Abstract
Non-synaptic mechanisms are being considered the common factor of brain damage in status epilepticus and alcohol intoxication. The present work reports the influence of the chronic use of ethanol on epileptic processes sustained by non-synaptic mechanisms. Adult male Wistar rats administered with ethanol (1, 2 e 3 g/kg/d) during 28 days were compared with Control. Non-synaptic epileptiform activities (NEAs) were induced by means of the zero-calcium and high-potassium model using hippocampal slices. The observed involvement of the dentate gyrus (DG) on the neurodegeneration promoted by ethanol motivated the monitoring of the electrophysiological activity in this region. The DG regions were analyzed for the presence of NKCC1, KCC2, GFAP and CD11b immunoreactivity and cell density. The treated groups showed extracellular potential measured at the granular layer with increased DC shift and population spikes (PS), which was remarkable for the group E1. The latencies to the NEAs onset were more prominent also for the treated groups, being correlated with the neuronal loss. In line with these findings were the predispositions of the treated slices for neuronal edema after NEAs induction, suggesting that restrict inter-cell space counteracts the neuronal loss and subsists the hyper-synchronism. The significant increase of the expressions of NKCC1 and CD11b for the treated groups confirms the existence of conditions favorable to the observed edematous necrosis. The data suggest that the ethanol consumption promotes changes on the non-synaptic mechanisms modulating the NEAs. For the lower ethanol dosage the neurophysiological changes were more effective suggesting to be due to the less intense neurodegenertation.
Highlights
Alcoholism is characterized by addiction to alcohol and persons with this addiction crave alcoholic beverages and develop tolerance to its intoxicating effects [1,2,3]
The highest DC shift and population spikes (PS) were encountered for the ethanol 1 (E1) group, which was significantly different from the other groups (Figure 2A and 2B)
The groups Control and E1 showed quiescent microglias with soma small and compact with thin ramified processes, on the other hand, the microglias of the groups ethanol 2 (E2) and ethanol 3 (E3) exhibited intense immune-reactivity characterized by active phenotype with remarkable cellular hypertrophy and retraction of the cytoplasmic processes. To our knowledge, it was shown the chronic alcoholization and its effects on the Non-synaptic epileptiform activities (NEAs) induced in hippocampus slice
Summary
Alcoholism is characterized by addiction to alcohol and persons with this addiction crave alcoholic beverages and develop tolerance to its intoxicating effects [1,2,3]. Recent studies indicate alcohol as one of the psychotropic drugs of greater negative impact on public health, personal safety and social structure [4]. Chronic alcoholism can induce alterations in the function and morphology of most if not all brain system and structure [5]. Changes in electrophysiological, morphological and neurochemical brain systems become even more heterogeneous when considering the relationship between alcohol and epilepsy. Experimental and clinical studies have been shown that seizures may occur during alcohol intoxication [9,10] and that people with epilepsy who drink moderate or heavy amounts of alcohol could increase the risk of seizures [8]. Alcohol is a risk factor for ischemic cerebral infarction [11] and increases the chances of head trauma [12], both of which are known factors in inducing epilepsy
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