This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator.
Specific Aims - Previously we characterized and compared mitochondrial cristae topography and connectivity, matrix volume and contact sites of rod and cone inner segments (RIS & CIS) from wild-type C57BL/6 mice using electron tomography. Since postnatal lead exposure produces rod-selective apoptosis, we also examined RIS mitochondria from wild-type and transgenic mice overexpressing Bcl-xL in photoreceptors (Tg) exposed to either water or lead (Pb) solution during postnatal development.
The aim of the study this year was to similarly characterize the mitochondria in synaptic terminals (ST) of wild-type rods (spherules) and cones (pedicles) and in rod spherules of wild-type and Tg mice exposed to either water or Pb solution during postnatal development and then to compare the respective mitochondrial ST and IS results. Publications: Johnson, J.E., Perkins, G.A., Brown, J., Lahsaei, P., Ghassemzadeh, S., Ellisman M.H., and Fox, D.A. (2006). A Three-Dimensional Electron Tomographic Analysis of Rod Photoreceptor Synaptic Terminal Mitochondria in Control, Lead-Exposed, and/or Bcl-xL Transgenic Mice. ARVO Meeting. Fort Lauderdale, FL. May 2006. Perkins, Guy A.; Brown, Joshua; Lahsaei, Peiman; Ghassemzadeh, Sassan; Ellisman, Mark H.; Johnson, Jerry E.; Fox, Donald A. (2006) Bcl-Xl Overexpression Protects Rod Photoreceptor Synaptic Terminal Mitochondria From Lead-Induced Permeability Transition. Society of Toxicology Meeting. San Diego, CA, Mar. 2006.
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