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At least 307 records · Page 17Linked to original sources
PubMed1978

Electrical activation of visual pathways substitutes for tonic light input in triggering EEG correlates of food reward during conditioned behavior in cats.

Cats trained to press a lever for 1 cc of milk reward normally show during the consummatory response high voltage 6--8 c/sec EEG synchronization associated with epicortical positive steady potential shift over the primary and secondary visual projections. The emergence of this postreinforcement synchronization (PRS) and Reward Contingent Positive Variation (RCPV) is known to depend upon appropriate gustatory input and presence of ambient light, although visual perception of reward and/or environment is not essential as shown in cats wearing translucent "milky" contact lenses. Training the animals in a paradigm in which a "light-off" cue signaled the availability of reward, and thus assigned positively reinforcing quality to the dark condition, also failed to restore the PRS-RCPV phenomenon in the absence of light. However, brief electrical stimuli applied to either the optic tract or the lateral geniculate nucleus substituted for unpatterned light input and fully restored the PRS-RCPV in the dark. The suprathreshold stimuli were effective only during the consummatory response. Maximum effect could be produced during a brief time period between 0.8 and 1.5 sec after the onset of consummatory response as judged by lapping activity, thus showing the specificity of the effect of visual input. Even during a relaxed wakefulness after satiation or during slow wave sleep or REM sleep the same electric stimuli were ineffective although they produced well-developed evoked potentials with all characteristic wave components. The results indicate that brain pathways utilize unpatterned i.e. noisy visual input in complex integrative processes involving gustatory input.

Animals↗
PubMed1994

Age-related effects of triphenyl phosphite-induced delayed neuropathy on central visual pathways in the European ferret (Mustela putorius furo).

The objective of this study was to investigate the relationship between the maturation of visual system neurons and the onset of their susceptibility to triphenyl phosphite (TPP)-induced delayed neurotoxicity in the European ferret. We administered single subcutaneous doses of TPP (1184 mg/kg body wt) to 1- to 10-week-old ferret kits to assess the effects on connections and neurons of the developing lateral geniculate thalamic nucleus (LGN) and primary visual cortex. Brains were processed with a modified Fink-Heimer silver-impregnation method. Axonal and terminal degeneration were first noted in the LGN of kits injected at 5 weeks of age. The severity of the degeneration increased in kits injected at later ages and reached adult densities and configurations in ferrets injected at 10 weeks of age. Degenerating neuronal cell bodies were also present in the LGN of kits injected at 7 weeks of age and older. In the visual cortex, axonal and terminal degeneration were consistently present in kits injected at 8 weeks of age and attained adult-like densities in kits injected at 10 weeks of age. Previous studies have reported that the ferret visual system appears to reach anatomical maturity (as defined by mature LGN lamination patterns, the location and density of axon terminals originating from neurons in the retina and LGN, and the migration and synaptic connections of cortical neurons) by 4-5 weeks of age. A temporal comparison of these normal developmental data with the degeneration data obtained in the present study suggests that immature neurons in the visual system of the ferret are not susceptible to TPP-induced delayed neurotoxicity but only become so after they have achieved some degree of maturity. Whether the LGN neurons undergoing degeneration are directly affected by TPP or are showing a transneuronal response to loss of afferent input remains unresolved.

Age Factors↗
PubMed1989

Balint's syndrome in Alzheimer's disease: specific disruption of the occipito-parietal visual pathway.

Previous quantitative neuropathologic analyses have shown that the association cortices of the temporal and frontal lobes are more damaged than the visual regions of the occipital lobe in Alzheimer's disease. In the present paper, we report on a subpopulation of Alzheimer's disease patients presenting a visual defect referred to as Balint's syndrome, and displaying a global caudal shift in pathology. Balint's syndrome is a defect in visuospatial skills, and the distribution of pathology suggests that the connections underlying this functional component of the visual system are devastated, whereas they are normally spared in Alzheimer's disease. These results suggest that multiple subtypes of Alzheimer's disease exist with differential distribution of pathology and corresponding neurologic symptomatology, and that neuritic plaque and neurofibrillary tangle formation involve the loss of specific corticocortical projections associated with specific functional deficits and identifiable neurologic syndromes.

