Research in VCAPP

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

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