The visual pathways of an albino green monkey have been studied electrophysiologically and by autoradiographic methods. The monkey had a white coat and pink eyes; it had a strabismus and a nystagmus. When comparisons were made with normal macaque and green monkeys, several abnormalities could be defined. In the retina there was no foveal pit. A whole mount preparation showed a central area of high ganglion cell density in which the ganglion cells were significantly larger than the most central ganglion cells of a normal monkey. More peripheral retinal areas showed an apparently normal distribution of ganglion cell sizes and packing densities. Within the optic tract the number of uncrossed retinofugal fibers was less than normal, the part of the tract that represents central vision showing almost no uncrossed component. The uncrossed input to the lateral geniculate nucleus and to the superior colliculus was similarly reduced. Regions normally receiving ipsilateral afferents from the central retina were innervated exclusively by crossed afferents. The pathways to the magnocellular geniculate layers showed a more extensive abnormality than did the pathways to the parvicellular layers. Not only were the afferents to the geniculate layers abnormal, but the laminar pattern in the nucleus was also clear than normal in some parts of the nucleus, and there were a number of abnormal laminar fusions. Within the visual cortex it was possible to demonstrate a normal mapping of the contralateral visual field through the contralateral nasal retina and through the peripheral parts of the ipsilateral temporal retina. The central parts of the temporal retina mapped abnormally in the contralateral visual cortex, so that there was a monocular map of the central parts of the visual field forming as a mirror reversal of the normal map. The normal map of the contralateral hemifield formed columns that alternated with the abnormal map of the ipsilateral hemifield. The peripheral parts of the visual field were represented as ocular dominance columns, demonstrable electrophysiologically and also by the transneuronal transport of 3H-proline.
1. This study describes the response properties of V1 cortical cells in a nocturnal primate and examines the receptive field organization of these cells in relationship to anatomically defined layers and cytochrome oxidase (CO) rich blobs and CO poor interblob compartments. Visual resolution and contrast sensitivity are consistent with other physiological and behavioral measures in this species. Comparisons are made with response properties of the same zones in macaque monkey, as well as of area 17 of a distantly related species (cat) that also occupies a nocturnal niche. 2. The responses of single cells to drifting sinusoidal gratings were recorded in V1 (striate cortex) of anesthetized, paralyzed bush babies (Galago crassicaudatus). Cells tended to be grouped with respect to ocular dominance, orientation preference, and direction selectivity. There was a high proportion of monocularly driven cells as in macaque monkey. Only 6% of the cells were nonoriented. These were poorly tuned complex cells and bore no resemblance to nonoriented lateral geniculate nucleus (LGN)-like cells reported in layer IV of macaque monkeys. Unidirectional cells were most frequently encountered in cortical layers that receive input from the magnocellular layers of the LGN. 3. Cells were classified as simple (31%) or complex (69%) according to standard criteria. Simple cells were significantly more narrowly tuned than complex cells for both orientation and spatial frequency. Complex cells had significantly higher average optimal spatial frequencies and spatial frequency cutoffs than simple cells. Contrast sensitivity of simple and complex cells averaged 38 and 34, respectively. Spatial resolution and sensitivity of these cells matches behavioral measures in bush baby. The spatial and temporal resolution of bush baby cells are similar to those of cats, which is likely related to the nocturnal niche of both species. 4. Cells in supragranular (I-III) and infragranular (V, VI) layers differed significantly in their response characteristics. The cells in the supragranular layers had significantly higher contrast sensitivity than did the cells in the infragranular layers. Cells in the supragranular layers likewise had higher temporal frequency cutoffs, significantly lower optimal spatial frequencies, lower spatial frequency cutoffs, and tighter orientation tuning than did cells in the infragranular layers. 5. Properties of cells in individual layers and CO blob and interblob compartments also showed differentiation. Layer III had the narrowest orientation and spatial frequency tuning with the tightest tuning in layer IIIC (IVB).(ABSTRACT TRUNCATED AT 400 WORDS)
Burst activity, defined by groups of two or more spikes with intervals of < or = 8 ms, was analyzed in responses to drifting sinewave gratings elicited from striate cortical neurons in anesthetized cats. Bursting varied broadly across a population of 507 simple and complex cells. Half of this population had > or = 42% of their spikes contained in bursts. The fraction of spikes in bursts did not vary as a function of average firing rate and was stationary over time. Peaks in the interspike interval histograms were found at both 3-5 ms and 10-30 ms. In many cells the locations of these peaks were independent of firing rate, indicating a quantized control of firing behavior at two different time scales. The activity at the shorter time scale most likely results from intrinsic properties of the cell membrane, and that at the longer scale from recurrent network excitation. Burst frequency (bursts per s) and burst length (spikes per burst) both depended on firing rate. Burst frequency was essentially linear with firing rate, whereas burst length was a nonlinear function of firing rate and was also governed by stimulus orientation. At a given firing rate, burst length was greater for optimal orientations than for nonoptimal orientations. No organized orientation dependence was seen in bursts from lateral geniculate nucleus cells. Activation of cortical contrast gain control at low response amplitudes resulted in no burst length modulation, but burst shortening at optimal orientations was found in responses characterized by supersaturation. At a given firing rate, cortical burst length was shortened by microinjection of gamma-aminobutyric acid (GABA), and bursts became longer in the presence of N-methyl-bicuculline, a GABA(A) receptor blocker. These results are consistent with a model in which responses are reduced at nonoptimal orientations, at least in part, by burst shortening that is mediated by GABA. A similar mechanism contributes to response supersaturation at high contrasts via recruitment of inhibitory responses that are tuned to adjacent orientations. Burst length modulation can serve as a form of coding by supporting dynamic, stimulus-dependent reorganization of the effectiveness of individual network connections.
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