Yonatan M. Kupchik

ORCID: 0000-0003-3732-4933
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurotransmitter Receptor Influence on Behavior
  • Receptor Mechanisms and Signaling
  • Regulation of Appetite and Obesity
  • Nicotinic Acetylcholine Receptors Study
  • Neuropeptides and Animal Physiology
  • Memory and Neural Mechanisms
  • Photoreceptor and optogenetics research
  • Biochemical Analysis and Sensing Techniques
  • Neural dynamics and brain function
  • Ion channel regulation and function
  • Lipid Membrane Structure and Behavior
  • Pharmacological Receptor Mechanisms and Effects
  • Cannabis and Cannabinoid Research
  • Neural and Behavioral Psychology Studies
  • Epilepsy research and treatment
  • Calpain Protease Function and Regulation
  • Innovative Teaching Methods
  • Nerve injury and regeneration
  • Neuroscience and Neural Engineering
  • Science Education and Pedagogy
  • Cellular transport and secretion
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Animal and Plant Science Education
  • Cardiovascular Disease and Adiposity

Hebrew University of Jerusalem
2010-2024

München Klinik
2017

John B. Pierce Laboratory
2017

Medical University of South Carolina
2011-2017

Centre de Recherche en Neurobiologie - Neurophysiologie de Marseille
2017

Centre National de la Recherche Scientifique
2017

Aix-Marseille Université
2017

Icahn School of Medicine at Mount Sinai
2016

Arizona State University
2016

Hebrew College
2015

Abstract Inhibitory optogenetics was used to examine the roles of prelimbic cortex ( PL ), nucleus accumbens core NAcore ) and projections in reinstatement cocaine seeking. Rats were microinjected into or with an adeno‐associated virus containing halorhodopsin archaerhodopsin. After 12 days self‐administration, followed by extinction training, animals underwent testing along presence/absence optically induced inhibition via laser light. Bilateral optical , fibers inhibited

10.1111/j.1369-1600.2012.00479.x article EN other-oa Addiction Biology 2012-07-24

Nicotine abuse and addiction is a major health liability. Nicotine, an active alkaloid in tobacco, self-administered by animals produces cellular adaptations brain regions associated with drug reward, such as the nucleus accumbens. However, it unknown whether, akin to illicit drugs of cocaine or heroin, endure contribute propensity relapse after discontinuing nicotine use. Using rat model cue-induced relapse, we made morphological electrophysiological measures synaptic plasticity, well...

10.1073/pnas.1220591110 article EN Proceedings of the National Academy of Sciences 2013-05-13

Distinct populations of D1- and D2-dopamine receptor-expressing medium spiny neurons (D1-/D2-MSNs) comprise the nucleus accumbens, activity in D1-MSNs promotes, whereas D2-MSNs inhibits, motivated behaviors. We used chemogenetics to extend D1-/D2-MSN cell specific regulation cue-reinstated cocaine seeking a mouse model self-administration relapse, found that either increasing or decreasing augmented cue-induced reinstatement. Both provide substantial GABAergic innervation ventral pallidum,...

10.1523/jneurosci.2659-16.2016 article EN cc-by-nc-sa Journal of Neuroscience 2016-12-01

The core subcompartment of the nucleus accumbens (NAcore) contributes significantly to behavioral responses following motivationally relevant stimuli, including drug-induced, stress-induced, and cue-induced reinstatement cocaine seeking. Projections from NAcore that could carry information necessary initiate reinstated seeking include outputs via indirect pathway dorsolateral ventral pallidum (dlVP) through direct medial substantia nigra (SN). Here we used an optogenetic strategy determine...

10.1523/jneurosci.1570-13.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-08-21

Nicotine self-administration is associated with decreased expression of the glial glutamate transporter (GLT-1) and cystine-glutamate exchange protein xCT within nucleus accumbens core (NAcore). N-acetylcysteine (NAC) has been shown to restore these proteins in a rodent model drug addiction relapse. However, specific molecular mechanisms driving its inhibitory effects on cue-induced nicotine reinstatement are unknown. Here, we confirm that extinction nicotine-seeking behavior impaired NAcore...

10.1111/adb.12797 article EN Addiction Biology 2019-07-22

The ventral pallidum (VP) is a target of dense nucleus accumbens projections. Many these projections coexpress GABA and the neuropeptide enkephalin, δ μ opioid receptor (MOR) ligand. Of two, MOR in VP known to be involved reward-related behaviors, such as hedonic responses palatable food, alcohol intake, reinstatement cocaine seeking. Stimulating MORs decreases extracellular GABA, indicating that effects on seeking are via modulating neurotransmission. Here, we use whole-cell patch-clamp rat...

10.1523/jneurosci.4336-13.2014 article EN cc-by-nc-sa Journal of Neuroscience 2014-01-15

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10.1001/jamapsychiatry.2013.2207 article EN JAMA Psychiatry 2013-08-01

Reliable neuronal communication depends on accurate temporal correlation between the action potential and neurotransmitter release. Although a requirement for Ca2+ in release is amply documented, recent studies have shown that voltage-sensitive G protein–coupled receptors (GPCRs) are also involved this process. However, how slow-acting GPCRs control fast an unsolved question. Here we examine whether recently discovered depolarization-induced charge movement M2-muscarinic receptor (M2R)...

10.1083/jcb.201007053 article EN cc-by-nc-sa The Journal of Cell Biology 2011-01-03

The ventral pallidum (VP) is a central node in the reward system that strongly implicated and addiction. Although majority of VP neurons are GABAergic encode reward, recent studies revealed novel glutamatergic neuronal population [VP expressing vesicular glutamate transporter 2 (VP VGluT2 )], whose activation generates aversion. Withdrawal from drugs has been shown to induce drastic synaptic changes populations associated with such as tegmental area (VTA) or nucleus accumbens neurons, but...

10.1523/jneurosci.0929-19.2019 article EN cc-by-nc-sa Journal of Neuroscience 2019-12-13

Relapse to cocaine seeking is associated with potentiated excitatory synapses in nucleus accumbens. α<sub>2</sub>δ-1 an auxiliary subunit of voltage-gated calcium channels that affects calcium-channel trafficking and kinetics, initiates extracellular signaling cascades, promotes synaptogenesis. Previous data demonstrate repeated exposure alcohol, nicotine, methamphetamine, morphine upregulates reward-related brain regions, but it was unclear whether this alteration generalized cocaine. Here,...

10.1523/jneurosci.1204-13.2014 article EN Journal of Neuroscience 2014-06-18

Cocaine-driven changes in the modulation of neurotransmission by neuromodulators are poorly understood. The ventral pallidum (VP) is a key structure reward system, which GABA regulated opioid neuropeptides, including dynorphin. However, it not known whether dynorphin acts differently on different cell types VP and its effects altered withdrawal from cocaine. Here, we trained wild-type, D1-Cre, A2A-Cre, or vGluT2-Cre:Ai9 male female mice cocaine conditioned place preference protocol followed...

10.1523/jneurosci.1262-19.2019 article EN cc-by-nc-sa Journal of Neuroscience 2019-12-13
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