Aged↗
PubMed1966

The central release of acetylcholine during stimulation of the visual pathway.

1. In rabbits anaesthetized with Dial ACh has been collected from the surface of the cerebral cortex during stimulation of the visual pathways.2. The spontaneous release of ACh from the visual and non-visual areas of the cortex was found to be similar.3. Stimulation of the retinae by diffuse light produced a large increase in ACh release from the primary visual receiving areas (4.3 times the spontaneous release) and a smaller increase (1.9 times the spontaneous release) from other parts of the cortex.4. Direct unilateral electrical stimulation of the lateral geniculate body evoked a large increase in ACh release (3.4 times the spontaneous release) from the ipsilateral visual cortex and a smaller increase (1.7 times the spontaneous release) from the contralateral visual area and other regions of the cerebral cortex. The evoked increase from the contralateral cortex was not mediated by transcallosal pathways.5. The increase in ACh release evoked from the visual cortex by stimulation of the ipsilateral lateral geniculate body was dependent on the frequency of stimulation. The evoked release was smallest at low stimulus frequencies and increased to a maximum at 20 stimuli/sec. The evoked ACh release from other areas of the cortex was independent of the frequency at which the lateral geniculate body was stimulated.6. The possible central nervous pathways associated with the spontaneous release of ACh and the release evoked by stimulation of the eyes by light and by direct stimulation of the lateral geniculate body are discussed.7. It is concluded that two ascending cholinergic systems may be involved; the non-specific reticulo-cortical pathways responsible for the e.e.g arousal response, and the more specific thalamo-cortical pathways associated with augmenting and repetitive after-discharge responses. The first system is thought to be concerned with the small but widespread increase in ACh release from the cortex following stimulation of the visual pathway while the second system could give rise to the larger increases evoked from the primary receiving areas of cortex. The spontaneous release of ACh from the surface of the brain may be the result of contributions from both systems.

Acetylcholine↗
PubMed1977

A comparison of visual pathways in Boston and Midwestern Siamese cats.

A genetic mutation in Siamese cats causes retinogeniculate fibers representing roughly the first 20 degrees of ipsilateral visual field in each eye to cross aberrantly in the optic chiasm and terminate in the wrong lateral geniculate nucleus (LGN). Previous investigations have shown that in the visual cortex this extra representation of ipsilateral visual field can be organized into one pattern in Boston Siamese cats, another in Midwestern. This finding was confirmed here. The possibility that the organization of the LGN might account for these two patterns was studied using combined anatomical and physiological methods. On the basis of microelectrode recordings from the visual cortex, 11 out of the 12 Siamese cats included here were Boston cats; one was Midwestern. The distribution of retinogeniculate terminals was examined in each cat using autoradiographic techniques following an eye-injection of 3H-proline. Overall, the LGN organization in Boston cats was similar to that of Midwestern: both lateral and medial normal segments of lamina A1 (mnA1) were present. In Boston cats, however, the mnA1 was remarkably small and shifted ventromedially in the nucleus to allow for the fusion between the medial borders of lamina A and the abnormal segment of A1. In the Midwestern cat this fusion was not apparent and the medial normal segment of A1 was significantly larger. These differences in organization of the LGN are consistent with those seen at the level of the visual cortex in Midwestern and Boston Siamese cats. It was not possible, however, to relate them clearly to the characteristic strabismus of these animals.

Animals↗
PubMed1990

Coding of image contrast in central visual pathways of the macaque monkey.

Measurements of contrast sensitivity were obtained from isolated neurons in the lateral geniculate nucleus, striate cortex, and middle temporal visual area of macaque monkeys. Between the lateral geniculate nucleus and the middle temporal area contrast sensitivity functions become progressively steeper. Furthermore, many neurons in the middle temporal area are more sensitive than any cell encountered in early stages. Measurements made with stimuli of different sizes show that this high sensitivity depends on areal summation across the receptive field.

Action Potentials↗