• We hypothesize that synaptic remodeling and changes of homeostasis in the medial prefrontal cortex (mPFC) following adolescent cocaine exposure may last for a long time, and these modifications may contribute to behavioral deficiencies in adulthood. (springer.com)
  • SIGNIFICANCE STATEMENT We show that cocaine-evoked synaptic changes onto ventral tegmental area (VTA) dopamine (DA) neurons leads to long-lasting increases in their burst firing. (jneurosci.org)
  • This study directly links synaptic changes to increased intrinsic excitability of VTA DA neurons after cocaine, and explains how acute cocaine induces long-lasting remodeling of the mesolimbic DA system. (jneurosci.org)
  • Cocaine exposure also resulted in decreased expression of the synaptic plasticity gene, Arc as evidenced by Western blotting. (thescipub.com)
  • Synaptic changes demonstrated that 5 d of cocaine exposure increased the inhibition of FSIs, potentially reducing the inhibition of pyramidal neurons and contributing to their hyperexcitability during relapse behavior. (eneuro.org)
  • Our studies highlight the impact of cocaine on PV and PNN levels and the intrinsic and synaptic properties of PNN-surrounded FSIs in the mPFC. (eneuro.org)
  • Finally, many results indicate that the state of synaptic transmission in the NAc after cocaine exposure is associated with impairment of AMPAR-dependent plasticity. (nih.gov)
  • METHODS: This is a secondary analysis of data from a multicenter project, the Maternal Lifestyle Study, designed to determine infant outcomes of in utero cocaine or opiates exposure. (rti.org)
  • CONCLUSION: In utero cocaine exposure is associated with growth deceleration involving all measurements, becoming more pronounced with advancing gestation. (rti.org)
  • The literature from multiple disciplines on in utero cocaine exposure and mother-infant interaction and attachment was examined for possible relationships and implications for occupational therapists. (aota.org)
  • Caffino L, Giannotti G, Malpighi C, Racagni G, Filip M, Fumagalli F (2014) Long-term abstinence from developmental cocaine exposure alters Arc/Arg3.1 modulation in the rat medial prefrontal cortex. (springer.com)
  • Caffino L, Calabrese F, Giannotti G, Barbon A, Verheij MM, Racagni G, Fumagalli F (2015a) Stress rapidly dysregulates the glutamatergic synapse in the prefrontal cortex of cocaine-withdrawn adolescent rats. (springer.com)
  • Prefrontal cortex (PFC)-dependent functions, such as executive function, explicit learning, and memory, are negatively affected in cocaine abusers and experimental animal models of cocaine treatment. (frontiersin.org)
  • To understand the possible mechanisms underlying cocaine-induced apoptosis in the developing brain, we measured the activities of caspase-3, caspase-8, and caspase-9 and examined the effects of cocaine on Bax and Bcl-2 protein expression in fetal rat brain. (medsci.org)
  • No additional suppression of GABA B R-Girk signaling was observed following repeated cocaine administration. (jneurosci.org)
  • In the present study, we performed transcriptome profiling of the dynamic changes in the PFC after repeated cocaine administration in mice. (frontiersin.org)
  • Methods: We applied surface-based anatomical modeling methods to magnetic resonance imaging (MRI) data to examine regional changes in the shape and volume of the caudate and putamen in adolescents with prenatal cocaine exposure (n = 40, including 28 exposed participants and 12 unexposed controls, age range 14 to 16 years). (ufl.edu)
  • Chronic cocaine treatment increases usage of the promoter encoding the Δ-Kalirin isoforms but does not alter full-length Kalirin promoter usage. (biomedcentral.com)
  • Usage of the 3'-terminal exon unique to Kalirin 7 increases following chronic cocaine exposure. (biomedcentral.com)
  • We found 463, 14, and 535 differentially expressed genes (DEGs) at 2 h, 24 h, and 7 days, respectively, after the withdrawal of chronic cocaine treatment. (frontiersin.org)
  • Our study found significant cognitive deficits with cocaine-exposed children twice as likely to have significant delay throughout the first 2 years of life. (drugwarfacts.org)
  • Thus cocaine-mediated changes in alternative splicing of the Kalrn gene may contribute importantly to the behavioral, morphological and biochemical responses observed. (biomedcentral.com)
  • Decreased volume of the thalamus and putamen, but not the cerebral cortex, was correlated with the reported level of maternal cocaine abuse. (drugabuse.gov)
  • Most recent studies have further suggested that maternal cocaine exposed may increase cell death in the fetal nervous system [ 23 - 25 ]. (medsci.org)
  • 24 ] has detected cocaine exposure-induced changes in expression of some apoptosis-related genes in the fetal mouse cerebral wall by microarray analysis and demonstrated that maternal cocaine exposure could influence transcriptional expression levels of multiple apoptosis related genes in fetal cerebral wall. (medsci.org)
