Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


HIPPOCAMPAL CA1 LONG-TERM POTENTIATION IS ALTERED FOLLOWING HIGH-FREQUENCY MAGNETIC STIMULATION
Abstract number: P166

Tokay1 T., *Kirschstein1 T., Zschorlich2 V., Kohling1 R.

Exposure of brain tissues to transcranial magnetic stimulation may induce persistent changes in neuronal activity and thus may influence synaptic transmission. However, data on the modulation of synaptic transmission by magnetic stimulation in vitro is scarce. We studied the effect of high-frequency magnetic stimulation (HFMS) on synaptic function in the rat hippocampal slice in vitro. To this end, synaptic transmission was monitored by electrical stimulation of Schaffer collateral axons and simultaneous recording of CA1 field potentials. HFMS was delivered through a circular coil positioned closely above the slice and consisted of 10 trains of 20 pulses at 100 Hz with 1 s intervals (5 repetitions with 10 s intervals). The intensity of the magnetic stimulus was adjusted to 60–75 A/ms. After the application of HFMS, electrically evoked CA1 field potentials showed a significant and long-lasting enhancement of synaptic strength at the Schaffer collateral-CA1 synapse. This enhancement was prevented in the presence of the selective N-methyl-D-aspartate (NMDA) receptor blocker D-AP5 (50 mM). Moreover, long-term potentiation induced by electrical tetanic stimulation was significantly reduced in slices that were treated with HFMS. In summary, we suggest that HFMS can elicit a NMDA receptor-dependent long-lasting enhancement of synaptic transmission in the rat CA1 region in vitro. In addition, HFMS appears to constrain the propensity of a slice to exhibit tetanus-induced long-term potentiation.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P166

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE