scholarly journals Perceptual decision related activity in the lateral geniculate nucleus

2015 ◽  
Vol 114 (1) ◽  
pp. 717-735 ◽  
Author(s):  
Yaoguang Jiang ◽  
Dmitry Yampolsky ◽  
Gopathy Purushothaman ◽  
Vivien A. Casagrande

Fundamental to neuroscience is the understanding of how the language of neurons relates to behavior. In the lateral geniculate nucleus (LGN), cells show distinct properties such as selectivity for particular wavelengths, increments or decrements in contrast, or preference for fine detail versus rapid motion. No studies, however, have measured how LGN cells respond when an animal is challenged to make a perceptual decision using information within the receptive fields of those LGN cells. In this study we measured neural activity in the macaque LGN during a two-alternative, forced-choice (2AFC) contrast detection task or during a passive fixation task and found that a small proportion (13.5%) of single LGN parvocellular (P) and magnocellular (M) neurons matched the psychophysical performance of the monkey. The majority of LGN neurons measured in both tasks were not as sensitive as the monkey. The covariation between neural response and behavior (quantified as choice probability) was significantly above chance during active detection, even when there was no external stimulus. Interneuronal correlations and task-related gain modulations were negligible under the same condition. A bottom-up pooling model that used sensory neural responses to compute perceptual choices in the absence of interneuronal correlations could fully explain these results at the level of the LGN, supporting the hypothesis that the perceptual decision pool consists of multiple sensory neurons and that response fluctuations in these neurons can influence perception.

1975 ◽  
Vol 38 (2) ◽  
pp. 395-404 ◽  
Author(s):  
A. J. Gabor ◽  
R. P. Scobey

In order to investigate if ectopic spike generation was ubiquitous in and specific generation was ubiquitous in and specific to epileptogenic cortex, a method was devised to determine the limits of such an area based on a well-accepted physiologic characteristic of epileptogenicity. The limits of the penicillin-induced epileptogenic cortex were defined in terms of a retinal activation field; this is a circumscribed area whose stimulation by light evokes a characteristic cortical epileptiform wave. All lateral geniculate nucleus (LGN) neurons manifesting ectopic spike generation during interictal epileptiform waves had receptive fields within the activation field. During organized seizures, ectopic spike generation was observed in neurons with receptive fields outside the activation field. Because of these findings it was concluded that ectopic spike generation is a characteristic and specific feature of epileptogenic cortex and that it is a characteristic of the epeleptogenic process rather than a peripheral event related entirely to the direct effect of penicillin on neurons.


2000 ◽  
Vol 17 (6) ◽  
pp. 871-885 ◽  
Author(s):  
G.T. EINEVOLL ◽  
P. HEGGELUND

Spatial receptive fields of relay cells in dorsal lateral geniculate nucleus (dLGN) have commonly been modeled as a difference of two Gaussian functions. We present alternative models for dLGN cells which take known physiological couplings between retina and dLGN and within dLGN into account. The models include excitatory input from a single retinal ganglion cell and feedforward inhibition via intrageniculate interneurons. Mathematical formulas describing the receptive field and response to circular spot stimuli are found both for models with a finite and an infinite number of ganglion-cell inputs to dLGN neurons. The advantage of these models compared to the common difference-of-Gaussians model is that they, in addition to providing mathematical descriptions of the receptive fields of dLGN neurons, also make explicit contributions from the geniculate circuit. Moreover, the model parameters have direct physiological relevance and can be manipulated and measured experimentally. The discrete model is applied to recently published data (Ruksenas et al., 2000) on response versus spot-diameter curves for dLGN cells and for the retinal input to the cell (S-potentials). The models are found to account well for the results for the X-cells in these experiments. Moreover, predictions from the discrete model regarding receptive-field sizes of interneurons, the amount of center-surround antagonism for interneurons compared to relay cells, and distance between neighboring retinal ganglion cells providing input to interneurons, are all compatible with data available in the literature.


2015 ◽  
Vol 114 (2) ◽  
pp. 1321-1330 ◽  
Author(s):  
Christopher A. Procyk ◽  
Cyril G. Eleftheriou ◽  
Riccardo Storchi ◽  
Annette E. Allen ◽  
Nina Milosavljevic ◽  
...  

In advanced retinal degeneration loss of rods and cones leaves melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) as the only source of visual information. ipRGCs drive non-image-forming responses (e.g., circadian photoentrainment) under such conditions but, despite projecting to the primary visual thalamus [dorsal lateral geniculate nucleus (dLGN)], do not support form vision. We wished to determine what precludes ipRGCs supporting spatial discrimination after photoreceptor loss, using a mouse model ( rd/rd cl) lacking rods and cones. Using multielectrode arrays, we found that both RGCs and neurons in the dLGN of this animal have clearly delineated spatial receptive fields. In the retina, they are typically symmetrical, lack inhibitory surrounds, and have diameters in the range of 10–30° of visual space. Receptive fields in the dLGN were larger (diameters typically 30–70°) but matched the retinotopic map of the mouse dLGN. Injections of a neuroanatomical tracer (cholera toxin β-subunit) into the dLGN confirmed that retinotopic order of ganglion cell projections to the dLGN and thalamic projections to the cortex is at least superficially intact in rd/rd cl mice. However, as previously reported for deafferented ipRGCs, onset and offset of light responses have long latencies in the rd/rd cl retina and dLGN. Accordingly, dLGN neurons failed to track dynamic changes in light intensity in this animal. Our data reveal that ipRGCs can convey spatial information in advanced retinal degeneration and identify their poor temporal fidelity as the major limitation in their ability to provide information about spatial patterns under natural viewing conditions.


2005 ◽  
Vol 93 (5) ◽  
pp. 2374-2387 ◽  
Author(s):  
Masayuki Matsumoto ◽  
Hidehiko Komatsu

Although there is no retinal input within the blind spot, it is filled with the same visual attributes as its surround. Earlier studies showed that neural responses are evoked at the retinotopic representation of the blind spot in the primary visual cortex (V1) when perceptual filling-in of a surface or completion of a bar occurs. To determine whether these neural responses correlate with perception, we recorded from V1 neurons whose receptive fields overlapped the blind spot. Bar stimuli of various lengths were presented at the blind spots of monkeys while they performed a fixation task. One end of the bar was fixed at a position outside the blind spot, and the position of the other end was varied. Perceived bar length was measured using a similar set of bar stimuli in human subjects. As long as one end of the bar was inside the blind spot, the perceived bar length remained constant, and when the bar exceeded the blind spot, perceptual completion occurred, and the perceived bar length increased substantially. Some V1 neurons of the monkey exhibited a significant increase in their activity when the bar exceeded the blind spot, even though the amount of the retinal stimulation increased only slightly. These response increases coincided with perceptual completion observed in human subjects and were much larger than would be expected from simple spatial summation and could not be explained by contextual modulation. We conclude that the completed bar appearing on the part of the receptive field embedded within the blind spot gave rise to the observed increase in neuronal activity.


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