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Hepatic encephalopathy (HE) is a neuropsychiatric hepatic‑induced syndrome in which several factors are involved in promoting brain perturbations, with ammonia being the primary factor. Motor impairment, incoordination, and gut dysbiosis are some of the well‑known symptoms of HE. Nevertheless, the link between the direct effect of hyperammonemia and associated gut dysbiosis in the pathogenesis of HE is not well established. Thus, this work aimed to assess motor function in hyperammonemia and gut dysbiosis in mice. Twenty‑eight Swiss mice were distributed into three groups: two‑week and four‑week hyperammonemia groups were fed with an ammonia‑rich diet (20% w/w), and the control group was pair‑fed with a standard diet. Motor performance in the three groups was measured through a battery of motor tests, namely the rotarod, parallel bars, beam walk, and static bars. Microbial analysis was then carried out on the intestine of the studied mice. The result showed motor impairments in both hyperammonemia groups. Qualitative and quantitative microbiological analysis revealed decreased bacterial load, diversity, and ratios of both aerobic and facultative anaerobic bacteria, following two and four weeks of ammonia supplementation. Moreover, the Shannon diversity index revealed a time‑dependent cutback of gut bacterial diversity in a treatment‑time‑dependent manner, with the presence of only Enterobacteriaceae, Streptococcaceae, and Enterococcaceaeat at four weeks. The data showed that ammonia‑induced motor coordination deficits may develop through direct and indirect pathways acting on the gut‑brain axis.

Copper (Cu) is an important trace element for the organism survival, which ensures the normal functioning of different biosystems. However, excessive levels of this heavy metal are responsible for profound physiological alterations including the central nervous system. Numerous findings sustain the involvement of heavy metals, as an environmental risk factor such as copper (Cu), in the neuropathology of Parkinson's disease (PD) which is a chronic neurodegenerative disorder that principally affects the motor system. The classic and evident symptoms of PD namely rigidity, tardiness of movement, and difficulty with walking, result from progressive dopaminergic neurons death within substantia nigra. Whereas, few pharmacological trials have shown a beneficial role against Cu neurotoxicity, Aloe arborescens is one of the powerful medicinal plants with an array of therapeutic effects. Thus, we aimed through the present study, to evaluate the impact of acute Cu intoxication (10μg/g B.W. i.p) for 3days on the dopaminergic system and locomotor performance, together with the possible restorative effect of oral administration of aqueous extract of Aloe arborescens gel (AEAAG) (200mg/kg B.W.). By means of immunohistochemistry, we noted, in the Cu intoxicated rats, a significant loss of TH (tyrosine hydroxylase) expression within substantia nigra compacta (SNc), ventral tegmental area (VTA) and the subsequent striatal outputs, those alterations were correlated to behavioral abnormalities such as a severe drop of locomotor performance. While AEAAG administration to Cu intoxicated rats showed a noticeable beneficial effect; this potential was featured by a complete recovery of the TH expression and locomotor behavior deficiencies in the intoxicated rats. The present investigation have brought, on the one hand, an experimental evidence of an altered dopaminergic innervations following Cu intoxication and on the other hand, a new pharmacological property of Aloe arborescens that may be used as a neuroprotective plant for neurodegenerative disorders, such as PD, touching the dopaminergic system trigged by heavy metals., (Copyright © 2017. Published by Elsevier GmbH.)

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs in both acute and chronic liver failure. However, the pathomechanisms of the disease remains obscure. Neuropathological studies have demonstrated a primary gliopathy in humans as well as in animal models of chronic and acute liver failure. Here, we have investigated in an animal model of mild HE: the bile duct ligated rat (BDL) at the cirrhotic stage (4 weeks after surgery), the expression of the key marker of mature astrocytes; the glial fibrillary acidic protein (GFAP) in different brain areas such as: Substantia nigra pars compacta (SNc), Ventral tegmental area (VTA), hippocampus, dorsal striatum and brain cortex by means of immunohistochemistry. The immunohistochemical study showed, in BDL compared to the operated controls (shams), a diminished astrocyte reactivity corresponding to a loss of GFAP expression within SNc, VTA, hippocampus and dorsal striatum (p<0.05),whereas in the brain cortex astrocytes appeared strongly immunoreactive with increased GFAP expression (p<0.05) as compared to shams. Our finding demonstrated differential astroglial responses which depend to the specificity of the area investigated and its particular neuronal neighboring environment, and could have possible outcomes on the diverse neuronal functions especially those observed during the different episodes of hepatic encephalopathy., (Copyright © 2016 Elsevier GmbH. All rights reserved.)