Quantitative studies of intracellular postsynaptic potentials in the lateral geniculate nucleus of the cat with respect to optic tract stimulus response latencies

Abstract

LGN cells were intracellularly recorded with glass micropipettes. Electrical stimuli of different amplitude and frequency were applied to the optic tract close to the optic chiasm. The cells were classified according to stimulus response latencies of action potentials as belonging to class I (1.0-16 msec) Or class II (1.7-3.0 MSEC). Class I EPSPs had shorter latencies (1.0-1.5 msec), durations (4-12 msec), rise times to peak (0.5-1.4 msec), and decay times (3.0-8.5 msec); the synaptic transmission time was on the average 0.41 msec. Class II EPSPs (1.6-2.6 msec latency) had longer durations (10-30 msec), rise times (1.6-3.7 msec), and decay times (9.0-25 msec); the synaptic transmission time was on the average 0.67 msec. With repetitive stimulation the EPSPs of latency class I revealed almost no stimulus frequency dependence between 1 and 120 HZ, while class 22 EPSPs decrease in amplitude between 30 and 70% with increasing frequency. Comparable temporal summation of excitation occurred in cells of both latency classes. Negative serial correlation coefficients of first order were found for consecutive EPSP amplitudes of all cells recorded for sufficient periods of time. The IPSPs were subdivided into two groups according to their optic tract response latency. Group 1 IPSPs had shorter latencies (2.0-2.6 msec), durations (15-50 msec), and times from the onset to maximal hyperpolarization (2.4-4.2 msec) than group 2 IPSPs (3.0-4.8 msec latency, 40-100 msec duration, 2.7-7.5 msec time from onset to extremum). The group 2 IPSPs decreased in amplitude by about 90% when the stimulus frequency was increased form 1 to 50 HZ, while the group 1 IPSPs displayed a comparable decrease in the frequency range between 50 and 120 HZ. Effective temporal summation was found in group 2 IPSPs in the frequency range below 70 HZ, and in group 1 IPSPs at stimulus frequencies between 70 and 120 HZ. The EPSP peak latencies and the latencies to the minimum of IPSPs proved to be invariant with respect to PSP amplitude and stimulus fre quency in individual cells. The latencies to the extrema of EPSPs and IPSPs as well as the amplitude values were symmetrically distributed.

Thalamic filtering of retinal spike trains by postsynaptic summation

“…In fact, synaptic current showed a 1-5% decrease at short EPSP intervals, indicating a slight depression rather than facilitation. These results agree with intracellular observations made in the lateral geniculate of cats, where subsequent EPSPs appear to be remarkably invariant (Eysel, 1976), and indicate that synaptic plasticityVparticularly facilitationVis unlikely to play a prominent role in retinogeniculate integration during natural vision.…”

“…We first measured postsynaptic potentials arising from the dominant retinal input and found no evidence for synaptic facilitation. The synaptic depression that we observed was modest, arguably smaller than seen in vitro (Alexander & Godwin, 2005;Blitz & Regehr, 2003;Chen et al, 2002) but highly consistent with intracellular in vivo recordings made in the cat (Eysel, 1976). We therefore constructed an extremely simple model of synaptic integration, one in which EPSPs have constant size irrespective of past history.…”

“…Plasticity is nearly ubiquitous at synapses in the central nervous system (Zucker & Regehr, 2002) and has been demonstrated at the retinogeniculate synapse in vitro (Alexander & Godwin, 2005;Blitz & Regehr, 2003;Chen, Blitz, & Regehr, 2002). However, the impact of plasticity appears to be quite minimal in intracellular recordings obtained in vivo (Eysel, 1976). Thus, the role of synaptic plasticity versus summation in the editing of retinal spike trains is not clear.…”

Computer-Based Training of Stimulus Detection Improves Color and Simple Pattern Recognition in the Defective Field of Hemianopic Subjects

“…Nevertheless, in recent years, we have witnessed a paradigm shift in neuroscience, namely that the brain is able to compensate for lost functions (see, e.g., Bach-y- Rita, 1990;Finger, LeVere, Almli, & Stein, 1988). Even the visual system, previously considered to be hard-wired both in animals and humans, has proven to possess a remarkable flexibility in adapting to damage (see, e.g., Chino, 1999;Sabel, 1999a,b;Werth & Moerenschlager, 1999;Kasten, Wuest, Behrens-Baumann, & Sabel, 1998c;Gilbert, Das, Ito, Kapadia, & Westheimer, 1996;Gilbert, 1998;Pöppel et al, 1987;Eysel, 1976;Eysel & Grüsser, 1978;Eysel & SchmidtKastner, 1991;Eysel, Eyding, & Schweigart, 1998;Eysel et al, 1999).…”

Vision restoration therapy does not benefit from costimulation: A pilot study

“…These proposals have been based on animal studies by Eysel (1976) and Eysel and Gruesser (1978) who were the first to document plasticity of receptive fields after lesions in retina and visual cortex. About 6-8 weeks after destruction of small, circumscribed areas in the retina, many cells in the geniculate body achieved about 50% of their normal function again.…”