Postnatal Development of Dopamine D&lt;sub&gt;1&lt;/sub&gt;-Like Receptors in Rat Cortical and Striatolimbic Brain Regions: An Autoradiographic Study

Tarazi, Frank I.; Tomasini, Eric C.; Baldessarini, R. J.

doi:10.1159/000017365

Cited by 152 publications

(123 citation statements)

References 42 publications

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“…Although all of the neurochemical "machinery" for dopaminergic transmission is present soon after birth, a number of indices of dopamine function change markedly during adolescence. Overexpression of dopamine D 1 , D 2 and D 4 receptors and subsequent decreases during adolescence have been reported in several studies [3,47,[65][66][67]. Such pruning has also been shown in postmortem studies of adolescent human brain for receptors and the dopamine transporter [44,57].…”

Section: Introductionmentioning

confidence: 71%

“…The mean age and range on the day of the experiment was 28 (27)(28)(29)(30) and 68 (60)(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77) for the PN28 and PN65 groups, respectively. Varying the frequency of electrical stimulation evokes steady-state responses at low frequencies (20 Hz) as uptake and release are balanced, and linear increases at high frequencies (60 Hz) as release overwhelms uptake.…”

Section: Resultsmentioning

confidence: 99%

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Cocaine increases stimulated dopamine release more in periadolescent than adult rats

Walker

Kuhn

2008

Neurotoxicology and Teratology

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The neural mechanisms responsible for the enhanced adolescent vulnerability for initiating drug abuse are unclear. We investigated whether age differences in dopamine neurotransmission could explain cocaine's enhanced psychomotor effects in the periadolescent rat. Electrical stimulation the medial forebrain bundle of anesthetized post-natal age 28 days (PN28) and PN65 rats elicited dopamine release in caudate nucleus and nucleus accumbens core before and after 15 mg/kg cocaine i.p. Extracellular dopamine concentrations were greater in PN65 than PN28 caudate following 20 and 60Hz stimulations and in the PN65 nucleus accumbens following 60Hz stimulations. Cocaine increased dopamine concentrations elicited by 20 Hz stimulations 3-fold in the adult, but almost 9-fold in periadolescent caudate. Dopamine release rate was lower in the periadolescent caudate although total dopamine clearance was similar to that of adults. The periadolescent caudate achieved adult levels of clearance by compensating for a lower V max with higher uptake affinity. Tighter regulation of extracellular dopamine by the higher uptake/release ratio in periadolescents led to greater increases after cocaine. In nucleus accumbens, dopamine release and V max were lower in periadolescents than adults, but uptake affinity and cocaine effects were similar. Immaturity of dopamine neurotransmission in dorsal striatum may underlie enhanced acute responses to psychostimulants in adolescent rats and suggests a mechanism for the greater vulnerability of adolescent humans to drug addiction.

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Section: Introductionmentioning

confidence: 71%

Section: Resultsmentioning

confidence: 99%

Cocaine increases stimulated dopamine release more in periadolescent than adult rats

Walker

Kuhn

2008

Neurotoxicology and Teratology

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“…This is one of only a limited number of investigations into the molecular underpinnings of age-related differential responses to psychostimulants, likely related to the increased plasticity of the brain during this period of extensive remodeling (Spear, 2000). Highly relevant to these studies is the literature documenting fluxes in levels of molecules identified as key mediators of cocaine's actions, including components of both the dopamine (Ehrlich et al, 1990;Tarazi et al, 1999) and neurotrophin BDNF (Ringstedt et al, 1993;Yurek et al, 1998;Costantini et al, 1999) pathways.…”

