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Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that is vital to the survival and function of sympathetic, parasympathetic and sensory neurons. Changes in GDNF expression may be involved in mediating the positive effects of exercise training on nervous system structure and function. Our aim was to test the hypothesis that increased physical activity will result in elevated GDNF protein expression in rat heart. Five eight week old Fisher 344 rats were exercised for three weeks, at a rate of 15m/min in involuntary running wheels for 30 min, six days per week. Five sedentary control rats were maintained in cages without running wheels. Exercised and sedentary animals were sacrificed after three weeks. Hearts were removed, rinsed to remove blood and separated into left and right atria and left and right ventricle. Tissue samples were pulverized, homogenized and the supernatant was analyzed using Enzyme linked immunosorbant assay (ELISA) for GDNF protein. Results showed no change in GDNF protein content of left atria or ventricles with exercise. However GDNF protein content of right atria decreased with exercise (1.2 ± 0.1 pg/mg versus 0.6 ± 0.1 pg/mg). This finding is contrary to what was observed with rats subjected to fourteen weeks of voluntary exercise. The difference between these studies may relate to type of exercise (involuntary vs voluntary) or intensity and duration of exercise. Future studies are planned to elucidate these differences. [ABSTRACT FROM AUTHOR]

The cardiac neuronal norepinephrine transporter (NET) is responsible for uptake of NE from the neuroeffector junction. There is ample evidence of reduced function of NET in hypertension, heart failure, and orthostatic intolerance. Studies on the localization of cardiac NET are limited, and suggest that NET is found in sympathetic fibers and intrinsic cardiac adrenergic cells. We hypothesized that NET would also be present in sensory terminals that innervate the heart. Histology and RT-PCR were used. Fixed atria and mesenteric vessels from normal, adult rats were stained for tyrosine hyrdoxylase (TH) and NET to confirm localization of NET to cardiac sympathetic nerve fibers (n=1). NET and TH were colocalized in the majority of fibers. However, there are NET-positive fibers that were TH-negative and presumably nonsympathetic. In these nerve fibers NET colocalized with calcitonin gene related peptide (CGRP), a marker of sensory neurons (n=2). The pattern of NET staining was the same in mesenteric blood vessels (n=1), suggesting that NET and CGRP colocalization is not unique to the heart. Dorsal root ganglion cell bodies, which receive sensory afferents from heart and mesentery, are positive for NET protein and express NET mRNA (n=4). In conclusion, sensory neurons are a source of NET in the heart that should be considered when assessing dysfunction of cardiac NET in disease. This is the first report of NET mRNA and protein in cardiac sensory nerves. [ABSTRACT FROM AUTHOR]

Sympathetic and sensory neurons innervate blood vessels and control blood pressure. Sympathetic and sensory neurons have been shown to respond to nerve growth factor (NGF). We have shown that NGF content significantly decreases in arteries and veins from rats between 1 and 7 months of age. As the rats aged there was more sympathetic innervation in blood vessels, while sensory innervation stayed the same or decreased. The present study examines involuntary exercise and the effects it plays on vessel innervation and hypertension. Four mouth old Fisher 344 rats were exercise for two weeks at 10m/min for 30 minutes/day. Blood pressures were measured using tail cuff plethysmography. Rats were sacrificed 24 hr following the last bout of exercise. Arteries and veins were removed and were processed for NGF analysis by ELISA, or were fixed and processed for immunochemical staining. Following 2 weeks of exercise the blood pressure in exercised rats (128±2.3 mmHg) was significantly lower than that in sedentary controls (137±3.5). We are currently processing vascular tissues for NGF content and changes in innervation. If NGF expression changes with exercise, this could provide a mechanism linking increased physical activity with changes in sympathetic and/or sensory innervation. [ABSTRACT FROM AUTHOR]