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PubMed1990

Directional tuning of cells in area 18 of the feline visual cortex for visual noise, bar and spot stimuli: a comparison with area 17.

Directional tuning for visual noise, bar and single spot stimuli was compared over a wide range of velocities in cells from areas 17 and 18 of the visual cortex in lightly-anaesthetized cats. In each area, S-cells were predominantly insensitive to motion of a field of visual noise. C-cells were more sensitive to noise motion than B-cells, but showed heterogeneity in noise sensitivity, which was associated with other response properties: strongly noise-sensitive C-cells had relatively high spontaneous activity and broad directional tuning, and were predominantly direction-selective and binocularly-driven. Frequently, directional tuning for noise was unimodal at low velocity, but became progressively more bimodal as velocity was increased: a trough of depressed response corresponding to the peak in tuning for the bar separated two progressively more widely disparate preferred directions. In area 18, cells with velocity tuned (VT) functions for bar motion developed bimodal tuning for noise well below the optimum velocity for bar or for noise motion, while velocity high-pass (VHP) cells became progressively more bimodally tuned for noise over a wide range of velocities, in parallel with a steep increase in response to bar and noise motion. A high proportion of VT and VHP cells was bimodally tuned for noise at all velocities, one VHP cell showing two discrete lobes of tuning for noise below the threshold velocity for bar motion. Among cells which remained unimodally tuned for noise, VT and VHP cells in area 18 had radically dissimilar preferred directions for noise and bar motion at all velocities. With the exception of VHP cells, velocity bandpass was higher for noise than for bar motion. These results, together with other novel observations on the modality of tuning for noise in preferred and opposite directions of motion, demonstrate that bimodality of tuning for noise cannot simply be an effect of upper cut-off velocity for bar motion (Movshon et al. 1980; Orban 1984). It is argued that the trough between the lobes of tuning arises through laterally-directed inhibitory convergence from superficial- and deep-layer, large basket cells. In 40% of noise-sensitive cells, tuning for bar motion was broader on the flank closest to the preferred direction for noise and for a moving sport, while some 25% of cells showed variations in tuning for bar motion with velocity, which were associated with velocity-dependent changes in tuning for noise.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

The temporal flexibility of attentional selection in the visual cortex.

Visual attention operates by biasing competitive interactions between neural representations, favoring relevant over irrelevant visual inputs. Attention can enhance the processing of relevant information using location-based, feature-based or object-based selection mechanisms. Studies using event-related potential and event-related magnetic field recordings, together with functional magnetic resonance imaging, show that the temporal sequencing of these different selection mechanisms is flexible. Depending on the specific processing demands of the experimental task, location-based, feature-based or object-based selection might be given temporal priority on a time scale of tens of milliseconds.

Animals↗
PubMed1999

Visual attention: spotlight on the primary visual cortex.

Visual search tasks appear to involve spatially selective attention to the target, but evidence for attentional modulation in the visual area with the most precise retinotopic organization V1 has been elusive. Recent imaging studies show that spatial attention can indeed enhance visual responses in human V1.

Animals↗
PubMed2004

Gamma oscillation maintains stimulus structure-dependent synchronization in cat visual cortex.

Visual cortical cells demonstrate both oscillation and synchronization, although the underlying causes and functional significance of these behaviors remain uncertain. We simultaneously recorded single-unit activity with microelectrode arrays in supragranular layers of area 17 of cats paralyzed and anesthetized with propofol and N(2)O. Rate-normalized autocorrelograms of 24 cells reveal bursting (100%) and gamma oscillation (63%). Renewal density analysis, used to explore the source of oscillation, suggests a contribution from extrinsic influences such as feedback. However, a bursting refractory period, presumably membrane-based, could also encourage oscillatory firing. When we investigated the source of synchronization for 60 cell pairs we found only moderate correlation of synchrony with bursts and oscillation. We did, nonetheless, discover a possible functional role for oscillation. In all cases of cross-correlograms that exhibited oscillation, the strength of the synchrony was maintained throughout the stimulation period. When no oscillation was apparent, 75% of the cell pairs showed decay in their synchronization. The synchrony between cells is strongly dependent on similar response onset latencies. We therefore propose that structured input, which yields tight organization of latency, is a more likely candidate for the source of synchronization than oscillation. The reliable synchrony at response onset could be driven by spatial and temporal correlation of the stimulus that is preserved through the earlier stages of the visual system. Oscillation then contributes to maintenance of the synchrony to enhance reliable transmission of the information for higher cognitive processing.

