1098-2302/asset/DEV_left.gif?v=1&s=de4a8863ac5f1ecdfa0b545e6a446f2f3a941009)
Research Article
Decline in age-dependent, MK801-induced injury coincides with developmental switch in parvalbumin expression: Somatosensory and motor cortex
Article first published online: 7 AUG 2008
DOI: 10.1002/dev.20325
Copyright © 2008 Wiley Periodicals, Inc.
1098-2302/asset/cover.gif?v=1&s=4a069b6f43d9b9804bdeb72039c0a49c9bb5628f "Developmental Psychobiology")
Additional Information
How to Cite
Lema Tomé, C. M., Miller, R., Bauer, C., Smith, C., Blackstone, K., Leigh, A., Busch, J. and Turner, C. P. (2008), Decline in age-dependent, MK801-induced injury coincides with developmental switch in parvalbumin expression: Somatosensory and motor cortex. Dev. Psychobiol., 50: 665–679. doi: 10.1002/dev.20325
Publication History
- Issue published online: 24 OCT 2008
- Article first published online: 7 AUG 2008
- Manuscript Accepted: 28 MAY 2008
- Manuscript Received: 28 JAN 2008
Funded by
- Wake Forest University Faculty Development Fund
- NIH. Grant Number: RO1 NS051632
- Abstract
- References
- Cited By
Keywords:
- glutamate;
- NMDA;
- antagonist;
- calcium buffering;
- development;
- rat;
- neonatal brain injury
Abstract
MK801-induced activation of caspase-3 is developmentally 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 (S1) 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. © 2008 Wiley Periodicals, Inc. Dev Psychobiol 50: 665-679, 2008.