Dopamine as an anorectic neuromodulator in the cockroach Rhyparobia maderae.

Insects, including cockroaches, self-select a balanced diet when faced with different nutrient choices. For self-selection to be carried out effectively, insects possess neuroregulatory systems to control their food intake. In the present study, we examined the role of the neurotransmitter dopamine (DA) in the feeding regulation of the Madeira cockroach (Rhyparobia maderae). When R. maderae nymphs were injected with 20 µl of 100 mmol l(-1) DA, they showed an 83.3% reduction in sucrose intake and a 78.9% reduction in total intake compared with saline-injected controls. The DA agonist, 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (6,7-ADTN) (100 mmol l(-1) in 1 µl), caused a significant reduction in sucrose feeding, reducing feeding by 47.3% compared with saline-injected controls. Protein feeding was also significantly reduced by 6,7-ADTN to 62%. Rhyparobia maderae nymphs injected with the DA antagonist chlorpromazine (100 mmol l(-1) in 1 µl) did not differ significantly from control nymphs in their feeding behavior. Interestingly, R. maderae nymphs injected with 2 µl or 5 µl chlorpromazine (100 mmol l(-1)) showed significantly increased mortality rates of 47.5% or 66.7%, respectively. The DA antagonist, spiperone (100 mmol l(-1) in 1 µl), caused a significant feeding response, showing an increase in feeding in both sucrose (310.6%) and total intake (236.3%). Casein feeding in R. maderae nymphs was also elevated (70.8%) but this was not statistically significant. The experiments with DA, the DA agonist 6,7-ADTN and the DA antagonist spiperone strongly suggest that the neurotransmitter DA is involved in regulating feeding in the cockroach R. maderae.

Exercise-induced neuroprotection in the spastic Han Wistar rat: the possible role of brain-derived neurotrophic factor.

Moderate aerobic exercise has been shown to enhance motor skills and protect the nervous system from neurodegenerative diseases, like ataxia. Our lab uses the spastic Han Wistar rat as a model of ataxia. Mutant rats develop forelimb tremor and hind limb rigidity and have a decreased lifespan. Our lab has shown that exercise reduced Purkinje cell degeneration and delayed motor dysfunction, significantly increasing lifespan. Our study investigated how moderate exercise may mediate neuroprotection by analyzing brain-derived neurotrophic factor (BDNF) and its receptor TrkB. To link BDNF to exercise-induced neuroprotection, mutant and normal rats were infused with the TrkB antagonist K252a or vehicle into the third ventricle. During infusion, rats were subjected to moderate exercise regimens on a treadmill. Exercised mutants receiving K252a exhibited a 21.4% loss in Purkinje cells compared to their controls. Cerebellar TrkB expression was evaluated using non-drug-treated mutants subjected to various treadmill running regimens. Running animals expressed three times more TrkB than sedentary animals. BDNF was quantified via Sandwich ELISA, and cerebellar expression was found to be 26.6% greater in mutant rats on 7-day treadmill exercise regimen compared to 30 days of treadmill exercise. These results suggest that BDNF is involved in mediating exercise-induced neuroprotection.

Neuroprotective effects of moderate aerobic exercise on the spastic Han-Wistar rat, a model of ataxia.

Research has shown that physical exercise may reduce degeneration in certain brain regions experiencing ataxia. Our laboratory utilized mutant spastic Han-Wistar rats (sHW) that display developmental abnormalities, including spastic paresis, fore limb tremors, hind limb rigidity, and a reduced life span (60-65 days of age). Concomitant neurodegeneration has been observed in the cerebellum (Purkinje cells). The purpose of this study was to investigate if moderate, aerobic exercise could reduce Purkinje cell neurodegeneration and improve the motor ability and survival of the mutant sHW rat. Mutant male littermates at the ages of 20 (n=11 pairs) and 30 (n=13 pairs) days old were divided into running groups and non-running groups. Mutant rats were run on a motorized treadmill at the rate of 15 m/min with a 10% slope. The "running" group ran for 30 min per day, 5 days a week; the "non-runners" remained nearby in the training facility. These conditions were held constant until the mutant runners could no longer run due to disease progression. Moderate exercise increased the lifespan of running mutant rats in both the 20-day start group (14% increase) and 30-day start group (13% increase). The rats exhibited improved motor function as open-field tests showed higher activity scores for runners after 50 days. Histological examination of the cerebellum revealed a 62% increase in Purkinje cell survival of the runners. These results suggest that aerobic exercise ameliorates, at least partially, cerebellar dysfunction in the sHW rat, an excellent model of ataxia.