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Nimodipine accelerates the postnatal development of parvalbumin and S-100 beta immunoreactivity in the rat brain
1Department of Animal Physiology, University of Groningen, Haren, The Netherlands.
Insights
Perinatal nimodipine treatment accelerated the development of parvalbumin (PV) and S-100 beta proteins in rat offspring
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Calcium (Ca2+) signaling plays a critical role in neuronal development and function.
- L-type Ca2+ channels are involved in various developmental processes in the brain.
- Understanding the impact of pharmacological interventions during development is crucial.
Purpose of the Study:
- To investigate the effects of chronic maternal nimodipine treatment on the expression of Ca2+-binding proteins in the developing rat brain.
- To examine the immunocytochemical distribution of parvalbumin (PV) and S-100 beta in the neocortex and hippocampus of offspring.
- To determine the developmental time course of these effects.
Main Methods:
- Pregnant rats received nimodipine (a Ca2+ antagonist) starting at postconceptual day 11.
- Offspring were analyzed at postnatal days (PD) 5, 7, 10, 14, and 20.
- Immunocytochemistry was used to assess the expression and distribution of PV and S-100 beta.
Main Results:
- Nimodipine treatment significantly increased parvalbumin (PV) expression in the neocortex and hippocampus by PD 10 (more than two-fold).
- This enhancement in PV expression was transient, disappearing by PD 14 and 20.
- Nimodipine also increased S-100 beta-immunopositive glial cells in the neocortex at PD 5 and 7, with effects diminishing after PD 10.
Conclusions:
- Perinatal blockade of L-type Ca2+ current by nimodipine accelerates the development of PV and S-100 beta immunoreactivity in the postnatal forebrain.
- These findings suggest a critical role for L-type Ca2+ channels in regulating the developmental timing of specific neuronal and glial protein expression.
- The transient nature of the observed effects highlights a sensitive developmental window for nimodipine's impact.
Abstract:
The effects of chronic maternal perinatal nimodipine treatment on the immunocytochemical distribution of the Ca(2+)-binding proteins parvalbumin (PV) and S-100 beta in neocortex and hippocampus were studied at the age of postnatal day (PD) 5, 7, 10, 14 and 20. The Ca2+ antagonist nimodipine (1000 ppm BAY e 9736 in daily food) was administered to pregnant rats starting at postconceptual day 11. The expression of PV exemplified in layer V of parietal and retrosplenial cortex and in all hippocampal layers of CA1 and CA3 was enhanced by more than two-fold in the offspring of nimodipine-treated dams at PD 10 compared with placebo-treated animals. The difference was no longer present at PD 14 and 20. Nimodipine administration also significantly increased the number of S-100 beta-immunopositive glial cells in upper neocortical layers I-III at PD 5 and 7. Again, the difference between nimodipine and placebo-treated animals disappeared after PD 10. The data indicate an accelerated development of PV and S-100 immunoreactivity in the postnatal forebrain as a result of perinatal blockade of the L-type Ca2+ current.