Jean‐Pol Tassin

ORCID: 0000-0001-6658-9581
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About
Contact & Profiles
Research Areas
  • Neurotransmitter Receptor Influence on Behavior
  • Receptor Mechanisms and Signaling
  • Neuroscience and Neuropharmacology Research
  • Neuropeptides and Animal Physiology
  • Neuroendocrine regulation and behavior
  • Memory and Neural Mechanisms
  • Neurological disorders and treatments
  • Psychoanalysis and Psychopathology Research
  • Attention Deficit Hyperactivity Disorder
  • Nicotinic Acetylcholine Receptors Study
  • Stress Responses and Cortisol
  • Parkinson's Disease Mechanisms and Treatments
  • French Urban and Social Studies
  • Diet and metabolism studies
  • Neural dynamics and brain function
  • Ion channel regulation and function
  • Functional Brain Connectivity Studies
  • Hypothalamic control of reproductive hormones
  • Treatment of Major Depression
  • Genetic Neurodegenerative Diseases
  • Tryptophan and brain disorders
  • Pharmacological Receptor Mechanisms and Effects
  • Enzyme Catalysis and Immobilization
  • Adipose Tissue and Metabolism
  • Cannabis and Cannabinoid Research

Inserm
2010-2024

Neurosciences Paris-Seine
2016-2024

Institut de Biologie Paris-Seine
2016-2024

Centre National de la Recherche Scientifique
2004-2023

Sorbonne Université
1974-2023

Université Paris-Seine
2018-2022

Université Paris 1 Panthéon-Sorbonne
2022

Sorbonne Paris Cité
2020

Collège de France
2002-2018

Centre de Coopération Internationale en Recherche Agronomique pour le Développement
2015

Drugs of abuse, such as psychostimulants and opiates, are generally considered exerting their locomotor rewarding effects through an increased dopaminergic transmission in the nucleus accumbens. Noradrenergic may also be implicated because most increase norepinephrine (NE) release, numerous studies have indicated interactions between noradrenergic neurons α1-adrenergic receptors. However, analysis after either destruction or pharmacological blockade receptors led to conflicting results. Here...

10.1523/jneurosci.22-07-02873.2002 article EN cc-by-nc-sa Journal of Neuroscience 2002-04-01

Using specific antibodies and cDNA probes, we have investigated, in rat basal ganglia, the distribution regulation of expression alpha subunits Gs G(olf), two GTP-binding proteins (G-proteins) that stimulate adenylyl cyclase. We confirmed G(olf) is highly expressed caudate-putamen, nucleus accumbens, olfactory tubercle, whereas less abundant these areas than other brain regions. Intrastriatal injections quinolinic acid decreased dramatically levels protein striatum substantia nigra, those...

10.1523/jneurosci.13-05-02237.1993 article EN cc-by-nc-sa Journal of Neuroscience 1993-05-01

The locomotor hyperactivity induced by systemic or local (nucleus accumbens) D-amphetamine injections can be blocked (prefrontal cortex) of prazosin, an alpha1-adrenergic antagonist (Blance et al., 1994). Microdialysis studies performed on freely moving animals indicated that prazosin (0.5 mg/kg, i.p.) does not modify the increase in extracellular dopamine (DA) levels nucleus accumbens are (2.0 i.p.), but it inhibits D-amphetamine-induced (-63%, p < 0.0001). No behavioral activation occurred...

10.1523/jneurosci.18-07-02729.1998 article EN cc-by-nc-sa Journal of Neuroscience 1998-04-01

10.1016/j.jcis.2004.09.043 article EN Journal of Colloid and Interface Science 2004-12-24

Repeated traumatic events induce long-lasting behavioral changes that are key to organism adaptation and affect cognitive, emotional, social behaviors. Rodents subjected repeated instances of aggression develop enduring aversion increased anxiety. Such aggressions trigger a stress response, resulting in glucocorticoid release activation the ascending dopamine (DA) system. We bred mice with selective inactivation gene encoding receptor (GR) along DA pathway, exposed them aggressions. GR...

10.1126/science.1226767 article EN Science 2013-01-17

10.1016/s0166-2236(84)80145-9 article EN Trends in Neurosciences 1984-11-01

Autosomal dominant DOPA-responsive dystonia (DRD) is usually caused by mutation in the gene encoding guanosine triphosphate-cyclohydrolase I (GTPCH I). We studied 22 families with a phenotype of levodopa-responsive sequencing six coding exons, 5'-untranslated region and exon-intron boundaries GTPCH gene. Eleven heterozygous mutations were identified, including five missense mutations, one splice site mutation, two small deletions nonsense 12 that included 27 patients 13 asymptomatic...

10.1093/brain/123.6.1112 article EN Brain 2000-06-01

Abstract Addictive properties of drugs misuse are generally considered to be mediated by an increased release dopamine (DA) in the ventral striatum. However, recent experiments indicated implication α1b‐adrenergic receptors behavioural responses psychostimulants and opiates. We show now that DA induced striatum morphine (20 mg/kg) is completely blocked prazosin (1 mg/kg), α1‐adrenergic antagonist. morphine‐induced increases were found similar mice deleted for receptor (α1b‐AR KO) wild‐type...

10.1111/j.1460-9568.2004.03805.x article EN European Journal of Neuroscience 2004-12-01

The possibility that the dopaminergic neurons innervating medial prefrontal cortex (mPFC) can inhibit locomotor behaviour has been suggested in several studies. evidence remains indirect, however, because manipulations tested aimed exclusively at permanently depleting mPFC dopamine. Here we demonstrate rats acute increases dopamine transmission this site by local injections of amphetamine known locomotor-activating effects nucleus accumbens (N.Acc.). Further, intra-mPFC D-1 receptor...

10.1111/j.1460-9568.1991.tb00036.x article EN European Journal of Neuroscience 1991-10-01

Abstract The stimulation of cortical dopaminergic D1 receptors can counteract the increased locomotor activity evoked by D‐amphetamine application in nucleus accumbens (Vezina et al., Eur. J. Neurosci. , 3 1001–1007, 1991). Moreover, an α1 antagonist, prazosin, prevents hyperactivity induced electrolytic lesions ventral tegmental area (Trovero Neuroscience 47 69–76, 1992). Attempts were thus made to see whether blockade α1‐adrenergic rat prefrontal cortex could reduce D‐amphetamine‐evoked...

10.1111/j.1460-9568.1994.tb00272.x article EN European Journal of Neuroscience 1994-03-01
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