Central dopamine (DA) activity is thought to play a role in fear motivation. The aim of the present study was to assess the involvement of DA D1 receptors in emotional learning. The authors report that peripheral and intraamygdalar administration of the specific D1 receptor antagonist SCH 23390 blocked the acquisition of fear-potentiated startle. Analysis of shock reactivity during footshock administration revealed that the learning impairment could not be explained by a diminution in the aversive properties of the unconditioned stimulus. Additionally, systemic and intraamygdalar injection of SCH 23390 did not alter fear expression as measured with the shock sensitization of acoustic startle. The potential contribution of mesoamygdaloid DA to the acquisition and retrieval of conditioned fear responses is discussed.
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http://dx.doi.org/10.1037//0735-7044.114.2.262 | DOI Listing |
J Neurosci
December 2024
Nash Family Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029
The neurotransmitter dopamine (DA) has a multifaceted role in healthy and disordered brains through its action on multiple subtypes of dopaminergic receptors. How modulation of these receptors influences learning and motivation by altering intrinsic brain-wide networks remains unclear. Here we performed parallel behavioral and resting-state functional MRI experiments after administration of two different DA receptor antagonists in male and female macaque monkeys.
View Article and Find Full Text PDFBehav Brain Res
March 2025
Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address:
Acting centrally, dopamine has been shown to induce ergogenic effects derived from its influence on thermoregulation, motivation, reward, and motor control. Thus, to evaluate the role of the central dopaminergic system in hypothalamic neuronal activation and its relationship with exercise performance, Wistar rats were intracerebroventricularly injected with saline (SAL) or SCH-23390 (SCH, dopamine D1 receptor blocker) at rest and before timed submaximal exercise (∼13 min) or exercise until fatigue. Core body and tail temperatures were recorded throughout the exercise.
View Article and Find Full Text PDFBehav Pharmacol
February 2025
Neuroscience Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences.
Exposure to stressful conditions such as forced swim stress (FSS) induces antinociception. Previous reports determined that dopamine receptors in the CA1 hippocampal area are important in chronic pain processing. Considering that neural mechanisms behind acute and chronic pain differ significantly, in this study, we have investigated the role of dopamine receptors within the CA1 region in the FSS-induced antinociceptive response in the acute pain induced by the tail-flick test in the rat.
View Article and Find Full Text PDFBehav Brain Res
March 2025
Department of Anatomy and Neurosciences, Amsterdam Neuroscience, Amsterdam University Medical Center, location VU Medical Center, Amsterdam, The Netherlands. Electronic address:
Modelling delay discounting behavior in rodents is important for understanding the neurobiological mechanisms underlying cognitive control and associated impulsivity disorders. Conventional rodent delay discounting procedures require extensive training and frequent experimenter interaction, as rodents are tested in separate operant chambers away from their home cage. To address these limitations, we adapted and characterize here a self-adjusting delay discounting procedure to an automated CombiCage setup.
View Article and Find Full Text PDFNeurobiol Learn Mem
January 2025
Department of Psychology and Collaborative Neuroscience Program, University of Guelph, 50 Stone Road E, Guelph, ON N1G 2W1, Canada.
Consolidated long-term memories can undergo strength or content modification via protein synthesis-dependent reconsolidation. This is the process by which a reminder cue initiates reactivation of the memory trace, triggering destabilization. Older and more strongly encoded spatial memories can resist destabilization due to biological boundary conditions.
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