Neuron-specific mechanisms for epilepsy self-termination

نویسندگان

  • Jin-Hui Wang
  • Wei Lu
  • Bo Wen
چکیده

Epilepsy is characterized as the ictal discharges of the cerebral brain in the sudden onset and self-termination for a few minutes. The seizure onset is presumably originated from the synchronous activity of excitatory neurons and the weakness of inhibitory synapses, which guide the suppression of the seizure onset by giving the exogenous reagents to enhance inhibitory synaptic transmission and to block action potentials. After long-term treatment, many epileptic patients become insensitive to such medications and the pathogenesis in the elevated ratio of cortical excitation to inhibition is still present. The lack of long-term therapeutic effectiveness may be reasoned from the facts that the current medication is not neuron-specific and the seizure self-termination has not been taken into account. Therefore, the new therapeutic strategies against epilepsy remains to be explored based on strengthening the endogenous mechanisms of seizure self-termination in a neuron-specific manner. We review the potential mechanisms of seizure self-termination and present our thoughts in anti-epilepsy by strengthening seizure self-termination in different neuronal compartments.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Activity-induced spontaneous spikes in GABAergic neurons suppress seizure discharges: an implication of computational modeling

BACKGROUND Epilepsy, a prevalent neurological disorder, appears self-termination. The endogenous mechanism for seizure self-termination remains to be addressed in order to develop new strategies for epilepsy treatment. We aim to examine the role of activity-induced spontaneous spikes at GABAergic neurons as an endogenous mechanism in the seizure self-termination. METHODS AND RESULTS Neuronal ...

متن کامل

Large scale brain models of epilepsy: dynamics meets connectomics.

The brain is in a constant state of dynamic change, for example switching between cognitive and behavioural tasks, and between wakefulness and sleep. The brains of people with epilepsy have additional features to their dynamic repertoire, particularly the paroxysmal occurrence of seizures. Substantial effort over decades has produced a detailed description of many human epilepsies and of specif...

متن کامل

PI3K-Akt signaling activates mTOR-mediated epileptogenesis in organotypic hippocampal culture model of post-traumatic epilepsy.

mTOR is activated in epilepsy, but the mechanisms of mTOR activation in post-traumatic epileptogenesis are unknown. It is also not clear whether mTOR inhibition has an anti-epileptogenic, or merely anticonvulsive effect. The rat hippocampal organotypic culture model of post-traumatic epilepsy was used to study the effects of long-term (four weeks) inhibition of signaling pathways that interact ...

متن کامل

P119: Animal Models of Epilepsy: The Impact of some Chemoconvalsants on Animal Models

We summarize some of the most frequenthly used rodent animal models of temporal lobe epileps and the impact of chemoconvulsants on them. Temporal lobe epilepsy is the most common epilepsy in humans in which seizures spread to the neighboring cortiase and hippocampal neuron loss and other neuropathological take place. Temporal lobe epilepsy and the other form of epilepsy cannot acquired in chini...

متن کامل

Generation of motor neurons from human amygdala-derived neural stem-like cells

Objective(s): Among several cell sources, adult human neural stem/progenitor cells (hNS/PCs) have been considered outstanding cells for performing mechanistic studies in in vitro and in vivo models of neurological disorders as well as for potential utility in cell-based therapeutic approaches. Previous studies addressed the isolation and culture of hNS/PCs from human neocortical and hippocampal...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2015