Section: Discussionmentioning

confidence: 99%

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

Niculescu¹,

Perrine²,

Miller³

et al. 2008

J. Neurosci.

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Responses to psychostimulants vary with age, but the molecular etiologies of these differences are largely unknown. The goal of the present research was to identify age-specific behavioral and molecular adaptations to cocaine and to elucidate the mechanisms involved therein. Postweanling, periadolescent, and adult male CD-1 mice were exposed to cocaine (20 mg/kg) for 7 d. The rewarding effects of cocaine were assessed, as were the response to a Trk antagonist and the regulation of dopamine and cAMP-regulated phosphoprotein, 32 kDa (DARPP-32). Cocaine was rewarding in both periadolescent and adult mice using a conditioned place preference procedure. In contrast, postweanling mice failed to demonstrate significant cocaine-induced place preference. Because components of the neurotrophin system including brain-derived neurotrophic factor and TrkB are developmentally regulated, their role in the age-specific effects of cocaine was determined using the Trk receptor antagonist K252a. Postweanling mice that received K252a before daily cocaine showed a significant place preference to the cocaine-paired environment that was not seen in the absence of K252a. DARPP-32 protein levels were significantly upregulated in the lateral region of the caudate-putamen exclusively in postweanling mice after chronic cocaine. Daily pretreatment with K252a attenuated the induction of DARPP-32 in the postweanling striatum. These data indicate that Trk neurotransmission plays a role in age-specific behavioral and molecular responses to cocaine and concurrently modulates DARPP-32 levels.

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“…In particular, the prefrontal cortex (PFC)-basolateral amygdala (BLA)-nucleus accumbens (NAc) triadic circuit, responsible for reward and motivated behavior, is dynamically developing during this period, as are its monoamine afferents (Ernst et al, 2006;Ernst and Fudge, 2009). Mesolimbic DA systems, which are integral to cocaine selfadministration and locomotor sensitization (Thomas et al, 2008), undergo major reorganization during adolescence (Tarazi et al, 1999;Cao et al, 2007b;Benoit-Marand and O'Donnell, 2008;Brenhouse et al, 2008;Andersen et al, 2000) and exhibit unique sensitivity to nicotine (Azam et al, 2007). Less is known about the adolescent maturation of 5-HT systems, which have a significant role in cocaine selfadministration (Rocha et al, 1997;Rodd et al, 2005;Fletcher et al, 2002) and locomotor sensitization (Tassin, 2008).…”

Section: Introductionmentioning

confidence: 99%

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Dao

McQuown

Loughlin

et al. 2011

Neuropsychopharmacol

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Epidemiological studies have shown that adolescent smoking is associated with health risk behaviors, including high-risk sexual activity and illicit drug use. Using rat as an animal model, we evaluated the behavioral and biochemical effects of a 4-day, low-dose nicotine pretreatment (60 mg/kg; intravenous) during adolescence and adulthood. Nicotine pretreatment significantly increased initial acquisition of cocaine self-administration, quinpirole-induced locomotor activity, and penile erection in adolescent rats, aged postnatal day (P)32. These effects were long lasting, remaining evident 10 days after the last nicotine treatment, and were observed when nicotine pretreatment was administered during early adolescence (P28-31), but not late adolescence (P38-41) or adulthood (P86-89). Neurochemical analyses of c-fos mRNA expression, and of monoamine transmitter and transporter levels, showed that forebrain limbic systems are continuing to develop during early adolescence, and that this maturation is critically altered by brief nicotine exposure. Nicotine selectively increased c-fos mRNA expression in the nucleus accumbens shell and basolateral amygdala in adolescent, but not adult animals, and altered serotonin markers in these regions as well as the prefrontal cortex. Nicotine enhancement of cocaine self-administration and quinpirole-induced locomotor activity was blocked by co-administration of WAY 100 635 (N-{2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl}-N-(2-pyridinyl)cyclohexanecarboxamide), a selective serotonin 1A (5-HT1A) receptor antagonist. Early adolescent pretreatment with the mixed autoreceptor/heteroceptor 5-HT1A receptor agonist, 8-OH-DPAT, but not the autoreceptor-selective agonist, S-15535, also enhanced quinpirole-induced locomotor activation. Nicotine enhancement of quinpirole-induced penile erection was not blocked by WAY 100 635 nor mimicked by 8-OH-DPAT. These findings indicate that early adolescent nicotine exposure uniquely alters limbic function by both 5-HT1A and non-5-HT1A receptor mechanisms.

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Postnatal Development of Dopamine D<sub>1</sub>-Like Receptors in Rat Cortical and Striatolimbic Brain Regions: An Autoradiographic Study

Cited by 152 publications

References 42 publications

Cocaine increases stimulated dopamine release more in periadolescent than adult rats

Cocaine increases stimulated dopamine release more in periadolescent than adult rats

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

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