Czaja Lab
Our lab is investigating the biology of postnatal neurogenesis
in vitro and in animal models utilizing technologies in cell
biology, molecular biology and neuroanatomy. Our long-term goal
is to understand the process of neural plasticity in
viscerosensory pathways after peripheral nerve injury and repair
in order to identify new therapeutic targets and develop
treatment strategies to restore functions in the damaged nervous
system.
Czaja Lab (2010): from left: Lee Cyr, Tin-Yan Lee, Vitaly Ryu,
Krzysztof Czaja, Hilary Carmichael, Zach Gallaher and
Jessamyn Dahmen. |
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Czaja lab (2011): from left: Rachel Wanty, Miguel Toscano,
Stephen Johnston, Zach Gallaher, Krzysztof Czaja,
Slater Weinstock, Casey Callahan.
Czaja Lab (2008): from left Zach Gallaher, Jay Jassal, Krzysztof Czaja,
Vitaly Ryu and Bo Herzog (click photo for
larger version) |
| |
Click on a Project Title for Details
Our long-term goal is to understand the process of injury-induced neurogenesis
and repair in the damaged nervous system. The objective of the proposed
research, which is the next step in pursuit of this goal, is to determine
whether destruction of peripheral afferent neurons results in their replacement
with newly generated neurons, and whether these new neurons can establish
appropriate connections, which might enable reestablishment of lost functions.
The central hypothesis of the project is that the neuronal destruction resulting
in the death of primary viscerosensory neurons is followed by altered neuronal
phenotype, neurogenesis, and neurite outgrowth, leading to reinnervation of the
target organ. This hypothesis is based on our recent discovery that, following
capsaicin-induced neuronal destruction, adult rat nodose ganglia exhibit
dramatically increased neurogenesis and growth of neurites into the vagal
trunks.
Findings that nearly all vagal afferents express NMDA receptors suggests that
hindbrain NMDA receptors, specifically those on the central vagal afferent
terminals themselves, play a role in control of food intake. However, vagal
afferents comprise a heterogeneous group of phenotypes, with regard to NMDA
receptor subtypes. The subpopulation and phenotype of vagal afferents that
participate in increased meal size following NTS NMDA receptor blockade is not
known. We hypothesize that increased food intake evoked by hindbrain application
of NMDA receptor antagonists depends on intact terminals of capsaicin-resistant
abdominal vagal afferents that co express NMDA NR2B and NR2C receptor subunits.
The overall objective of this project is to establish interactions between the
nutritional signal leptin and central pathways controlling gonadotropin
secretion in gilts. Our central hypothesis is that Kiss and RFRP-3 antagonize
each other to regulate the hypothalamic-pituitary axis. Leptin acts to
differentially regulate Kiss and RFRP-3 in the hypothalamus and support
gonadotropin secretion. Our approach, using intracerebroventricular injections
and immunocytochemistry, will be to establish the role of RFRP-3 in regulating
gonadotropin secretion and identify effects of leptin on Kiss and RFRP-3 neurons
in the hypothalamus of the gilt.
Our long-term goal is to understand the process of cocaine-induced neural
plasticity to identify new therapeutic targets and develop treatment strategies
to restore normal functions in the changed neuronal circuits. The objective of
the proposed research, which is the next step in pursuit of this goal, is to
determine how cocaine changes the neuronal circuits involved in drug addiction.
The central hypothesis of the project is that the cocaine treatment is followed
by synaptogensis or neurogenesis, leading to remodeling within the mesolimbic
dopaminergic system.
content of protocols
