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The Journal of Neuroscience, January 16, 2008, 28(3):732-736; doi:10.1523/JNEUROSCI.3665-07.2008

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Brief Communications
Thrombin Induces Long-Term Potentiation of Reactivity to Afferent Stimulation and Facilitates Epileptic Seizures in Rat Hippocampal Slices: Toward Understanding the Functional Consequences of Cerebrovascular Insults

Nicola Maggio,¹ Efrat Shavit,² Joab Chapman,² and Menahem Segal¹

¹Department of Neurobiology, The Weizmann Institute, 76100 Rehovot, Israel, and ²Departments of Physiology and Pharmacology and Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel

Correspondence should be addressed to Menahem Segal at the above address. Email: menahem.segal{at}weizmann.ac.il

The effects of thrombin, a blood coagulation serine protease, were studied in rat hippocampal slices, in an attempt to comprehend its devastating effects when released into the brain after stroke and head trauma. Thrombin acting through its receptor, protease-activated receptor 1 (PAR1), produced a long-lasting enhancement of the reactivity of CA1 neurons to afferent stimulation, an effect that saturated the ability of the tissue to undergo tetanus-induced long-term potentiation. This effect was mediated by activation of a PAR1 receptor, because it was shared by a PAR1 agonist, and was blocked by its selective antagonist. An independent effect of thrombin involved the lowering of the threshold for generating epileptic seizures in CA3 region of the hippocampus. Thus, the experiments in a slice mimicked epileptic and cognitive dysfunction induced by thrombin in the brain, and suggest that these effects are mediated by activation of the PAR1 receptor.

Key words: hippocampus; thrombin; LTP; seizure; PAR1; cerebrovascular insult

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Received Aug. 12, 2007; revised Dec. 2, 2007; accepted Dec. 4, 2007.

Correspondence should be addressed to Menahem Segal at the above address. Email: menahem.segal{at}weizmann.ac.il

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