Decrease of lymphoproliferative response by amphetamine is mediated by dopamine from the nucleus accumbens: Influence on splenic met-enkephalin levels

Assis, María Amparo; Valdomero, Analía; García‐Keller, Constanza; Sotomayor, Claudia Elena; Cancela, Liliana Marina

doi:10.1016/j.bbi.2011.01.001

Cited by 11 publications

(12 citation statements)

References 76 publications

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“…Furthermore, data from our lab demonstrate an increase in the levels of met-enkephalin in the nucleus accumbens from rats after acute amphetamine (5 mg/kg i.p.) following 4, but not 7 or 21 days after the last drug injection ( 18 , 49 , 50 ). Met-enkephalin elevation was also observed after 4 days withdrawal period from chronic amphetamine (5 × 2 mg/kg i.p) ( 49 ).…”

Section: Activation Of the Enkephalin System By Psychostimulants In Tmentioning

confidence: 93%

“…Similarly, the full D1 receptor agonist SKF-82958 induced PENK, prodynorphin and substance P gene expression in both the dorsal and ventral striatum ( 33 ). Interestingly, the increase in met-enkephalin induced by amphetamine ( 50 ) or PENK mRNA levels stimulated by SKF-82958 in striatal neurons ( 33 ) was blocked by the D1 receptor antagonist SCH-23390 ( 50 ) and by scopolamine, the muscarinic receptor antagonist ( 32 ). Oppositely, the D2 receptor antagonist eticlopride did not affect SKF-82958-induced PENK mRNA expression ( 33 ).…”

Section: Neurochemical and Molecular Mechanisms In Psychostimulant-inmentioning

confidence: 99%

“…Oppositely, the D2 receptor antagonist eticlopride did not affect SKF-82958-induced PENK mRNA expression ( 33 ). Similarly, amphetamine-induced met-enkephalin levels was not modified by raclopride, another D2 receptor antagonist ( 50 ). Thus, this evidence suggests that D1-mediated induction of PENK may involve trans-synaptic activation of cholinergic neurotransmission.…”

Section: Neurochemical and Molecular Mechanisms In Psychostimulant-inmentioning

confidence: 99%

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Enkephalin as a Pivotal Player in Neuroadaptations Related to Psychostimulant Addiction

et al. 2018

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Enkephalin expression is high in mesocorticolimbic areas associated with psychostimulant-induced behavioral and neurobiological effects, and may also modulate local neurotransmission in this circuit network. Psychostimulant drugs, like amphetamine and cocaine, significantly increase the content of enkephalin in these brain structures, but we do not yet understand the specific significance of this drug-induced adaptation. In this review, we summarize the neurochemical and molecular mechanism of psychostimulant-induced enkephalin activation in mesocorticolimbic brain areas, and the contribution of this opioid peptide in the pivotal neuroadaptations and long-term behavioral changes underlying psychostimulant addiction. There is evidence suggesting that adaptive changes in enkephalin content in the mesocorticolimbic circuit, induced by acute and chronic psychostimulant administration, may represent a key initial step in the long-term behavioral and neuronal plasticity induced by these drugs.

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Section: Activation Of the Enkephalin System By Psychostimulants In Tmentioning

confidence: 93%

Section: Neurochemical and Molecular Mechanisms In Psychostimulant-inmentioning

confidence: 99%

Section: Neurochemical and Molecular Mechanisms In Psychostimulant-inmentioning

confidence: 99%

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Enkephalin as a Pivotal Player in Neuroadaptations Related to Psychostimulant Addiction

et al. 2018

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“…The dopaminergic projections from the VTA to components of the limbic system are causally associated with motivated behavior and reward perception 10 , 11 . Pharmacological studies indicated a connection between reward system activity and immune modulation 12 – 14 , and we recently showed that reward system activity can boost antibacterial immunity 15 .…”

Section: Introductionmentioning

confidence: 98%

Modulation of anti-tumor immunity by the brain’s reward system

et al. 2018

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Regulating immunity is a leading target for cancer therapy. Here, we show that the anti-tumor immune response can be modulated by the brain’s reward system, a key circuitry in emotional processes. Activation of the reward system in tumor-bearing mice (Lewis lung carcinoma (LLC) and B16 melanoma) using chemogenetics (DREADDs), resulted in reduced tumor weight. This effect was mediated via the sympathetic nervous system (SNS), manifested by an attenuated noradrenergic input to a major immunological site, the bone marrow. Myeloid derived suppressor cells (MDSCs), which develop in the bone marrow, became less immunosuppressive following reward system activation. By depleting or adoptively transferring the MDSCs, we demonstrated that these cells are both necessary and sufficient to mediate reward system effects on tumor growth. Given the central role of the reward system in positive emotions, these findings introduce a physiological mechanism whereby the patient’s psychological state can impact anti-tumor immunity and cancer progression.

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“…Incubating human lymphocytes with DA inhibited Concanavalin A-stimulated proliferation and synthesis of IFNγ 13 . DA operates in human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV)-induced brain pathology 14 15 , and in lymphoproliferative response 16 . Gaskill et al 17 reported that DA activated macrophages, which express DA receptors, by increasing ERK 1 phosphorylation.…”

mentioning

confidence: 99%

Dopamine modulates hemocyte phagocytosis via a D1-like receptor in the rice stem borer, Chilo suppressalis

Stanley

et al. 2015

Sci Rep

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Dopamine (DA) is a signal moiety bridging the nervous and immune systems. DA dysregulation is linked to serious human diseases, including addiction, schizophrenia, and Parkinson’s disease. However, DA actions in the immune system remain incompletely understood. In this study, we found that DA modulates insect hemocyte phagocytosis using hemocytes prepared from the rice stem borer (RSB), Chilo suppressalis. We investigated whether insect hemocytes are capable of de novo DA production. Here we show that exposing hemocytes to lipopolysaccharide (LPS) led to induction of DA-generating enzymes. Exogenous DA induced rapid phosphorylation of extracellular signal-regulated kinase (ERK) in naïve hemocytes. Activation of ERK was inhibited by preincubating with a DOP1 receptor antagonist. Thus, DA signaling via the DOP1 receptor may contribute to early hemocyte activation. DA synthesized and released from hemocytes may act in an autocrine mechanism to stimulate or maintain phagocytic activity. Consistent with this hypothesis, we found that inhibition of DA synthesis with α-methyl-DL-tyrosine methyl ester hydrochloride or blockage of DOP1 receptor with antagonist SCH23390 impaired hemocyte phagocytosis. Topical DA application also significantly decreased RSB mortality following challenge with the insect pathogenic fungus, Beauveria bassiana. We infer that a DA-dependent signaling system operates in hemocytes to mediate phagocytotic functions.

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Decrease of lymphoproliferative response by amphetamine is mediated by dopamine from the nucleus accumbens: Influence on splenic met-enkephalin levels

Cited by 11 publications

References 76 publications

Enkephalin as a Pivotal Player in Neuroadaptations Related to Psychostimulant Addiction

Enkephalin as a Pivotal Player in Neuroadaptations Related to Psychostimulant Addiction

Modulation of anti-tumor immunity by the brain’s reward system

Dopamine modulates hemocyte phagocytosis via a D1-like receptor in the rice stem borer, Chilo suppressalis

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