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Visual cortex

The width of an ocular dominance column is approximately 0.4 mm (Hubei and Wiesel 1977). Two such columns containing the data for both eyes amount to roughly 1 mm. The orientation-selective cells are not arranged randomly. If a penetration is made horizontally to the cortical surface, recording the response of the cells, it is found that the optimal or preferred orientation to which the cell responds changes continuously. Roughly, a 1-mm displacement corresponds to a 180° change in orientation. In other words, a 2 x 2 mm2 [Pg.20]

The structure of layer 2 and 3 creates two new pathways the P-B (parvocellular-blob pathway) and the P-I (parvocellular-interblob pathway). The cells located inside the blobs of layer 2 and 3 are either color or brightness selective. They are not orientation selective. [Pg.21]

Most cells of the interblob region respond to lines or bars of a particular orientation. They do not respond to color or show any color opponency. In contrast to the cells found inside the blobs, the receptive field of the cells found in the interblob region is very small. The response characteristic of the neurons of the interblob regions is arranged [Pg.22]

VI mainly connects to area V2, which surrounds VI (Tov6e 1996). Area V2 seems to be organized into three types of stripes, the so-called thick, thin, and interstripes. The stripes seem to be used to process visual orientation (thick stripes), color (thin stripes), and retinal disparity (interstripes). Adjacent stripes respond to the same region of the visual field. Neurons of layer 4B of V1 connect to the thick stripes. Cells found inside the thick stripes are selective for orientation and movement. Many of the cells also respond to retinal disparity. The neurons of the blobs are connected to the thin stripes. These cells are not orientation selective. More than half of these cells respond to color. Most show a double opponent characteristic. The cells of the interblob region connect to the interstripes. Neurons of the interstripe region respond to different orientations but neither to color nor to motion. A condition know as chromatopsia is caused by damage to certain parts of VI and V2. Individuals who suffer from chromatopsia are not able to see shape or form. However, they are still able to see colors. [Pg.24]

Motion and color are processed by different cortical areas. A difference in the luminance of a moving stimulus is required for coherent motion perception (Ramachandran and Gregory 1978). Cells found in V3 respond to lines of different orientation and also to motion (Tovee 1996). They do not respond to color. V3 is believed to process dynamic form. Some cells of V3 are able to discount the movement of the eye. They only respond to a stimulus that moves relative to the eye. These cells also receive information about the eye position (Zeki 1999). Cells in V3 are connected to layer 4B of VI. V3 is also connected to the thick stripes of V2. [Pg.24]


Methanol intoxication can cause blindness due to damage to ganglion cells in the retina. The blindness results from the accumulation of formaldehyde and formic acid, which are metabolites of methanol. Chemical compounds can also damage the visual cortex, for example, visual damage was observed among the victims of organic mercury intoxication in Japan (the fishermen of Minamata Bay). ... [Pg.293]

An increased level of exploratory activity immediately after exposure, attributed to reduced anxiety on the part of the rats, was also observed in this study. Decreased avoidance was observed in rats exposed to 125 ppm trichloroethylene 4 hours per day, 5 days per week for 30 days (Goldberg et al. 1964a). Changes in visually evoked potentials (Blain et al. 1992) and electroretinal responses to flash stimulation (Blain et al. 1994) were seen in rabbits exposed to 350 ppm trichloroethylene for 12 weeks (4 days/week, 4 hours/day). The study authors suggested that binding of trichloroethanol to blood proteins may enable it to reach the visual cortex. [Pg.54]

At its most fundamental level, the circadian cycle rests on the influence of so-called clock genes . These genes have been studied most extensively in insects but they have also been found in humans. Their protein products enter the cell nucleus and regulate their own transcription. This feedback process is linked to exposure to light and so it is not surprising that visual inputs are important for maintenance of circadian rhythms. However, it is not the reception of specific visual information, transmitted in the optic nerve to the lateral geniculate nucleus (LGN) and visual cortex (i.e. visual discrimination), that is responsible for the rhythm but the more simple, almost subconscious, reception of light. [Pg.478]

Kosofsky, B.E. Molliver, M.E. Morrison, J.H. and Foote, S.L. The serotonin and norepinephrine innervation of primary visual cortex in the Cynomolgus monkey (Macaca fascicularis). J Comp Neurol 230 168-178, 1984. [Pg.300]

Morrison, J.H. Foote, S.L. Molliver, M.E. Bloom, F.E. and Lidov, H.G.W. Noradrenergic and serotonergic fibers innervate complementary layers in monkey primary visual cortex An immunohistochemi-cal study. Proc Natl Acad Sci USA 79 2401-2405, 1982. [Pg.301]

Altmann L,Gutowski M, Wiegand H. 1994. Effects of maternal lead exposure on functional plasticity in the visual cortex and hippocampus of immature rats. Develop Brain Res 81 50-56. [Pg.486]

The posterior parietal cortex is located posterior to the somatosensory cortex and serves as its unimodal association area. In addition to further processing of somatosensory input, information from the somatosensory cortex is integrated with visual inputs in this region. Association tracts from both the somatosensory cortex and the visual cortex terminate here. This activity is important for planning complex movements and for hand (prop-rioception)-eye (visual) coordination. [Pg.53]

Hilbig, H. Punkt, K. (1997). 24-hour rhythmicity of NADPH-diaphorase activity in the neuropil of rat visual cortex. Brain Res. Bull. 43, 337-40. [Pg.331]

Hensch, T. K., Fagiolini, M., Mataga, N. et al. Local GABA circuit control of experience-dependent plasticity in developing visual cortex. Science 282 1504-1508,1998. [Pg.300]

Pizzorusso, T., Medini, P., Berardi, N., Chierzi, S., Fawcett, J. W. and Maffei, L. Reactivation of ocular dominance plasticity in the adult visual cortex. Science 298 1248-1251, 2002. [Pg.527]

Prichard, J., Rothman, D., Novotny, E. etal. Lactate rise detected by H NMR in human visual cortex during physiologic stimulation. Proc. Natl Acad. Sci. U.S.A. 88 5829-5831,1991. [Pg.555]

Retinal responses to different light frequencies are encoded in the retina and conveyed to the thalamus and visual cortex 808... [Pg.807]

Paranoia, hallucinations Frontal cortex, visual cortex... [Pg.25]

Hallucinations, increased sexual drive Visual cortex, limbic system... [Pg.46]

Domino et al. (2000a) 18 Smokers i O-PET Nic nasal spray vs. pepper spray t Thai, pons, visual cortex, cereb... [Pg.148]


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Brain regions visual cortex

Brain visual cortex

Cortex

Cortexal

Involvement of the Visual Cortex in Color Constancy

Of visual cortex

Primary visual cortex

Synaptic plasticity visual cortex

Temporal visual cortex

Visual association cortex

Visual cortex critical period

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