The 5-HT1A serotonin receptor is located on calbindin- and parvalbumin-containing neurons in the rat brain

Aznar, Susana; Qian, Zhaoxia; Shah, Reshma; Rahbek, Birgitte; Knudsen, Gitte M.

doi:10.1016/s0006-8993(02)03727-7

Cited by 162 publications

(111 citation statements)

References 44 publications

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“…The companies of origin have previously tested the specificity of the 5-HT and 5HT receptor antisera. Moreover, their specificity in rat tissue has been confirmed in different studies (Aznar et al, 2003;Morales et al, 1996;Morales and Bloom, 1997;Willins et al, 1997). Overnight incubation of 5-HT3 antibody with an excess of its immunogenic peptide resulted in a total absence of 5HT-3 immunostaining in the mPFC.…”

Section: Double Immunofluorescencementioning

confidence: 72%

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Varea

Blasco-Ibáñez

Gómez-Climent

et al. 2006

Neuropsychopharmacol

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Recent hypotheses suggest that changes in neuronal structure and connectivity may underlie the etiology of depression. The medial prefrontal cortex (mPFC) is affected by depression and shows neuronal remodeling during adulthood. This plasticity may be mediated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), which is intensely expressed in the adult mPFC. As the expression of PSA-NCAM is increased by serotonin in other cerebral regions, antidepressants acting on serotonin reuptake may influence PSA-NCAM expression and thus counteract the effects of depression by modulating neuronal structural plasticity. Using immunohistochemistry, we have studied the relationship between serotoninergic fibers and PSA-NCAM expressing neurons in the adult rat mPFC and the expression of serotonin receptors in these cells. The effects of fluoxetine treatment for 14 days on mPFC PSA-NCAM expression have also been analyzed. Although serotoninergic fibers usually do not contact PSA-NCAM immunoreactive neurons, most of these cells express 5-HT3 receptors. In general, chronic fluoxetine treatment induces significant increases in the number of PSA-NCAM immunoreactive neurons and in neuropil immunostaining and coadministration of the 5-HT3 antagonist ondansetron blocks the effects of fluoxetine on PSA-NCAM expression. These results indicate that fluoxetine, acting through 5-HT3 receptors, can modulate PSA-NCAM expression in the mPFC. This modulation may mediate the structural plasticity of this cortical region and opens new perspectives on the study of the molecular bases of depression.

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Section: Double Immunofluorescencementioning

confidence: 72%

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Varea

Blasco-Ibáñez

Gómez-Climent

et al. 2006

Neuropsychopharmacol

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“…The ability of an SSRI to normalize GABA levels in depression and even increase it in healthy subjects (Bhagwagar et al, 2004b) suggests close interactions between these systems. Immunohistochemical studies reveal the presence of serotonin-1A (Aznar et al, 2003) and serotonin-2A (Jakab and Goldman-Rakic, 2000;Pazos et al, 1987b) receptors on nearly all CB-IR and PV-IR neurons. Moreover, serotonin-1A receptors are preferentially found in layer II of human prefrontal cortex (Burnet et al, 1995;Pazos et al, 1987a;Varnas et al, 2004) and PET studies show a significant reduction in radioligand binding to serotonin-1A receptors in depressed subjects (Bhagwagar et al, 2004a;Sargent et al, 2000).…”

Section: Discussionmentioning

confidence: 98%

GABAergic Neurons Immunoreactive for Calcium Binding Proteins are Reduced in the Prefrontal Cortex in Major Depression

