Analysis of NMDA‐independent long‐term potentiation induced at CA3—CA1 synapses in rat hippocampus in vitro

• Published in: The Journal of physiology 1999-10, Vol.520 (2), p.513-525
• Main Authors: Stricker, C., Cowan, A. I., Field, A.C., Redman, S. J.
• Format: Article
• Language: English
• Subjects: Animals; Calcium - metabolism; Cerebrospinal Fluid; Electrophysiology; Excitatory Postsynaptic Potentials - physiology; Female; Hippocampus - metabolism; Hippocampus - physiology; Long-Term Potentiation; Male; Original; Quinoxalines - pharmacology; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - metabolism; Signal Transduction - physiology; Synapses - physiology; Valine - analogs & derivatives; Valine - pharmacology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1999.00513.x

1 Excitatory postsynaptic currents (EPSCs) were evoked at synapses formed by Schaffer collaterals/commissural (CA3) axons with CA1 pyramidal cells using the rat hippocampal slice preparation. Long‐term potentiation (LTP) was induced at these synapses using a pairing protocol, with 50 μm d,l‐APV present in the artificial cerebrospinal fluid (ACSF). 2 Quantal analysis of the amplitudes of the control and conditioned EPSCs showed that the enhancement of synaptic strength was due entirely to an increase in quantal content of the EPSC. No change occurred in the quantal current. 3 These results were compared with those obtained from a previous quantal analysis of LTP induced in normal ACSF, where both quantal current and quantal content increased. The results suggest that calcium entering via NMDA receptors initiates the signalling cascade that results in enhanced AMPA currents because it is adding to cytoplasmic calcium from other sources to reach a threshold for this signalling pathway, or because calcium entering via NMDA receptors specifically activates this signalling pathway.