Olfaction in female Wistar rats is influenced by dopaminergic periglomerular neurons after nigral and bulbar lesions.

Hyposmia is found in Parkinsonian patients decades before the onset of motor disorders. The same occurs with sleep disorders, especially infuencing rapid eye movement (REM) sleep, which affect a large percentage of people who have Parkinson's disease. These two disturbances presumably are closely related to a dopaminergic dysfunction. Therefore, we propose that selective lesions, induced by rotenone, of the periglomerular neurons within the olfactory bulb or of the nigrostriatal pathway could result in hyposmia. In addition, we hypothesized that REM sleep deprivation (REMSD) could have potential to generate a synergistic olfactory impairment in both lesion paradigms. The results indicated that rotenone-induced nigrostriatal lesions in female Wistar rats were associated with odor preference changes, similar to hedonic tone impairment, but without a supposed potentiation triggered by REMSD. The nigrostriatal injury negatively affected olfaction performance, which was counteracted, functionally, by REMSD. However, injury to periglomerular neurons was less influenced by REMSD, as olfactory performance was restored after rebound sleep. We conclude that female rats present a pattern of olfactory discrimination/preference that is dependent on the activities of the nigrostriatal and the main olfactory pathways.

Does Parkinson's disease and type-2 diabetes mellitus present common pathophysiological mechanisms and treatments?

Parkinson's disease (PD) is the second most common neurodegenerative disease afflicting about 1% of people over 65 years old and 4-5% of people over 85 years. It is proposed that a cascade of deleterious factors is set in motion within that neuron made not of one, but rather of multiple factors such as free radicals, excitotoxicity, neuroinflammation, and apoptosis to cite only some of the most salient. In this scenario, chronic systemic inflammation, as well as impaired mitochondrial metabolism, have also been suspected of playing a role in the development of type-2 diabetes, and the possibility of a shared pathophysiology of PD and type-2 diabetes has been proposed. The discussion about the interactions between PD and type-2 diabetes mellitus began in the 1960's and there is still controversy. Insulin and dopamine may exert reciprocal regulation hence; hypoinsulinemia induced by streptozotocin decreased the amounts of dopamine transporter and tyrosine hydroxylase transcripts in the substantia nigra pars compacta. Accordingly, dopamine depletion in the striatum is able to decreases insulin signaling in basal ganglia, indicating that, perhaps, PD may be considered as a risk factor for the development of type-2 diabetes mellitus. In this sense, it is described that peroxisome proliferator-activated receptor-γ, ATP-sensitive K(+) channels, AMP-activated protein kinase, glucagon-like peptide-1 and dipeptidyl peptidase-4 are important therapeutic targets for PD and reinforces the association with diabetes. Therefore, the objective of the present review is to contextualize the mutual pathophysiological interactions between PD and type-2 diabetes mellitus, as well as the potential common treatments.