Regional amines levels in the rat brain following intra-accumbens cholecystokinin and intraperitoneal amphetamine pre-treatment

Heidbreder, Christian; Gewiss, M.; Depotter, W.; Witte, Philippe De

doi:10.3109/13813459208998113

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…However, it has been consistently demonstrated that CCK inhibits 5HT activity in the brain (Heidbreder et al 1992;Kaneyuki et al 1989;Rex et al 1997;Vasar et al 1985;Widerlöv et al 1983). It is not known whether these effects are mediated by CCK-A receptors.…”

Section: Discussionmentioning

confidence: 96%

SR146131, a cholecystokinin-A receptor agonist, antagonizes prepulse inhibition deficits produced by dizocilpine and DOI

Feifel

2002

Psychopharmacology

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The lack of an effect of SR146131 on amphetamine-induced disruption of PPI suggests that a selective nonpeptide CCK-A agonist may not produce antipsychotic-like effects on dopamine transmission. However, the unexpected effects of SR146131 on dizocilpine and DOI-induced PPI deficits are consistent with the effects of drugs that inhibit transmission in the 5HT2A receptor system, including atypical antipsychotic drugs. Possible mechanisms underlying these findings are discussed.

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Section: Discussionmentioning

confidence: 96%

SR146131, a cholecystokinin-A receptor agonist, antagonizes prepulse inhibition deficits produced by dizocilpine and DOI

Feifel

2002

Psychopharmacology

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“…Cholecystokinin (CCK) is a neurotransmitter that is very widely distributed throughout the brain, as are its receptors (principally CCK-B type) [154]. CCK interacts with serotonin, dopamine and noradrenaline systems [155][156][157] and in general antagonizes enkephalins. It is co-localized with dopamine in some neurons [158].…”

Section: Possibilities For Specific Pharmacological Therapymentioning

confidence: 99%

Chronic fatigue syndrome—aetiological aspects

Dickinson

1997

Eur J Clin Investigation

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The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.

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“…Specifically, CCK stimulates DA release by acting on CCK-1 receptors [4], while activation of the CCK-2 receptor confers an inhibitory effect on DA release [22]. In contrast to the ubiquitous presence of CCK-2 receptors throughout the brain, populations of central CCK-1 receptors are only known to exist within limited regions, such as the dorsomedial hypothalamus [23,30] and striatum [10], with specifically high intensity in the caudo-medial shell of the nucleus accumbens (NAcc) [17,20]. In the caudal NAcc, DA and CCK are co-released in vivo after administration of drugs that increase DA neuronal firing rate [4,19].…”

Section: Introductionmentioning

confidence: 99%

Brief intermittent access to sucrose differentially modulates prepulse inhibition and acoustic startle response in obese CCK-1 receptor deficient rats

Jonghe¹,

Martino²,

Hajnal³

et al. 2005

Brain Research

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Otsuka Long-Evans Tokushima Fatty (OLETF) rats lack the CCK-1 receptor and are hyperphagic and obese. CCK-1 receptors play a role in prepulse inhibition (PPI) by modulating mesolimbic dopamine transmission, a modulator of sensorimotor gating. Therefore, the present study assessed the effects of brief, daily sucrose access on PPI and acoustic startle response (ASR) in OLETF rat and age-matched non-mutant Long-Evans Tokushima Otsuka (LETO) rats. The results revealed that OLETF rats with sucrose access showed an increased ASR [F(1,16) = 6.84; P < 0.01)], relative to sucrose receiving LETO rats. No significant sucrose effect (P = 0.283) on PPI was noted in OLETF rats, whereas sucrose receiving LETO rats had a significantly lower (P < 0.05) PPI percentage than non-sucrose controls. In contrast, sucrose-receiving OLETF rats expressed significantly higher PPI percentage than LETO rats with identical sucrose presentation (P < 0.01). Taken together, these results suggest that sucrose access alters PPI and ASR in general, and the CCK-1 receptors play a modulatory role in facilitating or inhibiting these responses, respectively. A similar effect may be contributory to the hyperphagic behavioral phenotype of obese animal models with altered central dopamine regulation.

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Regional amines levels in the rat brain following intra-accumbens cholecystokinin and intraperitoneal amphetamine pre-treatment

Cited by 5 publications

References 10 publications

SR146131, a cholecystokinin-A receptor agonist, antagonizes prepulse inhibition deficits produced by dizocilpine and DOI

SR146131, a cholecystokinin-A receptor agonist, antagonizes prepulse inhibition deficits produced by dizocilpine and DOI

Chronic fatigue syndrome—aetiological aspects

Brief intermittent access to sucrose differentially modulates prepulse inhibition and acoustic startle response in obese CCK-1 receptor deficient rats

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