[The neurochemical mechanisms of temporal lobe epilepsy: an update].
BACKGROUND
Last decade witnessed a remarkable progress in understanding the molecular background of temporal lobe epilepsy. That success was due not only to undisputable achievements in the development of electrochemical and biological techniques, but also to the well-defined neuropathological features of partial epilepsy and the availability of appropriate animal models.


OBJECTIVE
The aim of the present paper was to review recent reports concerning those issues. Special emphasis was put on glutamatergic and GABAergic systems, but the putative role of some neuropeptides, ion channels and intracellular signaling pathways in the pathomechanism of temporal epilepsy was also discussed.


RESULTS
The most intriguing and still unsolved problem with studying the basic mechanism of partial epilepsy is a mutual relationship between hippocampal damage and epileptogenesis, in particular the interaction of glia and neuronal factors in this long-term dynamic process.


CONCLUSIONS
It is pointed out that better understanding of these molecular processes may have clinical implications in the future as regards preventing partial seizures, an accurate diagnosis and obtaining safer and more efficient antiepileptic drugs.
Leśkiewicz
Monika
M
Instytut Farmakologii Polskiej Akademii Nauk w Krakowie, Zaklad Neuroendokrynologii.
Lasoń
Władysław
W
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D017136:Ion Transport; D009474:Neurons / Q000378:metabolism*; D018079:Receptors, GABA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D015220:Calcium Channels; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid