scholarly journals Evidence for long-term functional plasticity in the visual cortex of adult cats

1982 ◽  
Vol 324 (1) ◽  
pp. 239-248 ◽  
Author(s):  
W. Singer ◽  
F. Tretter ◽  
U. Yinon
Keyword(s):  
Visual Cortex ◽  
Functional Plasticity ◽  
Adult Cats

Critical periods for functional and anatomical compensation in lateral suprasylvian visual area following removal of visual cortex in cats

1984 ◽  
Vol 52 (5) ◽  
pp. 941-960 ◽  
Author(s):  
L. Tong ◽  
R. E. Kalil ◽  
P. D. Spear
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Direction Selectivity ◽  
Visual Area ◽  
Critical Periods ◽  
Cortex Lesion ◽  
Thalamic Projections ◽  
Adult Cats ◽  
Visual Cortical

Previous experiments have found that neurons in the cat's lateral suprasylvian (LS) visual area of cortex show functional compensation following removal of visual cortical areas 17, 18, and 19 on the day of birth. Correspondingly, an enhanced retino-thalamic pathway to LS cortex develops in these cats. The present experiments investigated the critical periods for these changes. Unilateral lesions of areas 17, 18, and 19 were made in cats ranging in age from 1 day postnatal to 26 wk. When the cats were adult, single-cell recordings were made from LS cortex ipsilateral to the lesion. In addition, transneuronal autoradiographic methods were used to trace the retino-thalamic projections to LS cortex in many of the same animals. Following lesions in 18- and 26-wk-old cats, there is a marked reduction in direction-selective LS cortex cells and an increase in cells that respond best to stationary flashing stimuli. These results are similar to those following visual cortex lesions in adult cats. In contrast, the percentages of cells with these properties are normal following lesions made from 1 day to 12 wk of age. Thus the critical period for development of direction selectivity and greater responses to moving than to stationary flashing stimuli in LS cortex following a visual cortex lesion ends between 12 and 18 wk of age. Following lesions in 26-wk-old cats, there is a decrease in the percentage of cells that respond to the ipsilateral eye, which is similar to results following visual cortex lesions in adult cats. However, ocular dominance is normal following lesions made from 1 day to 18 wk of age. Thus the critical period for development of responses to the ipsilateral eye following a lesion ends between 18 and 26 wk of age. Following visual cortex lesions in 2-, 4-, or 8-wk-old cats, about 30% of the LS cortex cells display orientation selectivity to elongated slits of light. In contrast, few or no cells display this property in normal adult cats, cats with lesions made on the day of birth, or cats with lesions made at 12 wk of age or later. Thus an anomalous property develops for many LS cells, and the critical period for this property begins later (between 1 day and 2 wk) and ends earlier (between 8 and 12 wk) than those for other properties.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Rapid, long-term labeling of cells in the developing and adult rodent visual cortex using double-stranded adeno-associated viral vectors

2009 ◽  
Vol 69 (10) ◽  
pp. 674-688 ◽  
Author(s):  
Rebecca L. Lowery ◽  
Yu Zhang ◽  
Emily A. Kelly ◽  
Cassandra E. Lamantia ◽  
Brandon K. Harvey ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Viral Vectors

Oscillations and Long-Lasting Correlations in a Model of the Lateral Geniculate Nucleus and Visual Cortex

2000 ◽  
Vol 84 (4) ◽  
pp. 1863-1868 ◽  
Author(s):  
Kyle L. Kirkland ◽  
Adam M. Sillito ◽  
Helen E. Jones ◽  
David C. West ◽  
George L. Gerstein
Keyword(s):  
Experimental Data ◽  
Visual Cortex ◽  
Cell Membrane ◽  
Lateral Geniculate Nucleus ◽  
Feedback Inhibition ◽  
Frequency Range ◽  
Lateral Geniculate ◽  
Low Threshold ◽  
Thalamocortical System

We have previously developed a model of the corticogeniculate system to explore cortically induced synchronization of lateral geniculate nucleus (LGN) neurons. Our model was based on the experiments of Sillito et al. Recently Brody discovered that the LGN events found by Sillito et al. correlate over a much longer period of time than expected from the stimulus-driven responses and proposed a cortically induced slow covariation in LGN cell membrane potentials to account for this phenomenon. We have examined the data from our model, and we found, to our surprise, that the model shows the same long-term correlation. The model's behavior was the result of a previously unsuspected oscillatory effect, not a slow covariation. The oscillations were in the same frequency range as the well-known spindle oscillations of the thalamocortical system. In the model, the strength of feedback inhibition from the cortex and the presence of low-threshold calcium channels in LGN cells were important. We also found that by making the oscillations more pronounced, we could get a better fit to the experimental data.

scholarly journals NMDAR-independent acetylcholine, serotonin, and norepinephrine mediated modulation of synaptic eligibility traces into LTD in mice visual cortex

2020 ◽  
Author(s):  
Shumsuzzaman Khan
Keyword(s):  
Visual Cortex ◽  
Ex Vivo ◽  
Brain Slices ◽  
Low Frequency ◽  
Decay Kinetics ◽  
Low Frequency Stimulation ◽  
Long Term Changes ◽  
Frequency Stimulation ◽  
Mouse Visual Cortex

AbstractIn reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.

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