Catecholamines and serotonin in the rat central nervous system after 6-OHDA, 5-7-DHT and p-CPA

Reader, Tomás A.; Gauthier, Pierre

doi:10.1007/bf01250009

Cited by 80 publications

(33 citation statements)

References 61 publications

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“…Biochemical and functional interac tions between the noradrenergic locus ceruleus and serotonergic raphe systems are well documented (e.g., Kostowski et aI., 1974;Saavedra et aI., 1976;Pujol, 1979;Pujol et aI., 198 1;Agren et aI., 1986;Brassard et aI., 1987) and both systems are affected by brain injury (Pappius andDadoun, 1986, 1987). PCPA has been reported to affect NE levels in brain under some conditions (Miller et aI., 1970;Rebec et aI., 1981;Reader and Gauthier, 1984;Reader et aI., 1986;Vanderwolf and Baker, 1986); in all cases, however, following higher doses than used in the present experiments. The decrease in cortical NE resulting from traumatization was statistically sig nificant when pooled groups were compared with pooled controls.…”

Section: Discussioncontrasting

confidence: 51%

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Pappius

Dadoun

McHugh

1988

J Cereb Blood Flow Metab

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Summary: It was shown previously that focal cortical freezing lesions in rats cause widespread decrease in local cerebral glucose utilization (LCGU) in cortical areas of the lesioned hemisphere. This was interpreted as reflecting a depression of cortical activity. It was then demonstrated that cortical serotonin (5-HT) metabolism was increased throughout the lesioned hemisphere of a focally injured brain. To find out if the changes in the serotonergic system are of functional importance and me diate the observed changes in LCG U, the effects of the inhibition of 5-HT synthesis with p-chlorophenylalanine (PCP A) on cerebral metabolism and biogenic amine con tent in injured brain were studied. PCPA in doses up to 300 mg/kg had little, if any, effect on LCG U in intact brain and in doses up to 100 mg/kg did not modify the depressed LCGU in injured brain. In doses of 200 and 300 mg/kg, PCP A selectively increased cortical glucose utilization in the lesioned hemisphere where it was de pressed following injury. PCPA decreased 5-HT levels in U sing focal cortical freezing in the rat as a model of cerebral injury and the deoxyglucose (DG) method as developed and described by Sokoloff et al. (1977) to assess the functional state of trauma tized brain, earlier studies (Pappius, 1981) showed that a widespread, but not uniformly distributed, depression of local cerebral glucose utilization Abbreviations used: DG, deoxyglucose; DHBA, dihydroxy benzylamine; 5-HIAA, 5-hydroxyindoleacetic acid; 5-HT, sero tonin; LCGU, local cerebral glucose utilization; NE, norepi nephrine; PCPA, p-chlorophenylalanine . 324the cortical and raphe areas of both intact and injured brain in a dose-dependent manner. However, at doses of PCPA ineffective on LCGU (50 and 100 mg/kg), traumati zation still resulted in increased 5-HT metabolism. Doses of PCPA that ameliorated the depression of LCGU in in jured brain completely prevented increases in both 5-HT and its metabolite 5-hydroxyindoleacetic acid seen fol lowing traumatization in untreated animals. These results provide evidence that decreased LCGU in lesioned brain is due to an activation of the serotonergic system by trau matization. The data are in agreement with the postulated inhibitory role of serotonin in the cortex and its involve ment in functional alterations associated with injury. They suggest that blockage of this neurotransmitter system may have a potential in the development of novel therapeutic approaches to brain injury. Key Words: Brain injury-p-Chlorophenylalanine-Local cerebral glucose utilization -Norepinephrine -Serotonin.(LCGU ) developed with time after lesioning. The effects were not related to the location of the le sion, which was regularly placed in the parietal cortex, but could be made more frontally or cau dally with the same results (Colle et aI., 1986). The most severe metabolic depression occurred in all the cortical regions of the lesioned hemisphere were 3 days after the lesion LCGU was -50% of normal from frontal to visual cortex (Pappius, 198 1). Thus, the ...

