Abstract:
:Following neonatal hypoxia-ischemia (HI) serotonin (5-hydroxytryptamine, 5-HT) levels are decreased in the brain. The regulation of brain 5-HT is dependent on the serotonin transporter (SERT) localised at the neuronal pre-synaptic cell membrane. However SERT can also traffic away from the cell membrane into the cytosol and, after injury, may contribute to the cell's inability to maintain 5-HT levels. Whether this occurs after neonatal HI brain injury is not known. In addition, there is contradictory evidence that glial cells may also contribute to the clearance of 5-HT in the brain. Using a postnatal day 3 (P3) HI rat pup model (right carotid ligation+30 min 6% O(2)), we found, in both control and P3 HI animals, that SERT is retained on the cell membrane and is not internalised in the cytosol. In addition, SERT was only detected on neurons. We found no evidence of SERT co-localisation on microglia or astrocytes. We conclude that neuronal SERT is the primary regulator of synaptic 5-HT availability in the intact and P3 HI-injured neonatal brain. Furthermore, since concomitant reductions in 5-HT, SERT and serotonergic neurons occur after neonatal HI, it is plausible that the decrease in brain 5-HT is a consequence of SERT being lost as neurons degenerate as opposed to remaining neurons internalising SERT or clearance by glial cells.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Wixey JA,Reinebrant HE,Buller KMdoi
10.1016/j.neures.2012.04.002subject
Has Abstractpub_date
2012-07-01 00:00:00pages
252-6issue
3eissn
0168-0102issn
1872-8111pii
S0168-0102(12)00077-6journal_volume
73pub_type
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