Action Potentials↗
PubMed1992

How complete is physiological compensation in extrastriate cortex after visual cortex damage in kittens?

Previous studies indicate that neurons in the cat's posteromedial lateral suprasylvian (PMLS) visual area of cortex show physiological compensation after neonatal but not adult damage to areas 17, 18, and 19 of the visual cortex (collectively, VC). Thus, VC damage in adults produces a loss of direction selectivity and a decrease in response to the ipsilateral eye among PMLS cells, but these changes are not seen in adult cats that received VC damage as kittens. This represents compensation for early VC damage in the sense that PMLS neurons develop properties they would have had if there had been no brain damage. However, this is only a partial compensation for the effects of VC damage. A full compensation would involve development of properties of the VC cells that were removed in the damage. The present study investigated whether this type of compensation occurs for detailed spatial- and temporal-frequency processing. Single-cell recordings were made in PMLS cortex of adult cats that had received a VC lesion on the day of birth or at 8 weeks of age. Responses to sine-wave gratings that varied in spatial frequency, contrast, and temporal frequency were assessed quantitatively. We found that the spatial- and temporal-frequency processing of PMLS cells in adult cats that had neonatal VC damage were not significantly different from PMLS cells in normal cats. Therefore, there was no evidence that PMLS cells can compensate for VC damage by developing properties that are better than normal and like those of the striate cortex cells that were damaged. We also assessed the effects of long-term VC damage in adult cats to determine whether the normal properties seen in cats with neonatal VC damage represent a compensation for abnormalities in PMLS cortex present after adult damage. In a previous study, we found that acute VC damage in adult cats has small but reliable effects on maximal response amplitude, maximal contrast sensitivity, and spatial resolution (Guido et al. 1990b). In the present study, we found that long-term VC damage in adult cats does not increase these abnormalities as a result of secondary degenerative changes. In fact, the minor abnormalities that were present after an acute VC lesion were virtually absent following a long-term adult lesion, perhaps because they were due to transient traumatic effects. Therefore, there was little evidence for abnormalities in spatial- or temporal-frequency processing following long-term adult VC damage for which PMLS cells might show compensation following long-term neonatal damage.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1996

Imaging a Computational Process in the Visual Cortex.

Visual perception is a computational process reconstructing the 3D visual world based on the 2D images viewed by the two eyes, which inherently contains ill-posed problems due to information deficiency. A typical example is the correspondence problem in finding partner points between the two retinal images. A neural network model for solution of the correspondence problem was proposed by Marr (1982, Vision. San Francisco: Freeman and Co.), constructed of groups of neurons selectively responsive to different disparities of visual stimuli shown to the two eyes. This model solves the correspondence problem as a relaxation process of excitation working between the neuronal groups responding to the same disparity antagonized by inhibition working between those responding to different disparity. Optical recording of responses evoked in the rat visual cortical slice by electrical stimulation of the white matter demonstrated the relaxation process of excitation antagonized by inhibition. Copyright 1996 Elsevier Science Ltd.

Journal Article↗
PubMed1991

Inhibitory effects of beta-phenylethylamine on photic-evoked potentials in the visual cortex of the cat.

We investigated the effects of beta-phenylethylamine (PEA) on photic-evoked potentials recorded from the cerebral cortex (visual cortex) in the anesthetized cat. The photic-evoked potential consisted of negative (N) and positive (P) components in the cerebral cortex, with peak times of 39.4 +/- 15.4 msec and 57.5 +/- 16.3 msec, respectively. Intravenous administration of PEA (6.5, 12.5 and 25 mg/kg) induced a dose-dependent decrease in the amplitude of the N component of photic-evoked potentials. PEA-induced decreases in the amplitude of photic-evoked potentials (at 12.5 mg/kg) were antagonized by yohimbine (2 mg/kg). Prazocin (2 mg/kg, i.v.) and propranolol (0.5 mg/kg, i.v.) did not change the PEA-induced decrease of photic-evoked potentials. Methysergide (2 mg/kg, i.v.), haloperidol (1 mg/kg, i.v.) and naloxone (0.5 mg/kg, i.v.) also failed to alter the inhibitory effect of PEA. Pretreatment with alpha-methyl-p-tyrosine or reserpine did not completely attenuate the PEA-induced decrease of photic-evoked potentials. According to these results, PEA inhibits the photic-evoked potentials in the visual cortex partially through the noradrenergic alpha 2-receptor.

