Prenatal cocaine exposure has been associated with a variety of adverse neurological effects in infants and laboratory animals. Of particular interest, one group of investigators reported that exposed neonates have an abnormality in the brainstem auditory-evoked potential (BAEP). The particular abnormality, a prolongation in the wave I-V interpeak latency, suggested delayed or desynchronized transmission of subcortical auditory information. To further investigate this possible consequence of prenatal cocaine exposure, pregnant Long-Evans rats were injected daily with 60, 80 or 100 mg/kg cocaine HCl (SC, 2% solution) with half the daily dose given in the morning and the other half given in the afternoon. Treatment was given from gestation days 7 to 20 (sperm positive = GD 0). Ad lib-fed and pair-fed control groups were also used. Offspring were evaluated at the age of 35 days (birth = PD 0) and as adults (6-10 months). BAEPs were elicited by click stimuli presented over a broad range of intensities and repetition rates. Prolongation of the interpeak latencies and a reduction in BAEP amplitudes were observed only in the highest dose (C100) group, only at the age of 35 days, and only at the highest stimulus intensity. While these results support those found in exposed neonates, our data suggest a) that the effects are developmental delays which dissipate with aging and b) that the effects require high cocaine exposure.
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http://dx.doi.org/10.1016/0892-0362(90)90053-f | DOI Listing |
J Stud Alcohol Drugs
January 2025
Department of Population Health Sciences, University of Wisconsin-Madison, Madison, Wisconsin, United States.
Objective: Substance use patterns vary considerably in the general population, yet little is known about patterns before and during pregnancy. The purpose of this study was to describe single substance and polysubstance use (PSU) before and during pregnancy among recent births in the United States (US) and compare exposure patterns.
Methods: We used data from the Pregnancy and Risk Assessment Monitoring System (PRAMS) postpartum survey for 2016-2018 to estimate the prevalence and identify patterns of substance use by participants one to three months before and during pregnancy.
Aim: Chronic cocaine use is associated with decreases in neuroactive steroid levels. These adaptations may contribute to continued cocaine use and high relapse risk in individuals with cocaine use disorder (CUD). Thus, this pilot study assessed chronic treatment with 2 supraphysiologic doses of the neuroactive steroid precursor pregnenolone (PREG, 300 mg/day; 500 mg/day) to boost endogenous neuroactive steroid levels and assess its impact on provoked craving and cocaine use outcomes in an 8-week trial in men and women with CUD.
View Article and Find Full Text PDFJ Adolesc Health
January 2025
Department of Public Health & Primary Care, Institute of Population Health, School of Medicine, Trinity College Dublin, Dublin, Ireland.
Purpose: Despite growing concerns about trends in cocaine use, there is a shortage of longitudinal research that prospectively examines risk and protective factors associated with cocaine initiation and use in general youth populations. This study addresses this gap.
Methods: Growing Up in Ireland is a nationally representative cohort.
ACS Chem Neurosci
January 2025
School of Pharmacy, University of Wisconsin─Madison, Madison, Wisconsin 53705, United States.
Addiction to psychostimulants, including cocaine, causes widespread morbidity and mortality and is a major threat to global public health. Currently, no pharmacotherapies can successfully treat psychostimulant addiction. The neuroactive effects of cocaine and other psychostimulants have been studied extensively with respect to their modulation of monoamine systems (particularly dopamine); effects on neuropeptide systems have received less attention.
View Article and Find Full Text PDFPharmacol Rep
January 2025
Department of Translational Neuroscience, Center for Addiction Research, Wake Forest University School of Medicine, 115 South Chestnut St, Winston-Salem, NC, 27101, USA.
Background: Cocaine Use Disorder (CUD) remains a significant problem in the United States, with high rates of relapse and no present FDA-approved treatment. The acetylcholine neurotransmitter system, specifically through modulation of muscarinic acetylcholine receptor (mAChR) function, has shown promise as a therapeutic target for multiple aspects of CUD. Enhancement of the M mAChR subtype via positive allosteric modulation has been shown to inhibit the behavioral and neurochemical effects of cocaine across several rodent models of CUD.
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