Transient Synaptic Potentiation in the Visual Cortex. I. Cellular Mechanisms

• Published in: Journal of neurophysiology 1997-03, Vol.77 (3), p.1269-1283
• Main Authors: Harsanyi, Krisztina, Friedlander, Michael J
• Format: Article
• Language: English
• Subjects: Animals; Calcium - physiology; Chloride Channels - drug effects; Chloride Channels - physiology; Electric Stimulation; Electrophysiology; Guinea Pigs; In Vitro Techniques; Information Systems; Membrane Potentials - physiology; Neuronal Plasticity - physiology; Neurons - physiology; Nitric Oxide - physiology; Patch-Clamp Techniques; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Receptors, N-Methyl-D-Aspartate - physiology; Synapses - physiology; Visual Cortex - cytology; Visual Cortex - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.1997.77.3.1269

Krisztina Harsanyi and Michael J. Friedlander Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 Harsanyi, Krisztina and Michael J. Friedlander. Transient synaptic potentiation in the visual cortex. I. Cellular mechanisms. J. Neurophysiol. 77: 1269-1283, 1997. The cellular mechanisms that underlie transient synaptic potentiation were studied in visual cortical slices of adult guinea pigs ( age 5 wk postnatal). Postsynaptic potentials (PSPs) elicited by stimulation of the white matter/layer VI border were recorded with conventional intracellular techniques from layer II/III neurons. Transient potentiation (average duration 23 ± 3 min, mean ± SE) was evoked by 60 low-frequency (0.1 Hz) pairings of weak afferent stimulation with coincident intracellular depolarizing pulses (80 ms) of the postsynaptic cell. Fifty-one percent (47 of 92) of the pairing protocols led to significant enhancement (+26 ± 3%) of the PSP peak amplitude. Blockade of action potential output from the recorded neuron during pairing with Lidocaine, N -ethyl bromide quaternary salt in the recording micropipette did not reduce the likelihood of potentiation (7 of 14 protocols = 50%). Thus transient synaptic potentiation does not require action potential output from the paired cell or recurrent synaptic activation in the local cortical circuit. Rather, the modification occurs at synaptic sites that directly impinge onto the activated neuron. Intracellular postsynaptic blockade of inhibitory PSPs only onto the paired cell with the chloride channel blocker 4,4 -dinitro-stilbene-2,2 -disulfonic acid and the potassium channel blocker cesium in the micropipette also did not reduce the likelihood of induction of potentiation (6 of 9 protocols = 67%). These results suggest that the potentiation is due to a true up-regulation of excitatory synaptic transmission and that it does not require a reduction of inhibitory components of the compoundPSP for induction. Chelation of postsynaptic intracellular calciumwith 1,2-bis-2-aminophenoxy ethane- N,N,N ,N -tetraacetic acid (BAPTA) in all cases effectively blocked the induction of potentiation (no change in the PSP, 9 of 13 protocols; induction of synaptic depression, 4 of 13 protocols), suggesting that a rise in the intracellular postsynaptic calcium level is critical for the pairing-induced synaptic potentiation to occur. Bath application of the N -methyl- D -aspartate (NMDA) receptor antagonist 2-amino-5-phosphonova