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Section: Discussioncontrasting

confidence: 51%

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Pappius

Dadoun

McHugh

1988

J Cereb Blood Flow Metab

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“…It has been shown that DHT injected into the brain region that is rich in dopaminergic terminals could change dopamine levels as well as serotonin at the injected region (Ludwig and Schwarting, 2007). However, intracerebroventricular injection of DHT as in the present study has been reported to generally spare dopaminergic neurons (Fischette et al, 1987;Reader and Gauthier, 1984;Winstanley et al, 2003). Therefore, the result of our DHT experiment suggests that the integrity of the serotonergic system is essential for the effect of fluoxetine on the dopaminergic modulation.…”

Section: Discussionmentioning

confidence: 34%

Chronic Fluoxetine Selectively Upregulates Dopamine D1-Like Receptors in the Hippocampus

Kobayashi

Haneda

Higuchi³

et al. 2012

Neuropsychopharmacol

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The dentate gyrus of the hippocampus has been implicated in mechanisms of action of selective serotonin reuptake inhibitors (SSRIs). We have recently demonstrated that the SSRI fluoxetine can reverse the state of maturation of the adult dentate granule cells and enhances serotonin 5-HT 4 receptor-mediated synaptic potentiation at the synapses formed by their mossy fiber axons. Here, we show that fluoxetine can induce long-lasting enhancement of dopaminergic modulation at the mossy fiber synapse. Synaptic responses arising from the mossy fiber-CA3 pyramidal cell synapse were recorded using acute mouse hippocampal slices. Dopamine potentiates mossy fiber synaptic transmission by activating D 1 -like receptors. Chronic fluoxetine treatment induced a prominent increase in the magnitude of dopamine-induced synaptic potentiation, and this effect was maintained at least up to 1 month after withdrawal of fluoxetine. Quantitative autoradiography revealed that binding of the D 1 -like receptor ligand [ 3 H]SCH23390 was selectively increased in the dentate gyrus and along the mossy fiber in fluoxetine-treated mice. However, binding of the 5-HT 4 receptor ligand [ 3 H]GR113808 was not significantly changed. These results suggest that chronic fluoxetine enhanced the dopaminergic modulation at least in part by upregulating expression of D 1 -like receptors, while the enhanced serotonergic modulation may be mediated by modifications of downstream signaling pathways. These enhanced monoaminergic modulations would greatly increase excitatory drive to the hippocampal circuit through the dentate gyrus. The highly localized upregulation of D 1 -like receptors further supports the importance of the dentate gyrus in the mechanism of action of SSRIs.

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“…The reasons for these contradictory results are not clear, but there are several possible explanations. Whereas PCPA is very effective in depleting central 5-HT, it can also deplete peripheral 5-HT (Koe and Weissman, 1966) and other monoamines (Reader and Gauthier, 1984;Dailly et al, 2006), and does not affect neuropeptides colocalized in 5-HT neurons, such as thyrotropin-releasing hormone and substance P (Walker et al, 1990;Przegalinski et al, 1992). Possibly for these reasons, data obtained using PCPA have contributed previously to erroneous conclusions about the role of 5-HT in sleep (Jouvet, 1999).…”

Section: Role Of Central 5-ht Neurons In Respiratory Controlmentioning

confidence: 91%

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

Hodges¹,

Tattersall²,

Harris³

et al. 2008

J. Neurosci.

294

348

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f/f/p mice was decreased by 50% compared with wild-type mice, whereas baseline ventilation and the hypoxic ventilatory response were normal. In addition, Lmx1b f/f/p mice rapidly became hypothermic when exposed to an ambient temperature of 4°C, decreasing core temperature to 30°C within 120 min. This failure of thermoregulation was caused by impaired shivering and nonshivering thermogenesis, whereas thermosensory perception and heat conservation were normal. Finally, intracerebroventricular infusion of 5-HT stimulated baseline ventilation, and rescued the blunted hypercapnic ventilatory response. These data identify a previously unrecognized role of 5-HT neurons in the CO 2 chemoreflex, whereby they enhance the response of the rest of the respiratory network to CO 2 . We conclude that the proper function of the 5-HT system is particularly important under conditions of environmental stress and contributes significantly to the hypercapnic ventilatory response and thermoregulatory cold defense.

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Catecholamines and serotonin in the rat central nervous system after 6-OHDA, 5-7-DHT and p-CPA

Cited by 80 publications

References 61 publications

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Chronic Fluoxetine Selectively Upregulates Dopamine D1-Like Receptors in the Hippocampus

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

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