Objective: Amygdala has been demonstrated as one of the brain sites involved in the control of cardiorespiratory functioning. The structural and physiological alterations induced by epileptic activity are also present in the amygdala and reflect functional changes that may be directly associated with a sudden unexpected death. Seizures are always associated with neuronal damage and changes in the expression of cation-chloride cotransporters and Na/K pumps. In this study, the authors aimed to investigate if these changes are present in the amygdala after induction of status epilepticus with pilocarpine, which may be directly correlated with Sudden Unexpected Death in Epilepsy (SUDEP). Methods: Pilocarpine-treated wistar rats 60 days after Status Epilepticus (SE) were compared with control rats. Amygdala nuclei of brain slices immunostained for NKCC1, KCC2 and α1-Na+/K+-ATPase, were quantified by optical densitometry. Results: The amygdaloid complex of the animals submitted to SE had no significant difference in the NKCC1 immunoreactivity, but KCC2 immunoreactivity reduced drastically in the peri-somatic sites and in the dendritic-like processes. The α1-Na+/K+-ATPase peri-somatic immunoreactivity was intense in the rats submitted to pilocarpine SE when compared with control rats. The pilocarpine SE also promoted intense GFAP staining, specifically in the basolateral and baso-medial nuclei with astrogliosis and cellular debris deposition. Interpretation: The findings revealed that SE induces lesion changes in the expression of KCC2 and α1-Na + /K + -ATPase meaning intense change in the chloride regulation in the amygdaloid complex. These changes may contribute to cardiorespiratory dysfunction leading to SUDEP.

Abstract Background The 6-OHDA nigro-striatal lesion model has already been related to disorders in the excitability and synchronicity of neural networks and variation in the expression of transmembrane proteins that control intra and extracellular ionic concentrations, such as cation-chloride cotransporters (NKCC1 and KCC2) and Na+/K+-ATPase and, also, to the glial proliferation after injury. All these non-synaptic mechanisms have already been related to neuronal injury and hyper-synchronism processes. Objective The main objective of this study is to verify whether mechanisms not directly related to synaptic neurotransmission could be involved in the modulation of nigrostriatal pathways. Methods Male Wistar rats, 3 months old, were submitted to a unilateral injection of 24 µg of 6-OHDA, in the striatum (n= 8). The animals in the Control group (n= 8) were submitted to the same protocol, with the replacement of 6-OHDA by 0.9% saline. The analysis by optical densitometry was performed to quantify the immunoreactivity intensity of GFAP, NKCC1, KCC2, Na+/K+-ATPase, TH and Cx36. Results The 6-OHDA induced lesions in the striatum, were not followed by changes in the expression cation-chloride cotransporters and Na+/K+-ATPase, but with astrocytic reactivity in the lesioned and adjacent regions of the nigrostriatal. Moreover, the dopaminergic degeneration caused by 6-OHDA is followed by changes in the expression of connexin-36. Conclusions The use of the GJ blockers directly along the nigrostriatal pathways to control PD motor symptoms is conjectured. Electrophysiology of the striatum and the substantia nigra, to verify changes in neuronal synchronism, comparing brain slices of control animals and experimental models of PD, is needed.

Abstract Guillain-Barre Syndrome (GBS) has been repeatedly reported as a neurological complication of COVID-19 (post-COVID GBS [PCG]). Whether the introduction of SARS-CoV-2 vaccines reduced the prevalence of PCG is unknown. This narrative review aimed to compare the number of published PCG cases between the second half of 2020 (no vaccination available) with those of the first half of 2021 (vaccination available). A total of 124 articles reported 300 patients with PCG between January 2020 and June 2021. The ages ranged from 7 to 94y. There was male dominance. The latency between the onset of COVID-19 and the onset of PCG ranged from -10 to 90d Acute, inflammatory, demyelinating polyneuropathy was diagnosed in 171 patients, acute, motor axonal neuropathy in 24, and acute, motor, and sensory axonal neuropathy in 16 patients. Regarding treatment, 241 patients received immunoglobulins, 28 patients' plasmaphereses, and 7 patients' steroids. Artificial ventilation was required in 59 patients. Full recovery was achieved in 42 cases, partial recovery in 163 cases, and 17 patients died. The number of published PCG patients fell from 192 in the second half of 2020 to 75 patients in the first half of 2021. It is concluded that the prevalence of PCG has decreased since the introduction of SARS-CoV-2 vaccines. SARS-CoV-2 vaccinations have a positive effect on the prevalence of PCG. HIGHLIGHTS SARS-CoV-2 infections can be complicated by Guillain-Barre Syndrome (GBS). The prevalence of SARS-CoV-2 associated GBS declined since the introduction of SARS-CoV-2 vaccines. The outcome of SARS-CoV-2 associated GBS is worse among those with comorbidities compared to those without.