Journal
DEVELOPMENTAL PSYCHOBIOLOGY
Volume 50, Issue 7, Pages 665-679Publisher
JOHN WILEY & SONS INC
DOI: 10.1002/dev.20325
Keywords
glutamate; NMDA; antagonist; calcium buffering; development; rat; neonatal brain injury
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Funding
- Wake Forest University Faculty Development Fund
- NIH [RO1 NS051632]
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MK801-induced activation of caspase-3 is developulentally regulated, peaking at postnatal day (P) 7 and decreasing with increasing postnatal age thereafter. Further, at P7, cells displaying activation of caspase-3 lack expression of calcium binding proteins (CaBPs). To further explore this relationship, we investigated postnatal expression of calbindin (CB), calretinin (CR) and parvalbumin (PV) in two brain regions susceptible to MK801-induced injury, the somatosensory cortex (SI) and layer II/III of motor cortex (M1/M2). Expression of CB and especially PV was low to absent prior to P7 but substantially increased from P7 through to P21 and adulthood. In contrast, CR expression was more variable at early developmental ages, stabilized to lower levels after P7 and showed a marked decline by P21. The results suggest that not only does calcium buffering capacity increase developmentally but also acquisition of enhanced buffering may be one mechanism by which neurons survive agent-induced alterations in calcium homeostasis. (c) 2008 Wiley Periodicals, Inc. Dev Psychobiol 50: 665-679, 2008.
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