M
Merab Kokaia
Researcher at Lund University
Publications - 152
Citations - 8911
Merab Kokaia is an academic researcher from Lund University. The author has contributed to research in topics: Hippocampal formation & Epilepsy. The author has an hindex of 48, co-authored 144 publications receiving 8448 citations. Previous affiliations of Merab Kokaia include Beritashvili Institute of Physiology.
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Apoptosis and proliferation of dentate gyrus neurons after single and intermittent limbic seizures
TL;DR: The present data show that single and intermittent, brief seizures induce both apoptotic death and proliferation of dentate gyrus neurons, and it is hypothesized that these processes, occurring early during epileptogenesis, are primary events in the development of hippocampal pathology in animals and possibly also in patients suffering from temporal lobe epilepsy.
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Neurotrophins and brain insults
TL;DR: Insight into the regulation and role of the neurotrophins after brain insults should increase the understanding of pathophysiological mechanisms in epileptogenesis and cell death, and could lead to new therapeutic strategies.
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Increased production of the TrkB protein tyrosine kinase receptor after brain insults
Jean-Philippe Merlio,Patrik Ernfors,Zaal Kokaia,David S. Middlemas,Johan Bengzon,Merab Kokaia,Maj-Lis Smith,Bo K. Siesjö,Tony Hunter,Olle Lindvall,Håkan Persson +10 more
TL;DR: It is shown that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus, suggesting that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.
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Forebrain acetylcholine regulates adult hippocampal neurogenesis and learning.
TL;DR: The data provide evidence that forebrain ACh promotes neurogenesis, and suggest that the impaired cholinergic function in AD may in part contribute to deficits in learning and memory through reductions in the formation of new hippocampal neurons.
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Optogenetic control of epileptiform activity
TL;DR: It is proved a principle, that selective hyperpolarization of principal cortical neurons by NpHR is sufficient to curtail paroxysmal activity in transduced neurons and can inhibit stimulation train-induced bursting in hippocampal organotypic slice cultures, which represents a model tissue of pharmacoresistant epilepsy.