Chronic administration of citalopram in olfactory bulbectomy rats restores brain 5-HT synthesis rates: an autoradiographic study

Hasegawa, Shu; Watanabe, Arata; Nguyen, Khanh Q.; Debonnel, Guy; Dikšić, Mirko

doi:10.1007/s00213-004-2122-1

Cited by 33 publications

(44 citation statements)

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“…We have shown that elevated 5-HT synthesis rates in an animal model of depression, olfactory bulbectomized (OBX) rats, were normalized following chronic SSRI treatment [30]. It was thought that normalized 5-HT synthesis rates resulted in the desensitization of the 5-HT 1A receptor [30].…”

Section: Discussionmentioning

confidence: 99%

“…A set of representative autoradiograms illustrating 5-HT synthesis in the rat brain as determined by the α-MTrp method have been presented in many previous publications [49,37,24,52,75,30,31] and their addition would not provide any new information, because the logarithmic scale between the tracer concentration (represented by 5-HT synthesis) and optical density. All that can be seen from these images is the brain non-homogenous distribution.…”

Section: Measurement Of the α-Mtrp Trapping And Calculation Of 5-ht Smentioning

confidence: 99%

“…All that can be seen from these images is the brain non-homogenous distribution. The resultant images on the X-ray film were analyzed using a microcomputerbased image analyzing system (MCID/M4-Image Analysis System, Imaging Research Inc., Canada) and tissue equivalent calibrated standards as detailed in previous publications [49,37,23,30]. The optical densities were converted into tissue radioactivity concentration (nCi/g).…”

Section: Measurement Of the α-Mtrp Trapping And Calculation Of 5-ht Smentioning

confidence: 99%

“…It is also important to investigate whether 5-HT 2A receptors play a role in the modulation of 5-HT synthesis, as the modulation of regional 5-HT synthesis appears to be part of antidepressant action [37,23,10,30,46]. This question was studied by investigating the influence of a selective 5-HT 2A antagonist, M100907.…”

Section: Introductionmentioning

confidence: 99%

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5-HT2A receptor antagonist M100907 reduces serotonin synthesis: An autoradiographic study

Hasegawa

Fikre-Merid

Dikšić

2012

Brain Research Bulletin

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The effects of the administration of the serotonin (5-HT) 2A antagonist, M100907, on 5-HT synthesis rates, were evaluated using the α-[ 14 C]methyl-L-tryptophan (α-MTrp) autoradiographic method. In the treatment study, M100907 (10 mg/kg) was injected intraperitoneally 30 min before the α-MTrp injection (30 μCi over 2 min). A single dose of M100907 caused a significant decrease in the synthesis in the anterior olfactory nucleus, accumbens nucleus, frontal cortex, sensory-motor cortex, cingulate cortex, medial caudate-putamen, dorsal thalamus, substantia nigra, inferior collicus, raphe magnus nucleus, superior olive, and raphe pallidus nucleus.These data suggest that the terminal 5-HT 2A receptors are involved in the regulation of 5-HT synthesis in the entire brain. Further, 5-HT synthesis is likely regulated by the 5-HT 2A antagonistic property of M100907 in the cortices, anterior olfactory nucleus, caudate putamen, and nucleus accumbens.

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Section: Discussionmentioning

confidence: 99%

Section: Measurement Of the α-Mtrp Trapping And Calculation Of 5-ht Smentioning

confidence: 99%

Section: Measurement Of the α-Mtrp Trapping And Calculation Of 5-ht Smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

5-HT2A receptor antagonist M100907 reduces serotonin synthesis: An autoradiographic study

Hasegawa

Fikre-Merid

Dikšić

2012

Brain Research Bulletin

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“…Several neurochemical and behavioural studies [3][4][5] have found alterations in serotonergic neurotransmission after treatment with various classes of antidepressant drugs, including selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors (SSRI), such as fluvoxamine [6].…”

