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Published on: March 23, 2011
Decline in age-dependent, MK801-induced injury coincides with developmental switch in parvalbumin expression:
Carla M Lema Tomé1, Ryan Miller, Clayton Bauer
1Neurobiology & Anatomy, Wake Forest University Medical School, Medical Center Boulevard, Winston Salem, NC 27157-1010, USA. cltome@wfubmc.edu
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.
Insights
MK801 drug causes caspase-3 activation in developing brains, peaking at postnatal day 7. Increased calcium binding proteins (CaBPs) after this period may protect neurons from MK801-induced injury.
Area of Science:
- Neuroscience
- Developmental Biology
- Neuropharmacology
Background:
- MK801 induces caspase-3 activation, a marker of cell death, in a developmentally regulated manner.
- At postnatal day 7 (P7), caspase-3 activation occurs in cells lacking calcium binding proteins (CaBPs).
Purpose of the Study:
- To investigate the postnatal expression of key CaBPs: calbindin (CB), calretinin (CR), and parvalbumin (PV).
- To examine CaBP expression in the somatosensory cortex (S1) and motor cortex (M1/M2) following MK801 exposure.
Main Methods:
- Immunohistochemical analysis of CaBP expression (CB, CR, PV) in developing rat brain regions (S1, M1/M2).
- Assessment of developmental changes in CaBP expression from P7 to adulthood.
Main Results:
- CB and PV expression increased significantly from P7 through P21 and into adulthood.
- CR expression showed variability early on, stabilizing at lower levels post-P7 and declining by P21.
- MK801-induced caspase-3 activation was inversely correlated with developmental increases in CaBP expression.
Conclusions:
- Developing neurons gain increased calcium buffering capacity with age, particularly from P7 onwards.
- Enhanced calcium buffering by CaBPs may be a critical mechanism protecting neurons against excitotoxicity and MK801-induced damage.
