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Rigshospitalet - en del af Københavns Universitetshospital
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Aging and depression vulnerability interaction results in decreased serotonin innervation associated with reduced BDNF levels in hippocampus of rats bred for learned helplessness

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  1. Similar serotonin-2A receptor binding in rats with different coping styles or levels of aggression

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  2. Acute social defeat does not alter cerebral 5-HT2A receptor binding in male Wistar rats

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  3. Transient activation of mTOR following forced treadmill exercise in rats

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  4. Direct comparison of [(18) F]MH.MZ and [(18) F]altanserin for 5-HT(2A) receptor imaging with PET

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  1. Blocking of efflux transporters in rats improves translational validation of brain radioligands

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  2. Glucagon-like peptide-1 receptor regulation of basal dopamine transporter activity is species-dependent

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  3. Different preprocessing strategies lead to different conclusions: A [11C]DASB-PET reproducibility study

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  4. Towards selective CNS PET imaging of the 5-HT7 receptor system: Past, present and future

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Vis graf over relationer
Epidemiological studies have revealed a strong genetic contribution to the risk for depression. Both reduced hippocampal serotonin neurotransmission and brain-derived neurotrophic factor (BDNF) levels have been associated with increased depression vulnerability and are also regulated during aging. Brains from young (5 months old) and old (13 months old) congenital Learned Helplessness rats (cLH), and congenital Non Learned Helplessness rats (cNLH) were immunohistochemically stained for the serotonin transporter and subsequently stereologically quantified for estimating hippocampal serotonin fiber density. Hippocampal BDNF protein levels were measured by ELISA. An exacerbated age-related loss of serotonin fiber density specific for the CA1 area was observed in the cLH animals, whereas reduced hippocampal BDNF levels were seen in young and old cLH when compared with age-matched cNLH controls. These observations indicate that aging should be taken into account when studying the neurobiological factors behind the vulnerability for depression and that understanding the effect of aging on genetically predisposed individuals may contribute to a better understanding of the pathophysiology behind depression, particularly in the elderly.
OriginalsprogEngelsk
TidsskriftSynapse (New York, N.Y.)
Vol/bind64
Udgave nummer7
Sider (fra-til)561-5
Antal sider5
DOI
StatusUdgivet - 1 jul. 2010

ID: 32197997