Biomedical subjects

M Castelo-Branco

Publications and source records attributed to M Castelo-Branco.

4 recordsLinked to original sources

PubMed2005

Independent patterns of damage within magno-, parvo- and koniocellular pathways in Parkinson's disease.

Sensory deficits have been documented in Parkinson's disease, in particular within the visual domain. However, ageing factors related to the brain and to neural and non-neural ocular structures could explain some of the previously reported results, in particular the claimed impairment within the koniocellular pathway. This study addressed visual impairment attributable to the magno- (luminance), parvo- (red-green) and koniocellular (blue-yellow) pathways in a population of Parkinson's disease patients. To avoid potentially confounding factors, all subjects underwent a full neurophthalmological assessment which led to exclusion of subjects with increased intraocular pressure, diabetes even in the absence of retinopathy, and ocular abnormalities (from a total of 72 patients' eyes, 12 were excluded). Both parvo- and koniocellular pathways were studied by means of contrast sensitivity (CS) measurements along protan, tritan and deutan axes and also by fitting chromatic discrimination ellipses using eight measured contrast axes. Magnocellular function was assessed, using stimuli that induce a frequency doubling illusion, in 17 locations in the fovea and periphery. Achromatic (luminance modulation) thresholds were significantly higher in Parkinson's disease both in foveal and peripheral locations. A significant impairment was observed along protan and deutan axes, but only marginally along the tritan axis. These results were corroborated by a significant elongation of chromatic discrimination ellipses in our Parkinson's disease group. Correlation analysis showed that achromatic and chromatic CS measures were independent, which implies that multiple visual pathways are affected independently in Parkinson's disease. Magnocellular impairment was significantly correlated with age and disease stage, in contrast to the measured chromatic deficits. We conclude that in Parkinson's disease, independent damage occurs in the early magno- and parvocellular pathways. Furthermore, traditional koniocellular probing strategies in Parkinson's disease may be confounded by ageing factors, which may reconcile the previously reported controversial findings concerning chromatic impairment in Parkinson's disease.

Aging↗

PubMed2000

Neural synchrony correlates with surface segregation rules.

To analyse an image, the visual system must decompose the scene into its relevant parts. Identifying distinct surfaces is a basic operation in such analysis, and is believed to precede object recognition. Two superimposed gratings moving in different directions (plaid stimuli) may be perceived either as two surfaces, one being transparent and sliding on top of the other (component motion) or as a single pattern whose direction of motion is intermediate to the component vectors (pattern motion). The degree of transparency, and hence the perception, can be manipulated by changing only the luminance of the grating intersections. Here we show that neurons in two visual cortical areas--A18 and PMLS--synchronize their discharges when responding to contours of the same surface but not when responding to contours belonging to different surfaces. The amplitudes of responses correspond to previously described rate predictions for component and pattern motion, but, in contrast to synchrony, failed to reflect the transition from component to pattern motion induced by manipulating the degree of transparency. Thus, dynamic changes in synchronization could encode, in a context-dependent way, relations among simultaneous responses to spatially superimposed contours and thereby bias their association with distinct surfaces.

Animals↗

PubMed1999

Synchronous oscillations in the cat retina.

Retinal ganglion cells exhibit oscillatory responses which are precisely synchronized over large distances. Here we examined, with multi-electrode recordings, the time course of synchronization during spontaneous and stimulus-driven oscillatory activity. Spontaneous discharges showed synchronized oscillations at approximately 30 Hz, which were occasionally associated with slower superimposed oscillations in the range of 1-5 Hz. Stationary stimuli or moving gratings induced synchronous oscillations at higher frequencies (mean of 79.0 +/- 20.0 Hz for OFF- and 91.7 +/- 11.7 Hz for ON-responses), with time lags of a few milliseconds. At response onset, the first few oscillatory cycles were occasionally time locked to the stimulus. Thereafter, synchronization became independent of stimulus coordination and was exclusively due to neuronal interactions. Oscillatory modulation emerged rapidly and was sustained throughout the responses while oscillation frequency decreased gradually. This periodic patterning of responses persisted despite brief and local occlusion of stimuli, suggesting that synchronous oscillations emerge from population dynamics and entrain cells even if they are intermittently silenced.

Action Potentials↗

PubMed1998

Synchronization of visual responses between the cortex, lateral geniculate nucleus, and retina in the anesthetized cat.

Synchronization of spatially distributed responses in the cortex is often associated with periodic activity. Recently, synchronous oscillatory patterning was described for visual responses in retinal ganglion cells that is reliably transmitted by the lateral geniculate nucleus (LGN), raising the question of whether oscillatory inputs contribute to synchronous oscillatory responses in the cortex. We have made simultaneous multi-unit recordings from visual areas 17 and 18 as well as the LGN and the retina to examine the interactions between subcortical and cortical synchronization mechanisms. Strong correlations of oscillatory responses were observed between retina, LGN, and cortex, indicating that cortical neurons can become synchronized by oscillatory activity relayed through the LGN. This feedforward synchronization occurred with oscillation frequencies in the range of 60-120 Hz and was most pronounced for responses to stationary flashed stimuli and more frequent for cells in area 18 than in area 17. In response to moving stimuli, by contrast, subcortical and cortical oscillations dissociated, proving the existence of independent subcortical and cortical mechanisms. Subcortical oscillations maintained their high frequencies but became transient. Cortical oscillations were now dominated by a cortical synchronizing mechanism operating in the 30-60 Hz frequency range. When the cortical mechanism dominated, LGN responses could become phase-locked to the cortical oscillations via corticothalamic feedback. In summary, synchronization of cortical responses can result from two independent but interacting mechanisms. First, a transient feedforward synchronization to high-frequency retinal oscillations, and second, an intracortical mechanism, which operates in a lower frequency range and induces more sustained synchronization.

Animals↗