Anesthesia↗
PubMed2002

Visual cortex excitability increases during visual mental imagery--a TMS study in healthy human subjects.

Previous neuroimaging studies provided evidence that visual mental imagery relies, in part, on the primary visual cortex. We hypothesized that, analogous to the finding that motor imagery increases the excitability of motor cortex, visual imagery should increase visual cortex excitability, as indexed by a decrease in the phosphene threshold (PT). In order to test visual cortex excitability, the primary visual cortex was stimulated with transcranial magnetic stimulation (TMS), so as to elicit phosphenes in the right lower visual quadrant. Subjects performed a visual imagery task and an auditory control task. We applied TMS with increasing intensity to determine the PT for each subject. Independent of the quadrant in which subjects placed their visual images, imagery decreased PT compared to baseline PT; in contrast, the auditory task did not change PT. These findings demonstrate for the first time a short-term, task-dependent modulation of PT. These results constitute evidence that early visual areas participate in visual imagery processing.

Adult↗
PubMed1990

Molecular and morphological changes in the cat lateral geniculate nucleus and visual cortex induced by visual deprivation are revealed by monoclonal antibodies Cat-304 and Cat-301.

Monoclonal antibody Cat-301 recognizes a surface-associated proteoglycan on subsets of neurons in the mammalian CNS (Hockfield and McKay, 1983). The expression of Cat-301 immunoreactivity on Y cells in the cat LGN is sharply reduced by early visual deprivation (Sur et al., 1988). We employed an immunosuppression strategy (Hockfield, 1987) to further study alterations in the expression of experience-dependent molecules. Newborn BALB/c mice were injected with LGN from dark-reared cats to induce a suppression of the immune response to antigens expressed in visually deprived animals. These mice were then immunized with LGN from normal cats to elicit an immune response to antigens with an expression dependent on normal early visual experience. This strategy permitted the generation of monoclonal antibody Cat-304, which recognizes a surface-associated antigen on neuronal cell bodies and proximal dendrites, and which appears histologically identical to Cat-301. Further analyses show that Cat-304 and Cat-301 recognize different epitopes on the same 680-kDa chondroitin sulfate proteoglycan. We examined the effects of early visual deprivation on Cat-304 immunoreactivity in the LGN and visual cortex of cats. In LGN from normal cats, Cat-304 labels neurons in layers A, A1, and C, in interlaminar zones, and in the medial interlaminar nucleus. In LGN from dark-reared cats, the number of antibody-positive neurons is markedly reduced, and the cross-sectional area of the remaining positive neurons is smaller than normal. In cortical area 17 of normally reared cats, Cat 304-positive neurons are densely distributed in 2 bands, in layers IV and V/VI. Labeled neurons are also present in layers II and III. In area 17 of dark-reared cats, the number of antibody-positive neurons is reduced. The reduction in the number of labeled neurons is most pronounced in layers II/III and V/VI. Antibody-positive neurons are smaller in all cortical layers of dark-reared cats. The changes in the expression of Cat-301 immunoreactivity in dark-reared visual cortex and LGN are identical to those of Cat-304. The laminar differences in the effect of dark rearing on Cat-301 and Cat-304 expression in the visual cortex provides support for the suggestion that layer IV of cortical area 17 may be less susceptible to prolongation of plasticity by dark rearing than layers II/III and V/VI. Further, the biochemical and histological studies reported provide evidence that early visual experience regulates protein expression in the cat LGN and visual cortex.

Animals↗
PubMed2004

Regulation of the CREB signaling cascade in the visual cortex by visual experience and neuronal activity.