Rajkowska

O'Dwyer

Teleki

et al. 2006

Neuropsychopharmacol

373

234

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Post-mortem morphometric studies report reductions in the average density and size of cortical neurons in the dorsolateral prefrontal cortex (dlPFC) and orbitofrontal cortex (ORB) in major depressive disorder (MDD). The contribution of specific neuronal phenotypes to this general pathology in depression is still unclear. Post-mortem sections from the dlPFC and ORB regions of 14 subjects with MDD and 11 controls were immunostained to visualize calbindin-immunoreactive (CB-IR) and parvalbumin-immunoreactive (PV-IR) presumptive GABAergic neurons. A three-dimensional cell counting probe was used to assess the cell packing density and size of CB-IR neurons in layers II + IIIa and PV-IR neurons in layers III-VI. The density of CB-IR neurons was significantly reduced by 50% in depression in the dlPFC and there was a trend toward reduction in the ORB. The size of CB-IR somata was significantly decreased (18%) in depression in the dlPFC with a trend toward reduction in the ORB. In contrast, there was no difference in the density of PV-IR neurons between the depressed and control groups in the dlPFC. The size of PV-IR neuronal soma was unchanged in depressed compared to control subjects in either dlPFC or ORB. In depression, subpopulations of GABAergic neurons may be affected differently in dlPFC and ORB. A significant reduction in the density and size of GABAergic interneurons immunoreactive for calcium binding proteins was found predominantly in the dlPFC region. These cellular changes are consistent with recent neuroimaging studies revealing a reduction in the cortical levels of GABA in depression.

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“…Because a specific antibody that distinctly labels 5-HT 7 receptors in hamster brain tissue is not available, we have been unable to investigate whether 5-HT 7 receptor protein is co-localized at the cellular level with calbindin protein. It is interesting to note that immunohistochemical studies have shown that another serotonin receptor subtype, the 5-HT 1A receptor, is co-localized with calbindin in several rat brain regions, including the hippocampus, the thalamus and the septum (Aznar et al, 2003). As well as modulating photic phase shifts (Hamada et al, 2003), as described above, calbindin has been implicated in several other functions, including spatial memory, long-term potentiation in the hippocampus, synaptic plasticity, and either neuroprotection or enhanced vulnerability to neurodegeneration (Jouvenceau et al, 1999;Chard et al, 1995;Molinari et al, 1996;Nagerl et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

Duncan

Franklin

2007

Brain Research

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Aging affects several processes modulated by the 5-HT 7 receptor subtype, including circadian rhythms, learning and memory, and depression. Previously, we showed that aging induces a decrease in the hamster dorsal raphe (DRN) in both 5-HT 7 receptor binding and circadian phase resetting responses to 8-OH-DPAT microinjection. To elucidate the mechanisms underlying the aging decrease in 5-HT 7 receptors, we investigated aging modulation of 5-HT 7 receptor mRNA expression in the DRN, brain regions afferent to the DRN, and brain regions regulating circadian rhythms or memory. In situ hybridization for 5-HT 7 receptor mRNA was performed on coronal sections prepared from the brains of young, middle-aged, and old male Syrian hamsters. 5-HT 7 receptor mRNA expression was quantified by densitometry of X-ray film autoradiograms. The results showed that aging did not significantly affect 5-HT 7 receptor mRNA expression in the DRN or most other brain regions examined, with the exception of the cingulate cortex and paraventricular thalamic nucleus. Within the suprachiasmatic nucleus, the site of the master circadian pacemaker in mammals, 5-HT 7 receptor mRNA expression was localized in a discrete subregion resembling the calbindin subnucleus previously described. A second experiment using adjacent tissue sections showed that 5-HT 7 receptor mRNA and calbindin mRNAs were concentrated in the same region of the SCN, and as well as in the same region of several other brain structures. The localization of 5-HT 7 receptors and calbindin mRNAs within the same regions suggests that proteins they encode may interact to modulate processes such as circadian timekeeping.

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The 5-HT1A serotonin receptor is located on calbindin- and parvalbumin-containing neurons in the rat brain

Cited by 162 publications

References 44 publications

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

GABAergic Neurons Immunoreactive for Calcium Binding Proteins are Reduced in the Prefrontal Cortex in Major Depression

Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

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