Francisco Gonzalez-Aguilar

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High-intensity photocoagulator lesions placed nasally to the optic disc one eye destroyed all retinal layers and led to visual deafferentation of the lateral part of layer A in the contralateral lateral geniculate nucleus (LGN) of adult cats. The retino-geniculate topography was determined with vertical tungsten microelectrode penetrations through LGN(More)
Small, round photocoagulator lesions of 3-6 degrees (0.6-1.2 mm) diameter were placed nasally on the retina of adult cats. Histological controls proved the complete destruction of all retinal layers within the lesions. Changes in lesion size by shrinkage of the retinal scar did not exceed 0.1 mm or 0.5 degrees. At different times after photocoagulation,(More)
Late spreading of excitation occurs in the lateral geniculate nucleus following partial retinal lesions. The extent of spreading remained the same when reducing the size of the lesions to one fifth. This is incompatible with the idea that the spreading could be caused by displacement of normal cells into the deafferented area as a consequence of(More)
Brief vascular perfusion of the rat brain with a mixture of concentrated aldehydes completely insolubilized the brain protein in less than 30 s and yielded excellent ultrastructural preservation. Abundant synaptic vesicles closely and specifically attached to the presynaptic membrane were constantly detected. These vesicles appeared to undergo progressive(More)
Layers of the lateral geniculate nucleus (LGN) of mature cats were completely or partially deafferentated by precisely defined photocoagulation of the retina. Single neuron recordings were performed with microelectrodes from an experimentally modified layer and compared with neurons from a normally innervated layer in the same animal. The spontaneous(More)
The intersynaptic membranes of the rat brain cortex were found to remain firmly attached to one another after perfusion of strongly anisotonic solutions. Brains perfused with depolarizing and excitotoxic agents showed abundant, apparent intermingling of mitochondria and synaptic vesicles. The results suggest (i) that the intersynaptic membranes are not(More)
Perfusion fixation with highly concentrated aldehydes suggests that the synaptic vesicles undergo disintegration within the presynaptic ending upon touching the presynaptic membrane rather than being released by exocytosis into the intersynaptic cleft. Three factors have been explored in order to inquire further into the possible significance of the(More)
It is proposed that presynaptic potassium efflux triggered by the nerve impulse may generate either excitatory or inhibitory responses depending on the neurotransmitter which more or less steadily impregnates the postsynaptic membrane. The jelly intersynaptic matrix may potentiate the efficiency of inoic intersynaptic signals. The synaptic vesicles are(More)
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