Peter W. Kalivas

ORCID: 0000-0001-9487-0119
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About
Contact & Profiles
Research Areas
  • Neurotransmitter Receptor Influence on Behavior
  • Neuroscience and Neuropharmacology Research
  • Receptor Mechanisms and Signaling
  • Memory and Neural Mechanisms
  • Neuropeptides and Animal Physiology
  • Ion channel regulation and function
  • Stress Responses and Cortisol
  • Neuroendocrine regulation and behavior
  • Pain Mechanisms and Treatments
  • Attention Deficit Hyperactivity Disorder
  • Cannabis and Cannabinoid Research
  • Nicotinic Acetylcholine Receptors Study
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Tryptophan and brain disorders
  • Pharmacological Effects and Toxicity Studies
  • Electroconvulsive Therapy Studies
  • Schizophrenia research and treatment
  • Forensic Toxicology and Drug Analysis
  • Treatment of Major Depression
  • Epilepsy research and treatment
  • Diet and metabolism studies
  • Amino Acid Enzymes and Metabolism
  • Neural dynamics and brain function
  • Adipose Tissue and Metabolism
  • Neurological and metabolic disorders

Medical University of South Carolina
2016-2025

Ralph H. Johnson VA Medical Center
2020-2025

University of California, San Diego
2024-2025

Università di Camerino
2024-2025

Jacksonville State University
2025

Wake Forest University
2025

College of Charleston
2024

The Ohio State University
2024

ORCID
2021

Université Laval
2020

Neuroplasticity can be defined as the ability of nervous system to respond intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. Major advances in understanding neuroplasticity have date yielded few established interventions. To advance translation research towards clinical applications, National Institutes Health Blueprint for Neuroscience Research sponsored a workshop 2009. Basic researchers disciplines from central injury/stroke, mental/addictive...

10.1093/brain/awr039 article EN Brain 2011-04-10

The role of limbic-striato-pallidal circuitry in cocaine-induced reinstatement was evaluated. transient inhibition brain nuclei associated with motor systems [including the ventral tegmental area (VTA), dorsal prefrontal cortex (dPFC), core nucleus accumbens (NAcore), and pallidum (VP)] prevented reinstatement. However, only VP proved to be necessary for food reinstatement, suggesting that identified circuit is specific drug-related Supporting possibility VTA-dPFC-NAcore-VP a series...

10.1523/jneurosci.21-21-08655.2001 article EN Journal of Neuroscience 2001-11-01

The relative contributions of glutamate and dopamine within the nucleus accumbens to cocaine-induced reinstatement drug-seeking behavior were assessed. When extinguished cocaine self-administration was reinstated by a cocaine-priming injection, extracellular levels both elevated in accumbens. However, when yoked or saline control subjects administered prime, only elevated. Thus, increased animals lever pressing, whereas regardless behavior. increase not accounted for simply act pressing...

10.1523/jneurosci.23-08-03531.2003 article EN Journal of Neuroscience 2003-04-15

Basal extracellular glutamate sampled in vivo is present micromolar concentrations the space outside synaptic cleft, and neither origin nor function of this known. This report reveals that blockade release from cystine-glutamate antiporter produced a significant decrease (60%) extrasynaptic levels rat striatum, whereas voltage-dependent Na+ Ca2+ channels relatively minimal changes (0-30%). indicates primary striatum arises nonvesicular by antiporter. By measuring [35S]cystine uptake, it was...

10.1523/jneurosci.22-20-09134.2002 article EN Journal of Neuroscience 2002-10-15

Elevated dopamine transmission in the nucleus accumbens is thought to be a primary mediator of addiction cocaine.However, repeated exposure cocaine associated with recruitment glutamate transmission.This poses possibility that behaviors characterizing addiction, such as craving-induced relapse, may not preferentially mediated by transmission.An animal model relapse was used demonstrate glutamate, and accumbens, cocaineinduced reinstatement drug-seeking behavior.Reinstatement produced...

10.1523/jneurosci.20-15-j0006.2000 article EN cc-by-nc-sa Journal of Neuroscience 2000-08-01

Abstract The anatomical distribution of neurotensin perikarya and fibers in rat brain, spinal cord, pituitary has been studied by immunohistochemistry. Neurotensin immunoreactivity is widely distributed throughout the especially forebrain midbrain limbic structures, but also pons, medulla, cord. Areas with low immunoreactivity, or lack it, stand out include most hippocampus, isocortex, ventromedial dorsomedial hypothalamic nuclei, somatomotor cerebellum, dorsal column nuclei. Strong found...

10.1002/cne.902100302 article EN The Journal of Comparative Neurology 1982-09-20

Abstract The behavioral stimulant effect of peripheral cocaine injection into rats is augmented following daily adminstration. In vivo dialysis in the nucleus accumbens conscious was used to determine if increased response administration associated with increase extracellular dopamine concentration. Acute (15 mg/kg, ip) produced and elevation concentration accumbens. Following pretreatment ip × 4 days), a subsequent acute significantly elevated levels compared that by single injection....

10.1002/syn.890050104 article EN Synapse 1990-01-01

The rat prelimbic prefrontal cortex and nucleus accumbens core are critical for initiating cocaine seeking. In contrast, the neural circuitry responsible inhibiting seeking during extinction is unknown. present findings using inhibition of selected brain nuclei with GABA agonists show that suppression produced by previous training required activity in infralimbic cortex. Conversely, reinstatement drug a injection extinguished animals was suppressed increasing neuronal glutamate agonist AMPA....

10.1523/jneurosci.1045-08.2008 article EN Journal of Neuroscience 2008-06-04

The role of limbic, cortical, and striatal circuitry in a footshock reinstatement model relapse to cocaine seeking was evaluated. Transient inhibition the central extended amygdala [CEA; including nucleus (CN), ventral bed stria terminalis (BNSTv), accumbens shell (NAshell)], tegmental area (VTA), motor [including dorsal prefrontal cortex (PFCd), core (NAcore), pallidum (VP)] blocked ability stress reinstate lever pressing previously associated with delivery. However, basolateral amygdala,...

10.1523/jneurosci.4177-03.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-02-18
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