Opioid-dopaminergic mechanisms in the potentiation of d-amphetamine discrimination by interferon-α

Ho, Beng T.; Huo, Y Y; Lu, Junjun; Tansey, L. Wayne; Levin, Victor A.

doi:10.1016/0091-3057(92)90446-m

Cited by 22 publications

(12 citation statements)

References 22 publications

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“…Activation of MAPK signaling pathways have been shown to upregulate the activity and cell surface expression of the DA reuptake pump, which in turn may decrease DA synaptic availability (Moron et al 2003). Finally, IFN-alpha has been shown to bind to opioid receptors on nigrostriatal, mesolimbic, and mesocortical dopaminergic neurons, causing presynaptic DA release (Ho et al, 1992;Dafny et al, 1985;Di Chiara and Imperato, 1988). Long-term IFNalpha-induced DA release may lead to a compensatory reduction in the number and/or sensitivity of DA receptors (Cooper et al, 2003) and ultimately decreased dopaminergic tone.…”

Section: Discussionmentioning

confidence: 99%

IFN-alpha-induced motor slowing is associated with increased depression and fatigue in patients with chronic hepatitis C

Majer

Welberg

Capuron

et al. 2008

Brain, Behavior, and Immunity

106

102

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Interferon (IFN)-alpha has been used to investigate pathways by which innate immune cytokines influence the brain and behavior. Previous studies suggest that altered basal ganglia function may contribute to IFN-alpha-induced neuropsychological and behavioural changes. To further examine IFN-alpha effects on neuropsychological functions related to basal ganglia (as well as other brain regions), and explore the relationship between altered neuropsychological function and IFN-alphainduced depression and fatigue, a selected subset of the Cambridge Neuropsychological Test Automated Battery was administered to 32 hepatitis C patients at baseline (Visit 1) and following 12 weeks (Visit 2) of either no treatment (n=12) or treatment with IFN-alpha plus ribavirin (n=20). Symptoms of depression and fatigue were assessed using the Montgomery-Asberg Depression Rating Scale and the Multi-Dimensional Fatigue Inventory. Compared to control subjects, patients treated with IFN-alpha/ribavirin exhibited significant decreases in motor speed as measured in the simple and five-choice movement segments of the CANTAB reaction time task and slower response times in the rapid visual information processing task, a task of sustained attention. Decreased motor speed on the five-choice movement segments of the reaction time task were in turn correlated with increased symptoms of depression and fatigue (R=0.47, p<.05 and R=0.48, p<.05, respectively). IFN-alpha/ ribavirin treatment had no effects on executive function, decision time in the reaction time task, or target detection accuracy in the sustained attention task. Motor slowing and its correlation with psychiatric symptoms suggest that altered basal ganglia function may contribute to the pathogenesis of IFN-alpha-induced behavioural changes.

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Section: Discussionmentioning

confidence: 99%

IFN-alpha-induced motor slowing is associated with increased depression and fatigue in patients with chronic hepatitis C

Majer

Welberg

Capuron

et al. 2008

Brain, Behavior, and Immunity

106

102

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“…These discrepancies were likely due to differences in dosing, length of exposure, and, most importantly, the fact that speciesspecific IFN-α was variably used and rodents do not respond to human IFN-α with activation of classic type I IFN receptor signaling (Loftis et al, 2006a;Loftis et al, 2006b;Wang et al, 2008). Moreover, human IFN-α administered to rodents binds to opioid receptors, which may be responsible for some of the observed changes in brain monoamines (Blalock and Smith, 1981;Ho et al, 1992;Wang et al, 2006). Moreover, chronic (6 days to 4 weeks) peripheral administration of both human-and species-specific IFN-a administered to rodents has demonstrated only limited ability to reliably induce depressive behaviors (eg, see Rhesus monkeys exposed to chronic IFN-α exhibit immune, neuroendocrine, and behavioral responses similar to that of cytokine-treated patients, including decreases in psychomotor activity and increases in depressive-like huddling behavior (in~50% of animals; Felger et al, 2007;Felger and Miller, 2012).…”

