College of Veterinary Medicine

Research in IPN

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.





CzajaLab2010
Czaja Lab (2010): from left: Lee Cyr, Tin-Yan Lee, Vitaly Ryu, Krzysztof Czaja, Hilary Carmichael, Zach Gallaher and
Jessamyn Dahmen.
  2011
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)
 

Lab Projects

Along with the projects listed below, our laboratory is also investigating the brain plasticity following Roux-en-Y gastric bypass (RYGB), the most effective method to achieve major, long-term weight loss.  Specifically, we try to establish the role of the vagus nerve in the mechanism of RYGB.  This information may suggest treatments for obese individuals that would be less radical than surgery.  Moreover, establishing the role of brain reorganization in taste alterations may allow the development of novel therapies that can mimic the effects of RYGB surgery.

Injury induced neuronal proliferation and repair in the sensory pathways.
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.

The Role of Glutamate in the Control of Food Intake.
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

Rfamide-Like Peptides Mediate The Effects Of Nutrition On The Hypothalamic-Pituitary Axis Of The Gilt.
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.

Cocaine-induced plasticity of neural circuits involved in drug addiction.
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.

Mechanism of taste alterations following bariatric surgeries.
At present, Roux-en-Y gastric bypass (RYGB) is the most effective method to achieve major, long-term weight loss. Patients who have undergone RYGB often report an aversion to calorie-dense foods, such as fats, concentrated carbohydrates, ice cream, and sweetened beverages. However, mechanisms underlying the effects of RYGB on taste alterations are incompletely understood. Our long-term goal is to understand the mechanism of taste alterations following RYGB. Specifically, we want to determine whether destruction of subdiaphragmatic vagal afferents during the surgery modifies gustatory signaling in predictable ways. The central hypothesis of this proposal is that damage to dorsal and ventral gastric branches of the vagal trunks induces synaptic plasticity and phenotype changes in neurons of the rostral division of nucleus of the solitary tract (NTS), and that this will be reflected in lower preference for sweet foods. This hypothesis is based on our studies which revealed that vagotomy is followed by microglia activation and reorganization in the NTS, the target of both gustatory and gastrointestinal afferent neurons. Elucidating this mechanism is a high priority, because such knowledge may facilitate development of novel anti-obesity medications that could achieve some of the weight loss caused by RYGB, without surgical risks.
Last Edited: Feb 11, 2014 2:29 PM   

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