Section: Introductionmentioning

confidence: 99%

Acute treatment with fluvoxamine elevates rat brain serotonin synthesis in some terminal regions: An autoradiographic study

Mück‐Šeler

Pivac

Dikšić

2012

Nuclear Medicine and Biology

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Introduction-A considerable body of evidence indicates the involvement of the neurotransmitter serotonin (5-HT) in the pathogenesis and treatment of depression.Methods-The acute effect of fluvoxamine, on 5-HT synthesis rates was investigated in rat brain regions, using α-14 C-methyl-L-tryptophan as a tracer. Fluvoxamine (25 mg/kg) and saline (control) were injected intraperitoneally, one hour before the injection of the tracer (30 μCi).Results-There was no significant effect of fluvoxamine on plasma free tryptophan. After Benjamini-Hochberg False Discovery Rate correction, a significant decrease in the 5-HT synthesis rate in the fluvoxamine treated rats, was found in the raphe magnus (−32%), but not in the median (−14%) and dorsal (−3%) raphe nuclei. In the regions with serotonergic axon terminals, significant increases in synthesis rates were observed in the dorsal (+41%) and ventral (+43%) hippocampus, visual (+38%), auditory (+65%) and parietal (+37%) cortex, and the substantia nigra pars compacta (+56%). There were no significant changes in the 5-HT synthesis rates in the median (+11%) and lateral (+24%) part of the caudate-putamen, nucleus accumbens (+5%), VTA (+16%) or frontal cortex (+ 6%).Conclusions-The data show that the acute administration of fluvoxamine affects 5-HT synthesis rates in a regionally specific pattern, with a general elevation of the synthesis in the terminal regions and a reduction in some cell body structures. The reasons for the regional specific effect of fluvoxamine on 5-HT synthesis are unclear, but may be mediated by the presynaptic serotonergic autoreceptors. Keywords

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Evaluation of reward processes in an animal model of depression

2006

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Rationale Anhedonia is a core symptom of major depression. Deficits in reward function, which underlie anhedonia, can be readily assessed in animals. Therefore, anhedonia may serve as an endophenotype for understanding the neural circuitry and molecular pathways underlying depression.Objective Surprisingly, there is scant knowledge regarding alterations in brain reward function after olfactory bulbectomy (OB), an animal model which results in a behavioural syndrome responsive to chronic antidepressant treatment. Therefore, the present studies aimed to assess reward function after bulbectomy. Materials and methods The present study utilized sucrose preference, cocaine-induced hyperlocomotion and intracranial self-stimulation (ICSS) responding to examine reward processes in the OB model.Results Bulbectomized animals showed a marked preference (>90%) for 0.8% sucrose solution compared with water; similar to the preference exhibited by sham controls. Importantly, there were pronounced deficits in brain reward function, as assessed using ICSS, which lasted 8 days before returning to baseline levels. Furthermore, bulbectomized animals were hyper-responsive to the locomotor stimulating properties of an acute and a repeated cocaine regimen. However, no difference in ICSS facilitation was observed in response to an acute cocaine injection. Conclusions Taken together, these results suggest that bulbectomized rats display alterations in brain reward function, but these changes are not long-lasting and thus, not amenable to investigating the effects of pharmacological interventions. However, given that OB animals are hypersensitive to drugs of abuse, bulbectomy may be an appropriate inducing factor for the development of animal models of co-morbid depression and drug dependence.

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Chronic administration of citalopram in olfactory bulbectomy rats restores brain 5-HT synthesis rates: an autoradiographic study

Cited by 33 publications

References 50 publications

5-HT2A receptor antagonist M100907 reduces serotonin synthesis: An autoradiographic study

5-HT2A receptor antagonist M100907 reduces serotonin synthesis: An autoradiographic study

Acute treatment with fluvoxamine elevates rat brain serotonin synthesis in some terminal regions: An autoradiographic study

Evaluation of reward processes in an animal model of depression

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