The cAMP-responsive element (CRE) regulatory pathway has been studied as a model of signal-regulated transcription and is critical for some forms of learning and adaptation. In cell culture systems, the extracellular-regulated kinase (ERK) and ribosomal S6 kinase (RSK) couple synaptic signals to CRE-mediated gene expression by modulating CRE-binding protein (CREB) phosphorylation. However, it is not known whether sensory experience regulates gene expression in the brain by this mechanism. In this study, we ask: Are activated forms of ERK, RSK, and CREB colocalized in the cortex and are they coordinately regulated by synaptic signals? We find that these three signaling components are regulated in distinct ways. First, cells that show CRE-lacZ reporter expression, primarily excitatory neurons, do not colocalize with cells containing phospho-ERK. Second, while phosphorylation of ERK and RSK are modulated by visual experience, phosphorylation of CREB at serines 133, 142, or 143 is detected constitutively and is unaffected by experience. This finding suggests that neural activity might not regulate CREB phosphorylation in vivo. To test this hypothesis, we blocked action potentials by injection of tetrodotoxin and found no effect on CREB phosphorylation. These in vivo data show that, in contrast to cell culture systems, cortical synaptic activity controls CRE-mediated gene expression without affecting CREB phosphorylation, possibly by modification of RSK and CREB-associated coregulators.

Action Potentials↗
PubMed1981

[Correlation of infarctions of the visual cortex with homonymous visual field defects. A computer tomographic study (author's transl)].

Computed tomography (CT) is a simple and non-invasive method of demonstrating infarctions of the visual cortex. Seventy-eight CT-proven infarctions were correlated with the visual field defects. This correlation between cortical infarctions and visual field defects is difficult to achieve by angiography because of the variations in the vascular supply. CT, on the other hand, provides a far better correlation, showing the functional-anatomical structure of the visual cortex by projection in three planes (transverse, sagittal, coronar). CT, however, can not replace angiography in cases where arteriovenous malformations are suspected.

Acute Disease↗
PubMed2000

Spatial distribution of contextual interactions in primary visual cortex and in visual perception.

To examine the role of primary visual cortex in visuospatial integration, we studied the spatial arrangement of contextual interactions in the response properties of neurons in primary visual cortex of alert monkeys and in human perception. We found a spatial segregation of opposing contextual interactions. At the level of cortical neurons, excitatory interactions were located along the ends of receptive fields, while inhibitory interactions were strongest along the orthogonal axis. Parallel psychophysical studies in human observers showed opposing contextual interactions surrounding a target line with a similar spatial distribution. The results suggest that V1 neurons can participate in multiple perceptual processes via spatially segregated and functionally distinct components of their receptive fields.

Animals↗
PubMed2003

When is early visual cortex activated during visual mental imagery?

Although many neuroimaging studies of visual mental imagery have revealed activation in early visual cortex (Areas 17 or 18), many others have not. The authors review this literature and compare how well 3 models explain the disparate results. Each study was coded 1 or 0, indicating whether activation in early visual cortex was observed, and sets of variables associated with each model were fit to the observed results using logistic regression analysis. Three variables predicted all of the systematic differences in the probability of activation across studies. Two of these variables were identified with a perceptual anticipation theory, and the other was identified with a methodological factors theory. Thus, the variability in the literature is not random.

Humans↗
PubMed2006

Localizing sites of activation in primary visual cortex using visual-evoked potentials and functional magnetic resonance imaging.

This study compared retinotopic map identification in primary visual cortex (V1) using: (i) functional magnetic resonance imaging (fMRI) and (ii) visual evoked potentials (VEPs) coupled with dipole source localization (DSL). A multielectrode array was used to record VEPs while subjects viewed a flickering dartboard pattern modulated by a 16-bit m-sequence. The stimulus preferentially activates V1. Using a common time function DSL algorithm, the primary source of each stimulus patch was found independent of the fMRI. The VEP/DSL and fMRI localization data for each subject were aligned by a rigid translation and rotation. The average distance between VEP and corresponding fMRI sources was 10.8 mm +/- 3.8 mm. To assess the significance of the results, fMRI and DSL solutions were scrambled so the comparisons were no longer for corresponding patches. The average distance between the noncorresponding data sets was 17.2 mm for 50 million scrambles. The probability of the scrambled data yielding a better fit than the real data was p < 10(-7). The combination of multielectrode recording, multiinput visual stimulation and common time function DSL analysis can provide a detailed retinotopic map of visual cortex that has high correspondence with independent fMRI localization analysis on the same subject.

Brain Mapping↗