Section: Biochemical and Behavioral Studies In Laboratory Animalsmentioning

confidence: 99%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

319

237

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Motivational and motor deficits are common in patients with depression and other psychiatric disorders, and are related to symptoms of anhedonia and motor retardation. These deficits in motivation and motor function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnormalities in mesolimbic and mesostriatal dopamine (DA). One pathophysiologic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation. Biomarkers of inflammation such as inflammatory cytokines and acute-phase proteins are reliably elevated in a significant proportion of psychiatric patients. A variety of inflammatory stimuli have been found to preferentially target basal ganglia function to lead to impaired motivation and motor activity. Findings have included inflammation-associated reductions in ventral striatal neural responses to reward anticipation, decreased DA and DA metabolites in cerebrospinal fluid, and decreased availability, and release of striatal DA, all of which correlated with symptoms of reduced motivation and/or motor retardation. Importantly, inflammation-associated symptoms are often difficult to treat, and evidence suggests that inflammation may decrease DA synthesis and availability, thus circumventing the efficacy of standard pharmacotherapies. This review will highlight the impact of administration of inflammatory stimuli on the brain in relation to motivation and motor function. Recent data demonstrating similar relationships between increased inflammation and altered DAergic corticostriatal circuitry and behavior in patients with major depressive disorder will also be presented. Finally, we will discuss the mechanisms by which inflammation affects DA neurotransmission and relevance to novel therapeutic strategies to treat reduced motivation and motor symptoms in patients with high inflammation.

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“…Such S D effects of the μ-agonist d-amphetamine were potentiated by pretreatment with interferon-α which is naturally released in activation of the immune system. Naloxone suppressed the effect of interferon, suggesting an opioid-dopamine mechanism to explain the action of Interferon (Ho et a/., 1992). In summary these findings raise the hypothesis that in the process of operant conditioning reorganization of the receptor pattern in certain brain areas is evident.…”

Section: Introductionmentioning

confidence: 86%

Alterations in the Visual Cortex Receptor Pattern by Operant Conditioning in a Reward Paradigm

Löhrke

Franz²,

Brose³

et al. 1995

Biological Chemistry Hoppe-Seyler

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The aim of the study was to investigate the impact of operant conditioning on the receptor pattern in the visual cortex of calves. A reward paradigm was used to induce conditioned preference for colours. Binding sites in visual cortex specimens from conditioned and naive animals were assayed in vitro on cellular basis after dissociation of the tissue by collagenase, incubation with fluorescent ligands and flow-cytometry for fluorescence analysis. The cellular counts were subdivided according to sedimentation at 200 g as well as via the flow-cytometrical histogram by size and granularity. Binding sites of dopamine D1 and D2 receptor subtypes, glucocorticoids, opioids, casein as well as glycine and N-methyl-D-aspartic acid (NMDA) were detected by fluorescent molecular probes. In displacing naloxone fluorescein from NMDA- and mu-opioid receptors NMDA and meth-enkephalin were used. Comparisons between portions of fluorescent cellular counts from visual cortex tissue of conditioned and naive animals revealed a small increase (1.2-fold, P < 0.05) in opioid receptors of large and high granulated counts, bearing > 80% D1 receptors, and a decrease (0.70-fold, P < 0.05) in less granulated counts with variable portion of D1 receptors. Conditioning resulted in higher and lower displacing rates by meth-enkephalin and NMDA, resp., and in a reduce in counts with dopamine D1 (0.8-fold, P < 0.05), glycine and glucocorticoid binding sites (0.6-fold in both cases, P < 0.01). A tendency of elevated phagocyte marker expression occurred in high granulated counts. The data suggest that conditioning is accompanied with significant and in part marked change in binding sites studied. Induction of scavenger activity may parallel this process. As cellular portion with glycine and glucocorticoid receptors were most markedly altered by conditioning, the neurochemical needs of the used paradigm seem to focus to motility-related functions.

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Opioid-dopaminergic mechanisms in the potentiation of d-amphetamine discrimination by interferon-α

Cited by 22 publications

References 22 publications

IFN-alpha-induced motor slowing is associated with increased depression and fatigue in patients with chronic hepatitis C

IFN-alpha-induced motor slowing is associated with increased depression and fatigue in patients with chronic hepatitis C

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Alterations in the Visual Cortex Receptor Pattern by Operant Conditioning in a Reward Paradigm

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