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Attention helps us process potentially important objects by selectively increasing the activity of sensory neurons that represent the relevant locations and features of our environment. This selection process requires top-down feedback about what is important in our environment. We investigated how parietal cortical output influences neural activity in early sensory areas. Neural recordings were made simultaneously from the posterior parietal cortex and an earlier area in the visual pathway, the medial temporal area, of macaques performing a visual matching task. When the monkey selectively attended to a location, the timing of activities in the two regions became synchronized, with the parietal cortex leading the medial temporal area. Parietal neurons may thus selectively increase activity in earlier sensory areas to enable focused spatial attention.

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We studied the effects of reversible cooling between 35 and 7 °C on membrane properties and spike generation of cells in slices of rat visual cortex. Cooling led to a depolarization of the neurones and an increase of the input resistance, thus bringing the cells closer to spiking threshold. Excitability, measured with intracellular current steps, increased with cooling. Synaptic stimuli were most efficient in producing spikes at room temperature, but strong stimulation could evoke spikes even below 10 °C. Spike width and total area increased with cooling, and spike amplitude was maximal between 12 and 20 °C. Repetitive firing was enhanced in some cells by cooling to 20–25 °C, but was always suppressed at lower temperatures. With cooling, passive potassium conductance decreased and the voltage‐gated potassium current had a higher activation threshold and lower amplitude. At the same time, neither passive sodium conductance nor the activation threshold of voltage‐dependent sodium channels changed. Therefore changing the temperature modifies the ratio between potassium and sodium conductances, and thus alters basic membrane properties. Data from two cells recorded in slices of cat visual cortex suggest a similar temperature dependence of the membrane properties of neocortical neurones to that described above in the rat. These results provide a framework for comparison of the data recorded at different temperatures, but also show the limitations of extending the conclusions drawn from in vitro data obtained at room temperature to physiological temperatures. Further, when cooling is used as an inactivation tool in vivo, it should be taken into account that the mechanism of inactivation is a depolarization block. Only a region cooled below 10 °C is reliably silenced, but it is always surrounded by a domain of hyperexcitable cells.

We tested the hypothesis that in a cluttered visual scene, the magnocellular (M) pathway is crucial for focusing attention serially on the objects in the field. Since developmental dyslexia is commonly associated with an M pathway deficit, we compared reading impaired children and age-matched normal readers in a search task that required the detection of a target defined by the conjunction of two features, namely form and colour, that are processed by the parvocellular dominated ventral neocortical stream. The dyslexic group's performance was significantly poorer than the controls when there were a large number of distractor items. The scheme of selective attention proposed from these results provides a neural mechanism that underlies reading and explains the pathophysiology of dyslexia.

Orientation sensitivity was tested, using moving bars as stimuli, in 136 LGN cells in normal cats and 82 LGN cells in cats with areas 17 and 18 lesioned. The responses of most neurones showed some dependence on the orientation of the line stimulus. The orientation bias was more pronounced for long, narrow bars moving at rather slow velocities. Length-response curves revealed less end-inhibition along the optimum orientation than along the non-optimum orientation. Thiry-two percent of the cells in the normal cats and 50% in the lesioned animals responded best to orientations within 10 degrees of the vertical or horizontal. The oblique orientations were represented poorly in the lesioned group. Thus the corticogeniculate feedback may serve to confer a more uniform distribution of orientation preferences on the LGN. It is suggested that the orientation biases of LGN neurones may play a role in building orientation-selective cells in the visual cortex. Further, the preferences for horizontal and vertical orientations in the LGN may explain the preferences for these orientations reported for visual cortical cells.

Postsynaptic potentials (PSPs) were recorded from cat striate cortical cells by the whole-cell in vivo recording technique using patch-clamp electrodes. EPSPs and IPSPs evoked by flashing bars on the receptive field at different positions and orientations revealed the spatial structure of the excitatory and inhibitory inputs. The elongation of the excitatory input field (length:width ratio) was found to be minimal (mean ratio of 1.7) and much lower than those reported for spike discharges. Two-dimensional receptive field response profiles of early PSPs were recorded by flashing a small spot of light over a square matrix covering the receptive field. These recordings also showed only mild degrees of elongations of the receptive field. Such elongations could be the result of either an excitatory input from the geniculate that is already biased for orientation or an excitatory convergence from a limited number of LGN fields arranged in a row. In most first- order cells, we found that inhibition was contributing significantly to orientation selectivity. Often prominent IPSPs could be evoked by stimuli of nonoptimum orientations. Presence of inhibition could also be inferred by the way that EPSPs were sharply cut off by inhibition. When the amplitude of an EPSP was measured at different latencies after its onset, the EPSP was found to be very broadly tuned to orientation at the beginning, but showing increasing orientation selectivity with time. It is proposed that this progressive development of orientation selectivity is due to (1) inhibitory inputs arriving after the first wave of excitation, (2) intracortical excitatory inputs from other cells tuned to similar orientations, and (3) voltage-sensitive mechanisms such as NMDA channels.