Ultrasonic vocalization at 55kHz (55kHz-USVs) by rodents has been proposed to be a behavioral manifestation of affectively positive incentive motivation. To examine the extent to which 55kHz-USV emissions correlate with cocaine-induced locomotor activity, we measured cocaine-induced 55kHz-USVs and their relationship to cocaine-induced locomotor sensitization in rats. We demonstrate that similar to locomotor responses, 55kHz-USVs are also sensitized by exposure to cocaine. Furthermore, we show that the magnitude of cocaine-induced 55kHz-USV sensitization is positively correlated with that of locomotor sensitization. Moreover, we demonstrate that rats selectively bred for high rates of 55kHz-USVs exhibit higher levels of cocaine-induced 55kHz-USV sensitization than animals selectively bred for low levels of 55kHz USVs. These results suggest that the neural circuits underlying 55kHz-USV, which may directly reflect affective experience/motivation, can be sensitized by cocaine in a way that resembles locomotor sensitization.
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http://dx.doi.org/10.1016/j.neulet.2009.02.007 | DOI Listing |
Int J Mol Sci
January 2025
Azriele Faculty of Medicine in the Galilee, Bar-Ilan University, Safed 1311502, Israel.
Provoked vulvodynia (PV) is the leading cause of vulvar pain and dyspareunia. The etiology of PV is multifactorial and remains poorly understood. PV is associated with a history of repeated vulvar inflammation and is often accompanied by sensory neuromodulation as a result of activation of the metabotropic glutamate receptor 5 (mGluR5) in the sensory nerve terminals.
View Article and Find Full Text PDFNeuroscience
January 2025
Interdisciplinary Neuroscience Program, The University of Texas at Austin, Austin, TX, USA; Waggoner Center for Alcohol & Addiction Research, The University of Texas at Austin, Austin, TX, USA; Department of Neuroscience, The University of Texas at Austin, Austin, TX, USA; Department of Neurology, Dell Medical School, The University of Texas at Austin, Austin, TX, USA. Electronic address:
While our understanding of the neurobiological mechanisms underlying cocaine and opiate reward has historically been dopamine-focused, evidence from genetic and pharmacological approaches indicates that µ-opioid receptors (MORs) in the striatum are important contributors. Within the striatum, MORs are expressed in both dopamine D1-receptor and D2-receptor expressing GABAergic medium spiny neurons (MSNs), as well as in interneurons and various afferents. Thus, it remains unclear how these distinct MOR populations regulate drug reward.
View Article and Find Full Text PDFNeuropharmacology
January 2025
Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, USA.
Nicotine use remains one of the leading causes of preventable deaths in the United States and, while the prevalence of combustible cigarette use has declined over the past few years, the popularity of electronic nicotine delivery systems continues to rise. Vaping is not without risks, and its long-term effects, particularly in vulnerable populations, remain largely unknown. This study introduces a novel, oronasal-restricted, nicotine vapor self-administration mouse model to investigate the impact of nicotine concentration, genotype, sex, and age on self-administration and behavioral response to nicotine.
View Article and Find Full Text PDFFront Mol Neurosci
December 2024
Laboratory of Neuropsychiatry, Psychiatric Centre Copenhagen, Mental Health Services in the Capital Region of Denmark and University of Copenhagen, Copenhagen, Denmark.
Objective: Acetylcholine modulates the activity of the direct and indirect pathways within the striatum through interaction with muscarinic M and M receptors. M receptors are uniquely positioned to regulate plasticity within the direct pathway and play a substantial role in reward and addiction-related behaviors. However, the role of M receptors on cholinergic neurons has been less explored.
View Article and Find Full Text PDFTransl Psychiatry
December 2024
Center for Substance Abuse Research, Temple University, Philadelphia, PA, USA.
Recent progress in psychiatric research has highlighted neuroinflammation in the pathophysiology of opioid use disorder (OUD), suggesting that heightened immune responses in the brain may exacerbate opioid-related mechanisms. However, the molecular mechanisms resulting from neuroinflammation that impact opioid-induced behaviors and transcriptional pathways remain poorly understood. In this study, we have begun to address this critical knowledge gap by exploring the intersection between neuroinflammation and exposure to the opioid heroin, utilizing lipopolysaccharide (LPS)-induced neuroinflammation, to investigate transcriptional changes in the nucleus accumbens (NAc), an essential region in the mesolimbic dopamine system that mediates opioid reward.
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