Altered cocaine-induced behavioral sensitization in adult mice exposed to cocaine in utero

Crozatier, Claire; Guerriero, Réjean M.; Mathieu, Flavie; Giros, Bruno; Nosten‐Bertrand, Marika; Kosofsky, Barry E.

doi:10.1016/j.devbrainres.2003.10.006

Cited by 44 publications

(45 citation statements)

References 37 publications

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“…These results were in line with those obtained after prenatal exposure to cocaine (Collo et al, 2012), suggesting that some commonalities between nicotine and cocaine in generating structural plasticity of DAergic neurons can be related to the activation of D3R. Incidentally, prenatal exposure to nicotine and cocaine in human and rodents was associated with long-lasting postnatal neurobiological and behavioral effects (Crozatier et al, 2003;Bublitz and Stroud, 2012).…”

Section: Discussionsupporting

confidence: 77%

Nicotine-Induced Structural Plasticity in Mesencephalic Dopaminergic Neurons Is Mediated by Dopamine D3 Receptors and Akt-mTORC1 Signaling

et al. 2013

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Although long-term exposure to nicotine is highly addictive, one beneficial consequence of chronic tobacco use is a reduced risk for Parkinson's disease. Of interest, these effects both reflect structural and functional plasticity of brain circuits controlling reward and motor behavior and, specifically, recruitment of nicotinic acetylcholine receptors (nAChR) in mesencephalic dopaminergic neurons. Because the underlying cellular mechanisms are poorly understood, we addressed this issue with use of primary cultures of mouse mesencephalic dopaminergic neurons. Exposure to nicotine (1-10 mM) for 72 hours in vitro increased dendritic arborization and soma size in primary cultures. These effects were blocked by mecamylamine and dihydro-b-erythroidine, but not methyllycaconitine. The involvement of a4b2 nAChR was supported by the lack of nicotineinduced structural remodeling in neurons from a4 null mutant mice (KO). Challenge with nicotine triggered phosphorylation of the extracellular signal-regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mammalian target of rapamycin complex 1 (mTORC1)-dependent p70 ribosomal S6 protein kinase. Upstream pathway blockade using the phosphatidylinositol 3-kinase inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one hydrochloride] resulted in suppression of nicotine-induced phosphorylations and structural plasticity. These effects were dependent on functional DA D3 receptor (D3R), because nicotine was inactive both in cultures from D3R KO mice and after pharmacologic blockade with D3R antagonist trans-N-4-2-(6-cyano-1,2,3, 4-tetrahydroisoquinolin-2-yl)ethylcyclohexyl-4-quinolinecarboxamide (SB-277011-A) (50 nM). Finally, exposure to nicotine in utero (5 mg/kg/day for 5 days) resulted in increased soma area of DAergic neurons of newborn mice, effects not observed in D3 receptor null mutant mice mice. These findings indicate that nicotine-induced structural plasticity at mesencephalic dopaminergic neurons involves a4b2 nAChRs together with dopamine D3R-mediated recruitment of ERK/Akt-mTORC1 signaling.

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Section: Discussionsupporting

confidence: 77%

Nicotine-Induced Structural Plasticity in Mesencephalic Dopaminergic Neurons Is Mediated by Dopamine D3 Receptors and Akt-mTORC1 Signaling

et al. 2013

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“…However, as shown in Figure 9A, cocaine-induced increase in locomotor activity was higher in prenatal saline-treated group and lasted for a longer period than that found in the prenatal cocaine-treated group. This result is consistent with that obtained previously by using a mouse model of prenatal cocaine exposure (Crozatier et al, 2003). To further test the hypothesis that the reduced locomotor sensitivity to cocaine in prenatal cocaine-treated rats is related to dopamine system, we examine the effect of apomorphine, a dopamine receptor agonist, on the locomotor activity.…”

Section: Enhanced Excitatory Transmission and Neuronal Excitabilitysupporting

confidence: 77%

Cocaine ExposureIn UteroAlters Synaptic Plasticity in the Medial Prefrontal Cortex of Postnatal Rats

