Cobalt-induced neuro-behavioural alterations are accompanied by profound Purkinje cell and gut-associated responses in rats.

Metal ions including cobalt (Co) ions reportedly exhibit neurotoxic and antimicrobial properties. We hypothesized that oral exposure to Co may have implications for gut-dysbiosis with possible alterations of microbiota-gut-brain signaling in the host. In this preliminary study, we sought to examine whether exposure of male Wistar rats to cobalt chloride (CoCl2) at 0, 25, 50 and 100 mg/kg for two weeks affects select neurobehavioural indices, vagus nerve and brain morphology along with evaluation of associated changes in faecal bacterial flora, faecal fatty acids and the morphology of the intestines. CoCl2-exposed rats showed a dose-dependent reduction in hanging latency in the hanging wire (HW) test, reduced tendency to recognize novel objects in a Novel Object recognition (NOR) test, but increased interaction with open arms in the elevated plus maze (EPM) test, compared to controls. There were dose-dependent reductions in total heterotrophic count, coliforms, <italic>E. coli, Enterococcal</italic> and <italic>Lactobacilli</italic> counts in the faeces. Administration of CoCl2 at 100 mg/kg evoked the appearance of unsaturated fatty acids including palmitoleic, oleic and linoleic acids in the faeces as detected by gas chromatography-flame ion detection (GD-FID) analysis using fatty acid methyl esters (FAME) standards. Histopathological examination revealed chromatolysis of Purkinje cells in the cerebellum, although no significant lesions were present in the vagus nerve isolated from all the groups. In the intestines, there was moderate to severe infiltration of inflammatory cells into the duodenum, ileum, jejunum and colon while villi erosions were seen prominently in the ileum. These initial findings suggest that short-term exposure to Co can lead to gut-associated changes that may underlie neurotoxicity and alterations in behavior induced by Co.