  • The acute cocaine-induced weakening of somatodendritic Girk signaling complements the previously demonstrated cocaine-induced strengthening of glutamatergic neurotransmission, likely contributing to enhanced output of VTA DA neurons during the early stages of addiction. (jneurosci.org)
  • For acute cocaine studies, mice (4-5 weeks) were acclimated over a 4 d period to handling and open-field chambers (1 h/d), receiving saline injections on days 3 (s 1 ) and 4 (s 2 ). (jneurosci.org)
  • Caffino L, Giannotti G, Malpighi C, Racagni G, Fumagalli F (2015b) Short-term withdrawal from developmental exposure to cocaine activates the glucocorticoid receptor and alters spine dynamics. (springer.com)
  • Caffino L, Giannotti G, Mottarlini F, Racagni G, Fumagalli F (2017a) Developmental exposure to cocaine dynamically dysregulates cortical Arc/Arg3.1 Modulation in response to a challenge. (springer.com)
  • Thus the circadian system might be at the core of the developmental effects of cocaine and their inter-individual variability, she added. (bio-medicine.org)
  • According to Zhdanova, circadian factors, including melatonin, could provide new therapeutic strategies to counteract the developmental effects of prenatal cocaine exposure. (bio-medicine.org)
  • Early studies in the mid-1980s reported that cocaine use in pregnancy caused children to have severe problems including cognitive, developmental, and emotional disruption. (wikipedia.org)
  • It has been well documented that drugs of abuse such as cocaine can cause enhanced progression of HIV-Associated Neuropathological Disorders (HAND), the underlying mechanisms mediating these effects remain poorly understood. (thescipub.com)
  • In GluN3A knock-out mice, cocaine did not alter SK channel function or VTA DA neuron firing. (jneurosci.org)
  • A previous study demonstrated that cocaine induced apoptosis in cultured cortical neuronal cells of fetal mice [ 22 ]. (medsci.org)
  • Adult rats were exposed to 1 or 5 d of cocaine and stained for PNNs (using Wisteria floribunda agglutinin) and PV intensity 2 or 24 h later. (eneuro.org)
  • After controlling for confounders, at 40 weeks' gestation, cocaine exposure was estimated to be associated with a decrease of 151 g, 0.71 cm, and 0.43 cm in birth weight, length, and head circumference, respectively. (rti.org)
  • The mPFC is critical to relapse in cocaine addiction, yet few studies have focused on the impact of cocaine exposure on PV interneurons that profoundly control the output of the mPFC. (eneuro.org)
  • Then, we provide a detailed and critical analysis of literature demonstrating alterations in AMPAR transmission in association with behavioral sensitization to cocaine and cocaine self-administration. (nih.gov)
  • These early and rapid responses to cocaine may alter the network stability of PV FSIs that partially mediate the persistent and chronic nature of drug addiction. (eneuro.org)
  • We conclude that cocaine exposure leads to changes in AMPAR transmission that depend on many factors including whether exposure is contingent or non-contingent, the duration of withdrawal, and whether extinction training has occurred. (nih.gov)
  • After a careful 'review' of the data a few 'outliers' were removed and the data fell into line with expectations… That is not to say that cocaine (or any drug for that matter) is safe to consume while pregnant. (drugs-forum.com)
  • Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thereby exposes her fetus to the drug. (wikipedia.org)
  • Pregnant rats were treated with cocaine subcutaneously (30 & 60 mg/kg/day) from day 15 to 21 of gestation. (medsci.org)
  • Cocaine, for example, can readily cross the placenta and directly impact critical neurotransmitter systems in the fetal brain, including dopamine, serotonin, and norepinephrine systems. (drugabuse.gov)
  • The present study was to determine whether prenatal cocaine exposure induced apoptosis and the possible role of Bcl-2 family genes in the programming cell death in fetal rat brain. (medsci.org)
  • The increased apoptosis of neuronal cells in the fetal brain is likely to play a key role in cocaine-induced neuronal defects during fetal development. (medsci.org)
  • The present study was therefore designed to test the hypothesis that maternal administration of cocaine during pregnancy caused apoptotic cell death in fetal rat brain. (medsci.org)
  • Unexpected, the expression of molecules related to oxidative stress, inflammation and apoptosis showed no significant changes in mPFC following adolescent cocaine exposure. (springer.com)
  • Warner said that assumptions that kids exposed to cocaine in the womb will be problem kids are wrong. (drugs-forum.com)
  • Kinetic modeling using a cerebellum reference region was implemented in the PMOD software package to determine ligand binding potentials for D2/D3 receptors and dopamine transporters (DAT) in each of the ROIs to test whether fallypride and/or FECNT binding potentials, measures of D2/D3 and DAT levels respectively, were influenced by prenatal cocaine exposure. (vanderbilt.edu)
  • In the cocaine-experienced rats, both levels of synapse-related proteins (synapsin I and PSD-95) and density of synapse and dendrite spine in mPFC were significantly decreased when compared to controls. (springer.com)