Lü¹,

Lim²,

Poo³

2009

J. Neurosci.

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Cocaine exposure during pregnancy causes abnormality in fetal brain development, leading to cognitive dysfunction of the offspring, but the underlying cellular mechanism remains mostly unclear. In this study, we examined synaptic functions in the medial prefrontal cortex (mPFC) of postnatal rats that were exposed to cocaine in utero, using whole-cell recording from mPFC layer V pyramidal neurons in acute brain slices. Cocaine exposure in utero resulted in a facilitated activity-induced long-term potentiation (LTP) of excitatory synapses on these pyramidal neurons and an elevated neuronal excitability in postnatal rat pups after postnatal day 15 (P15). This facilitated LTP could be primarily attributed to the reduction of GABAergic inhibition. Biochemical assays of isolated mPFC tissue from postnatal rats further showed that cocaine exposure in utero caused a marked reduction in the surface expression of GABA A receptor subunits ␣1, ␤2, and ␤3, but had no effect on glutamate receptor subunit GluR1. Both facilitated LTP and reduced surface expression of GABA A receptors persisted in rats up to at least P42. Finally, the behavioral consequence of cocaine exposure in utero was reflected by the reduction in the sensitivity of locomotor activity in postnatal rats to cocaine and the dopamine receptor agonist apomorphine. Since the mPFC is an important part of the reward circuit in the rat brain and plays important roles in cognitive functions, these findings offer new insights into the cellular mechanism underlying the adverse effects of cocaine exposure in utero on brain development and cognitive functions.

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“…The exaggerated and persistent increase in D 1 receptor-mediated intracellular signaling is a potential mechanism contributing to other behavioral and neuro-anatomical anomalies we and others have observed in adult mice following prenatal exposure to cocaine (e.g., 13,14). Despite such persistent neuro-adaptations it is clear that prenatal cocaine treatment does not affect the acute locomotor response to cocaine, similar to what has previously been seen at various postnatal ages (16,79,80). , and an increase in D 1 receptor phosphorylation in the striatum of rabbits prenatally exposed to cocaine.…”

Section: Enhanced D 1 Receptor Signalingmentioning

confidence: 51%

“…To control for some of these variables we created an animal model of prenatal cocaine exposure which has provided support for the role of cocaine independently contributing to some but not all of the clinical findings (reviewed in (10)). Of note,, rodents exposed to cocaine in utero display an altered response to drugs of abuse when tested as adults including impaired conditioned place preference (11,12), increased acquisition to (13,14) and enhanced reinforcing ability of cocaine (13,14) in self-administration tests, augmented brain stimulation reward following administration of cocaine and D 1 agonists (15), and enhanced stereotypy during cocaine induced behavioral sensitization (16).…”

Section: Introductionmentioning

confidence: 99%

Augmented D1 Dopamine Receptor Signaling and Immediate-Early Gene Induction in Adult Striatum After Prenatal Cocaine

Tropea

Guerriero

Willuhn

et al. 2008

Biological Psychiatry

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Background-Prenatal exposure to cocaine can impede normal brain development triggering a range of neuroanatomical and behavioral anomalies that are evident throughout life. Mouse models have been especially helpful in delineating neuro-teratogenic consequences following prenatal exposure tococaine. The present study employed a mouse model to investigate alterations in D 1 dopamine receptor signaling and downstream immediate-early gene induction in the striatum of mice exposed to cocaine in utero.

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Altered cocaine-induced behavioral sensitization in adult mice exposed to cocaine in utero

Cited by 44 publications

References 37 publications

Nicotine-Induced Structural Plasticity in Mesencephalic Dopaminergic Neurons Is Mediated by Dopamine D3 Receptors and Akt-mTORC1 Signaling

Nicotine-Induced Structural Plasticity in Mesencephalic Dopaminergic Neurons Is Mediated by Dopamine D3 Receptors and Akt-mTORC1 Signaling

Cocaine ExposureIn UteroAlters Synaptic Plasticity in the Medial Prefrontal Cortex of Postnatal Rats

Augmented D1 Dopamine Receptor Signaling and Immediate-Early Gene Induction in Adult Striatum After Prenatal Cocaine

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