Title: Effects of guanidinosuccinic acid on potentiation of synaptic efficacy in rat hippocampal slices
Authors: D'Hooge, Rudi ×
Manil, J.
Colin, F.
De Deyn, P.P. #
Issue Date: 1991
Host Document: Abstract Booklet of the Third International symposium on Guanidino compounds in Biology and Medicine pages:51-51
Conference: Third International Symposium on Guanidino Compounds in Biology and Medicine edition:3 location:Antwerp date:2-3 September 1991
Abstract: Since guanidinosuccinic acid (GSA) is suggested to play a role in uremic en¬cephalopathy, we set out to investigate the effects of GSA on excitatory synaptic neurotransmission and on post-tetanic and long-term potentiation of this transmission in rat hippocampal slices. In addition, we investigated the influence of the allosteric NMDA receptor agonist D-serine on the GSA indu¬ced effects. A high-intensity stimulation paradigm was employed. Every 4.1 s, a bipolar nickel-chrome electrode stimulated the Schaffer collaterals in 300 µm thick parasagital hippocampal slices, with a maximal intensity of 2 mA. Glass micropipettes recorded the resulting field potentials in CA 1 region of the slices. Multiple tetanic bursts (100 Hz) were delivered at fixed intervals. Three measures were taken from the field potentials: surface of excitatory postsynaptic field potentials (EPSPs), surface of population spikes (PSs), and peak-to-peak amplitude of PSs. Under the influence of 1000, 100, and 50 µM GSA in the perfusion fluid, EPSP and PS surfaces and amplitudes remained the same or decreased in all slices tested, in contrast to the usual increase ob¬served under standard conditions. 25 or 10 µM GSA did not produce such ef¬fects. Thus, probit analysis yields a tentative ED50 (effective dose in 50% of the animals) of 35.4 µM GSA (total n = 20). The inhibitory effect of GSA (100 µM) on potentiation of synaptic efficacy was completely antagonized by the co-application of 100 µM D-serine. Application of 1 00 µM D-serine alone did not result in any significant distortion of the standard pattern. Although our results could indicate an involvement of NMDA receptors, the exact mechanism of GSA's interference with excitatory synaptic transmission in hippocampus remains to be investigated further
Publication status: published
KU Leuven publication type: IC
Appears in Collections:Laboratory for Biological Psychology
× corresponding author
# (joint) last author

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