New determinants for causal neural mechanism of dry mouth in Parkinson’s disease induced by destruction of superior salivatory nucleus, facial nerve, and submandibular gland circuitry: an experimental study

Abstract

Aim: Dry mouth has been considered a clinical finding of Parkinson’s disease (PD), but we think otherwise. We studied if the olfactory bulbectomy (OBX) might rely on the superior salivatory nucleus (SSN), submandibular ganglia (SMGn), and submandibular glands (SLGl) circuity disruption induced submandibular gland degeneration related dry mouth in rats. Material and Method: This study was carried out on twenty-six male rats. Five (GI-n=5), six (GII, n=6), and sixteen (GIII, n=15) of them were used as control, SHAM, and OBX groups, respectively, and followed eight weeks. PD-related clinical examinations were done before and after the experiment (1/day), and animals were decapitated. The olfactory bulb volumes (mm3), degenerated neuron densities of SSN/SMG (n/mm3 and SMGl follicles volumes were detected serologically. Olfactory bulb volume values and degenerated neuron density values of SSN/SMGn/SMGl follicles volumes were compared statistically. Results: OBX-applied animals showed anosmia, tremors, rigidity, and memory loss. The mean olfactory bulb volumes (mm3), degenerated neuron density of SSN (n/mm3), SMGn (n/mm3), and follicles volumes of SMGl (cubic micrometer/mm3) were measured in the order written as; (4.27±0.21), (4±1), (5±2), (81.23±13.34).106 in GI; (3.67±0.33), (14±3), (17±4), (72.45±11.78).106 in GII and (2.91±0.14), (23±5), (29±8), (57.19±11.93).106 in Group III. The mean P values between olfactory bulb volumes, degenerated neuron densities of SSN and SMGn, and salivary follicles volumes were: p