ArticlePrenatal exposure to cocaine disrupts discrimination learning in adult rabbits
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The Homer1 family of proteins at the crossroad of dopamine-glutamate signaling: An emerging molecular “Lego” in the pathophysiology of psychiatric disorders. A systematic review and translational insight
2022, Neuroscience and Biobehavioral ReviewsCitation Excerpt :On the other hand, an increase of Homer2 versus Homer1 isoforms in ventromedial PFC strengthens the cocaine preference and produces glutamate abnormalities in the shell of NAc, resulting in enhanced rewarding and reinforcing properties of cocaine in mice (Ary et al., 2013). Of interest, prenatal cocaine exposure appears to be related to an increase in mGLuR1 phosphorylation by protein kinase C, which uncouples this receptor from Homer1 and its signaling cascade components during early brain development (Bakshi et al., 2014), with a subsequent negative impact on cognitive processes such as reduced attention, motor and language skills (Bandstra et al., 2002; Delaney-Black et al., 1996; Mayes et al., 1995; Romano and Harvey, 1996; Wang et al., 2013; Zhen et al., 2001). In summary, converging evidence suggests an active role for Homer proteins in regulating various aspects of plasticity that underlie addiction behaviours.
Sex mediates dopamine and adrenergic receptor expression in adult rats exposed prenatally to cocaine
2007, International Journal of Developmental NeuroscienceCitation Excerpt :Our demonstration of sex-mediated alterations in D1 receptor binding in animals exposed to cocaine in utero supports the hypothesis that prenatal cocaine exposure differentially alters the DA system(s) thought to subserve sustained attention in male and female rats. These alterations are congruent with Harvey and colleagues hypothesis of morphological alterations and reduced coupling of D1 receptors in the frontocingulate cortex (Harvey, 2004); and related to studies showing adverse effects of prenatal cocaine on attention demanding tasks (Romano and Harvey, 1996; for review see Harvey, 2004). Furthermore, these studies as well as results from the current investigation converge with research showing prenatal cocaine exposure alters “normal” D1 receptor function (e.g., Friedman and Wang, 1998), as well as research on the influence and alterations of D1 receptors associated with postnatal cocaine abuse (for review see Hummel and Unterwald, 2002).
A meta-analysis of animal studies on disruption of spatial navigation by prenatal cocaine exposure
2007, Neurotoxicology and TeratologyCitation Excerpt :This may reflect the existence of reports of significant effects of PCOC exposure at varying offspring ages at the time of testing. For example, several studies have reported PCOC-induced effects in behavioral, anatomical, and neurochemical measures in juvenile offspring [40,102], while there has also been numerous reports of PCOC-induced changes in these measures which are long-lasting and persist into adulthood [11,25,58,62,73]. Relevant to animal models of PCOC exposure, the lone study with mice [41] displayed a more intense effect of prenatal treatment when compared to studies using rat models, finding increased latencies in the acquisition training in PCOC-exposed offspring.
Prenatal cocaine exposure enhances responsivity of locus coeruleus norepinephrine neurons: Role of autoreceptors
2007, NeuroscienceCitation Excerpt :The Maudsley reactive strain has a greater reactivity to stress than rats from the Maudsley non-reactive strain (Broadhurst, 1975), and investigations of the basis for this behavioral difference have revealed that the reactive strain has 30–40% less [125I]para-iodoclonidine binding sites in the LC (Sara et al., 1993), a decreased behavioral response to clonidine (Sara et al., 1993), and an increased noradrenergic response to stress (Buda et al., 1994). Thus, these studies support the contention that the degree of loss of α2-adrenergic binding observed in rats exposed to prenatal cocaine may be linked with the altered Fos and NE turnover measures reported here, and play a role in the altered behavior documented in other studies (Romano and Harvey, 1996; Spear et al., 1998; Garavan et al., 2000; Morrow et al., 2002; Gabriel et al., 2003; Thompson et al., 2005). In contrast to the finding in the LC, there was no difference between the groups in [125I]-p-iodoclonidine binding in the parabrachial nucleus.
Pharmacokinetic profile of cocaine following intravenous administration in the female rabbit
2007, European Journal of Pharmacology