We are interested in the general theme of environmental, disease and aging effects on neurodegeneration, and the development of protective strategies that can prevent these effects. We use a number of anatomical, neurochemical and pharmacological methods, including immunocytochemistry, in situ hybridization, autoradiography, electron microscopy, HPLC, in vivo electrochemistry, in vivo microdialysis, and in vitro superfusion to study both central and peripheral nervous system.

      Central dopaminergic systems are known to deteriorate with age and under the influence of a number of toxins. However, it is clear that there are changes in the brain long before damage is evident. Our laboratory is using a combination of in vivo monitoring techniques to monitor thse changes in dopamine systems in order to determine what mechanisms account for compensation. Based on these studies, strategies designed to protect the system from damage and promote plasticity are being investigated and include reuptake blockade, monoamine oxidase inhibition, and the use of pre- and post synaptic agonists to decrease release of endogenous transmitter. The age at which these protective strategies must be initiated to be effective is an important variable as is the presence and availability of various growth factors.

      We are also investigating similar mechanisms and protective strategies in the peripheral sympathetic system innervating lymphoid organs, which appears to change with age and autoimmune disease, and changes in cardiac innervation associated with congestive heart failure.

Liang CS, Mao W, Iwai C, Fukuoka S, Stevens SY. 2006. Cardiac sympathetic neuroprotective effect of desipramine in tachycardia-induced cardiomyopathy. Am J Physiol Heart Circ Physiol. Mar;290(3):H995-1003

Bellinger DL, Stevens SY, Thyaga Rajan S, Lorton D, Madden KS. 2005. Aging and sympathetic modulation of immune function in Fischer 344 rats: effects of chemical sympathectomy on primary antibody response. J Neuroimmunol. Aug;165(1-2):21-32.

Collier TJ, Greene JG, Felten DL, Stevens SY, and Collier KS. 2004. Reduced cortical noradrenergic neurotransmission is associated with increased neophobia and impaired spatial memory in aged rats. Neurobiol Aging. Feb;25(2):209-221.

Stevens SY, Cai S, Pellecchia M, and Zuiderweg ER. 2003. The solution structure of the bacterial HSP70 chaperone protein domain DnaK(393-507) in complex with the peptide NRLLLTG. Protein Sci. Nov;12(11):2588-2596.

Cai S, Stevens SY, Budor AP, and Zuiderweg ER. 2003. Solvent interaction of a Hsp70 chaperone substrate-binding domain investigated with water-NOE NMR experiments. Biochemistry. Sep 30;42(38):11100-11108.

Kelley SP, Moynihan JA, Stevens SY, Grota LJ, and Felten DL. 2003. Sympathetic nerve destruction in spleen in murine AIDS. Brain Behav Immun. Apr;17(2):94-109.

Liang CS, Yatani A, Himura Y, Kashiki M, and Stevens SY. 2003. Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion. Am J Physiol Heart Circ Physiol. May;284(5):H1729-1736.

Liang CS, Himura Y, Kashiki M, and Stevens SY. 2002. Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF. Am J Physiol Heart Circ Physiol. Nov;283(5):H1863-1867.

Kyrkanides S, Tallents RH, Macher DJ, Olschowka JA, and Stevens SY. 2002. Temporomandibular joint nociception: effects of capsaicin on substance P-like immunoreactivity in the rabbit brain stem. J Orofac Pain. 16(3):229-236.

Kelley SP, Moynihan JA, Stevens SY, Grota LJ, and Felten DL. 2002. Chemical Sympathectomy Has No Effect on the Severity of Murine AIDS: Murine AIDS Alone Depletes Norepinephrine Levels in Infected Spleen. Brain Behav Immun. Apr;16(2):118-139.

Rice PA, Boehm GW, Moynihan JA, Bellinger DL, and Stevens SY. 2002. Chemical sympathectomy alters numbers of splenic and peritoneal leukocytes. Brain Behav Immun. Feb;16(1):62-73.

Qin F, Vulapalli RS, Stevens SY, and Liang CS. 2002. Loss of cardiac sympathetic neurotransmitters in heart failure and NE infusion is associated with reduced NGF. Am J Physiol Heart Circ Physiol. Jan;282(1):H363-371