Aging of the serotonergic system in the rat forebrain: An immunocytochemical and neurochemical study

Luijtelaar, M. G. P. A. van; Tonnaer, J. A. D. M.; Steinbusch, Harry W.M.

doi:10.1016/0197-4580(92)90032-s

Cited by 85 publications

(59 citation statements)

References 43 publications

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“…Such features have already been reported for serotonergic and cholinergic systems in normal, aging rats [7,110,77,3], as well as in the entire monoaminergic system of Zitter mutant or microenchephalic rats [106,114]. Enlarged/swollen varicosities are generated by accumulations of intra-axonal materials as a result of impaired axonal transport due to destabilization of microtubules.…”

Section: Selective Noradrenergic Axonal Degeneration In Sstr2 -/-Brainsmentioning

confidence: 86%

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Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

et al. 2015

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Alzheimer's disease and other age-related neurodegenerative disorders are associated with deterioration of the noradrenergic locus coeruleus (LC), a probable trigger for mood and memory dysfunction. LC noradrenergic neurons exhibit particularly high levels of somatostatin binding sites. This is noteworthy since cortical and hypothalamic somatostatin content is reduced in neurodegenerative pathologies. Yet the role of a somatostatin signal-

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Section: Selective Noradrenergic Axonal Degeneration In Sstr2 -/-Brainsmentioning

confidence: 86%

“…Enlarged/swollen varicosities are generated by accumulations of intra-axonal materials as a result of impaired axonal transport due to destabilization of microtubules. The knot-like fiber clusters are formed following the gradual degeneration of intervaricose connections [110,109,4].…”

Section: Selective Noradrenergic Axonal Degeneration In Sstr2 -/-Brainsmentioning

confidence: 99%

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

et al. 2015

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“…14 Several lines of evidence suggest a role for 5-HT during aging, including structural and functional age-related changes in the 5-HT system in rodents [15][16][17] and in humans, as documented by post-mortem receptor binding studies, [18][19][20] RNA level studies, 21 in vivo imaging studies 22 and neuroendocrine challenges. 10 Depending on the brain region investigated, the 5-HT modulation of cerebral glucose metabolism increases or decreases during normal aging, suggesting a deregulated control of 5-HT 23 (see also 24 ). The mechanisms for age-related changes in 5-HT function are not known and may include gene variants, pharmacological manipulation in adult/old population or late-onset functional declines.…”

Section: Introductionmentioning

confidence: 99%

Lack of serotonin1B receptor expression leads to age-related motor dysfunction, early onset of brain molecular aging and reduced longevity

Sibille

Leman

et al. 2007

Mol Psychiatry

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Normal aging of the brain differs from pathological conditions and is associated with increased risk for psychiatric and neurological disorders. In addition to its role in the etiology and treatment of mood disorders, altered serotonin (5-HT) signaling is considered a contributing factor to aging; however, no causative role has been identified in aging. We hypothesized that a deregulation of the 5-HT system would reveal its contribution to agerelated processes and investigated behavioral and molecular changes throughout adult life in mice lacking the regulatory presynaptic 5-HT 1B receptor (5-HT 1B R), a candidate gene for 5-HTmediated age-related functions. We show that the lack of 5-HT 1B R (Htr1b KO mice) induced an early age-related motor decline and resulted in decreased longevity. Analysis of life-long transcriptome changes revealed an early and global shift of the gene expression signature of aging in the brain of Htr1b KO mice. Moreover, molecular changes reached an apparent maximum effect at 18-months in Htr1b KO mice, corresponding to the onset of early death in that group. A comparative analysis with our previous characterization of aging in the human brain revealed a phylogenetic conservation of age-effect from mice to humans, and confirmed the early onset of molecular aging in Htr1b KO mice. Potential mechanisms appear independent of known central mechanisms (Bdnf, inflammation), but may include interactions with previously identified age-related systems (IGF-1, sirtuins). In summary, our findings suggest that the onset of age-related events can be influenced by altered 5-HT function, thus identifying 5-HT as a modulator of brain aging, and suggesting age-related consequences to chronic manipulation of 5-HT.

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“…Based on their morphological similarities [9], the abnormal serotonergic fibers were assumed to be degenerative fibers. Such fibers have been reported in the brain and spinal cord of serotonergic neurotoxin-(5,7-dihydroxytryptamine or 5,6-dihydroxytryptamine) injected-rats [19], several amphetamine derivatives (p-chloramphetamine, 3,4-metylendioxymethamphetamine or fenfluamine) injectedrats [8, 14,16] and aged rats [10,20]. The production of free radicals has been associated with these treatments as well as aging.…”

Section: Discussionmentioning

confidence: 99%

Evidence for Degeneration of Monoaminergic Fibers in the Spinal Cord of Zitter Mutant Rats.

Okuda

Saitoh

Kitajima

et al. 1999

Acta Histochem. Cytochem

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Aging of the serotonergic system in the rat forebrain: An immunocytochemical and neurochemical study

Cited by 85 publications

References 43 publications

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

Lack of serotonin1B receptor expression leads to age-related motor dysfunction, early onset of brain molecular aging and reduced longevity

Evidence for Degeneration of Monoaminergic Fibers in the Spinal Cord of Zitter Mutant Rats.

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