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Adrian Corbett, Ph.D.
Associate Professor
Address: 250 Biological Sciences Building
Phone: (937) 775-2058
E-mail: adrian.corbett@wright.edu
University of Miami (Florida), 1984
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Research Interests:
My laboratory has three main areas of research: 1) excitation-contraction
coupling research in skeletal muscle, 2) study of voltage-gated sodium channel
subtypes in brain, with a particular interest in different localization,
and 3) changes in ligand receptor density or neuronal activity in brain in
response to stress, disease state, or environmental changes.
In excitation-contraction coupling research, my laboratory has used isolated
triads from skeletal muscle to examine the effect of various compounds and
ions on depolarization-induced calcium release. The triad is composed of
a transverse tubule and two physically attached terminal cisternae of the
sarcoplasmic reticiulum. Chemically-induced depolarization of the transverse
tubule initiates calcium release in a voltage-dependent manner from the calcium-loaded
terminal cisternae, which is monitored through changes in Fura fluorescence.
My work on sodium channel subtypes in brain has resulted in the generation
of subtype specific polyclonal antibodies, which have been used to study
sodium channel subtype localization in the brain. This work has pointed to
an interesting change in localization for the RII sodium channel subtype:
in every area of the brain this channel is localized in unmyelinated axons
EXCEPT in specific regions of the hypothalamus, which it is ALSO found on
the neuronal soma and on dendrites. This suggests that signal for specific
targeting of the RII sodium channel to unmyelinated axons may have been lost
in these areas, resulting in localization of this channel all over the neuron
cell membrane. My laboratory is pursuing isolation of RII sodium channels
from the hypothalamus and intends to compare peptide digests of these channels
with those which are normally targeted to unmyelinated neurons, through the
use of reverse phase chromatography. [Image]
Finally, my laboratory has pursued some small projects with high school
students in our Science Apprenticeship Program, using immunohistochemistry
to identify changes in neuronal activity or receptor density in response
to disease state, stress or environmental changes. In one project, we looked
at changes in c-fos expression in rat brain following initiation of decompression
sickness. In another project, we compared glutamate receptor density (AMPA
and kainite receptor types) in the solitary tract nucleus in control rats
versus spontaneously hypertensive rats.
Selected Publications:
Kramer JW, Ferguson DG,
Corbett AM. (2003) Enrichment of traidic and terminal cisternae vesicles
from rabbit skeletal muscles. J Membraine Biology 195:9-20 [Image]
Castaneda-Castellanos DR,
Cano M, Wang JKT, Corbett A, Benson D, Blanck JJ, Thornhill WB, Recio-Pinto
E (2000) CNS voltage-dependent Na+ channel expression and distribution in
an undifferentiated and differentiated CNS cell line. Brain Res 866:281-285.
Kramer JW, Corbett AM (1996)
1996. Comparison of calcium loading and retention in isolated skeletal muscle
triads and terminal cisternae. American J Physiology (Cell Physiology vol.
39) 270:C1602-1610.
Ritucci NA, Corbett AM (1995)
The effect of magnesium and ATP on depolarization induced calcium release
in isolated skeletal muscle traids. American Journal of Physiology (Cell
Physiology vol 38) 269:C85-C95.
Kramer JW, Corbett AM (1995)
The voltage dependence of depolarization-induced calcium release in isolated
skeletal muscle triads. J Membrane Biol 144:217-230.
Jarnot M, Corbett AM (1995)
High titer antibody to mammalian neuronal sodium channels produces sustained
channel block. Brain Res 674: 159-162. |