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Expression changes of somatostatin receptor subtypes sst2A, sst2B, sst3 and sst4 after a cortical contusion trauma in
Holger Braun1, Stefan Schulz, Volker Höllt
1Institut für Pharmakologie und Toxikologie, Otto-von-Guericke-Universität Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
Abstract:
The neuropeptide somatostatin acts as a neuromodulator in the CNS in a predominantly inhibitory manner. In this study, an ipsilateral cortical and hippocampal damage in the brain of adult rats was induced by a cortical contusion trauma in order to examine subsequent changes of expression of different somatostatin receptor subtypes (sst). By using subtype specific antibodies we found a clear decline of expression level for sst2A, sst2B, sst3 and sst4 subtypes in the pyramidal cell layer of the ipsilateral hippocampus. Nissl staining revealed that this decline of expression level is due to cell death of sst expressing neurons within the first 48 h after trauma. Additionally we found a progressive infiltration of sst4 positive cells into regions of cortical and hippocampal damage. The number of these cells increases strikingly within the first 3 days after trauma and it seems that their morphology changes from a round to an astrocyte-like shape. Moreover, sst4 and sst2A positive cells accumulate in the ipsilateral ependym and pyramidal-like cells expressing sst4 were found beneath the damaged CA3 pyramidal layer. Taken together, after trauma we found deterioration of sst positive neurons and an additional activation of sst4 and sst2A expressing cells the final fate of which has to be elucidated further.
Insights
Brain injury in rats caused somatostatin (sst) neuron death and altered sst receptor expression. Activated sst4 and sst2A cells infiltrated damaged areas, indicating complex post-trauma neural changes.
Area of Science:
- Neuroscience
- Cell Biology
Background:
- Somatostatin (sst) is a neuropeptide neuromodulator in the central nervous system (CNS).
- Its role in CNS injury response is not fully understood.
Purpose of the Study:
- To investigate changes in somatostatin receptor subtype expression after brain injury.
- To determine the fate of somatostatin-expressing neurons and identify infiltrating cells.
Main Methods:
- Induced ipsilateral cortical and hippocampal damage in adult rats using cortical contusion trauma.
- Utilized subtype-specific antibodies to analyze somatostatin receptor expression.
- Performed Nissl staining to assess neuronal survival.
Main Results:
- Significant decline in sst2A, sst2B, sst3, and sst4 receptor expression in the hippocampus due to neuronal death within 48 hours post-trauma.
- Progressive infiltration of sst4-positive cells into damaged cortical and hippocampal regions, with morphological changes suggesting astrocyte activation.
- Accumulation of sst4 and sst2A positive cells in the ependym and beneath the CA3 pyramidal layer.
Conclusions:
- Cortical contusion trauma leads to the deterioration of somatostatin-expressing neurons.
- An increase in sst4 and sst2A expressing cells suggests a reactive glial response post-injury.
- Further research is needed to elucidate the precise role of these activated cells.
