animal models of adolescence. Major findings from the emerging neuroscience of adolescence are then highlighted to establish the importance of studies of adolescent neurotoxicity. A variety of methodological issues that are of particular relevance to adolescent exposures are then discussed. These include consideration of pharmacokinetic factors, inclusion of other-aged comparison group(s), and issues involving timing, route of administration, and exposureinduced alterations in growth rate. Despite such methodological challenges, research to determine whether adolescence is a time of increased vulnerability (or greater resiliency) to specific drugs and environmental toxicants is progressing rapidly, as exemplified by the work presented in the articles of this special issue. Keywordsadolescence; neurotoxicity; behavior; animal models; brain sculpting; pharmacokinetics; drug metabolism; body weight; methodology Most of what we know about neural and behavioral consequences of developmental exposure to drugs and other chemicals is based on exposures during the prenatal and early postnatal period, with little emphasis on exposure periods that subsume adolescence. With the increasing recognition that adolescence is a time of considerable neural restructuring and sculpting of the brain (for review, see Spear, 2000), there likewise has been a growing interest in assessing whether this developmental transition is a vulnerable period for neurotoxicity. This special issue is designed to highlight research examining "the question of whether adolescence is a…. (time) of enhanced neurobehavioral toxic risk associated with exposure to drugs of abuse, therapeutic drugs, hormones and environmental toxicants." By presenting examples of the emerging research in this area, the goal of the special issue is to encourage additional high quality work in this area, and to draw attention to Neurotoxicology and Teratology as an outlet for this research.

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“…The frontal cortex in the rodent receives input from dopaminergic nuclei throughout postnatal development (Berger et al, 1983. Dopaminergic innervation density (Verney et al, 1982;Kalsbeek et al, 1988), concentrations (Chen et al, 1997) and receptor mRNA expression (Leslie et al, 1991;Schambra et al, 1994) peak postnatally, when parvalbumin expression is nearly mature. In fact, the entire population of GABAergic neurons continues to undergo dendritic differentiation through postnatal weeks two to three (Vincent et al, 1995).…”

Section: Dopamine Enhances Parvalbumin Expressionmentioning

confidence: 99%

“…Interestingly, DA receptor expression also peaks late, around 14-21 days postnatal (Leslie et al, 1991;Schambra et al, 1994). The concentrations of tyrosine hydroxylase (TH), the rate limiting enzyme for DA production, fluctuates developmentally in the rodent frontal cortex but, its highest level occurs at approximately 15 days postnatal (Chen et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Dopamine and Estrogen upon Cortical Parvalbumin Expression

Ross¹

2001

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Physiology and Genetics, and the Neuroscience ProgramEstrogen plays a protective role in several neurologic disorders known to involve alterations in both the dopamine system and (gamma amino butyric acid containing) GABAergic neurons that contain parvalbumin. Two studies were conducted to identify the effects of estrogen and dopamine upon cortical parvalbumin expression. In the first study, organotypic slice cultures of the frontal cortex were prepared from male rats (postnatal age 2/3) and maintained for 14 days in serum-enriched medium or media containing either: dopamine, estrogen, or a combination of the two. In control slices, parvalbumin immunoreactive neurons were primarily clustered near cortical layer V. All treatment conditions increased the distribution of parvalbumin labeled neurons in layer VI and enhanced the maturation of dendritic measures of labeled neurons in the deep layers (V-VI). Both estrogen and the combination treatment induced similar alterations in the superficial cortical layers, as well. In the second study, gonadectomy (male rats, postnatal age 2) induced long lasting decreased in the density of parvalbumin immunoreactive neurons throughout all cortical layers. Estrogen replacement restored parvalbumin expression to control levels in the superficial cortical layers, only. Gonadectomy also Report Documentation PageForm Public reporting burden for the collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to a penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. Estrogen plays a protective role in several neurologic disorders known to involve alterations in both the dopamine system and (gamma amino butyric acid containing) GABAergic neurons that contain parvalbumin. Two studies were conducted to identify the effects of estrogen and dopamine upon cortical parvalbumin expression. In the first study, organotypic slice cultures of the frontal cortex were prepared from male rats (postnatal age 2/3) and maintained for 14 days in serum-enriched medium or media containing either: dopamine, estrogen, or a combination of the two. In control slices, parvalbumin immunoreactive neurons were primarily clustered near cortical layer V. All treatment conditions increased the distribution of parvalbumin labeled neurons in layer VI and enhanced the maturation of dendritic measures of labeled neurons in the deep layers (V-VI). Both estrog...

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Postnatal development of D 1 dopamine receptors in the medial prefrontal cortex, striatum and nucleus accumbens of normal and neonatal 6-hydroxydopamine treated rats: a quantitative autoradiographic analysis

Cited by 116 publications

References 42 publications

Loss of dendrite stabilization by the Abl-related gene (Arg) kinase regulates behavioral flexibility and sensitivity to cocaine

Loss of dendrite stabilization by the Abl-related gene (Arg) kinase regulates behavioral flexibility and sensitivity to cocaine

Assessment of adolescent neurotoxicity: Rationale and methodological considerations

The Effects of Dopamine and Estrogen upon Cortical Parvalbumin Expression

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