Quantitative morphological effects of dark-rearing and light exposure on the synaptic connectivity of layer 4 in the rat visual cortex (area 17)

1987 ◽  
Vol 68 (1) ◽  
Author(s):  
P.L.A. Gabbott ◽  
M.G. Stewart
1988 ◽  
Vol 233 (1273) ◽  
pp. 385-391 ◽  

Evidence is presented for the synaptic connectivity between a physiologically characterized and intracellularly filled GABAergic interneuron and a corticotectal pyramidal neuron in area 17 of the cat visual cortex. The interneuron was located in layer 4 and had the morphological characteristics of a clutch cell. The physiological data demonstrated that the clutch cell received direct X-type innervation from the dorsal lateral geniculate nucleus. These results indicate that a GABAergic neuron is directly involved during the first cortical stages of geniculocorticotectal interactions. Furthermore, the proximal location of the clutch-cell inputs to the labelled dendrite suggests a strategic siting of intracortical feedforward inhibition.


1995 ◽  
Vol 81 (2) ◽  
pp. 463-466
Author(s):  
Carl G. Aurell

The perceptual model, discussed previously in Part II, is applied to the organization of the visual cortex in a search for “consciousness neurons,” i.e., sources of sensations, images, and percepts. It is hypothesized that these three conscious phenomena emerge in the primary visual cortex, Area VI, possibly from neurons in its Layer 4.


1981 ◽  
Vol 41 (2) ◽  
Author(s):  
J.G. Parnavelas ◽  
A. Chatzissavidou ◽  
R.A. Burne
Keyword(s):  
Area 17 ◽  

1999 ◽  
Vol 82 (1) ◽  
pp. 86-93 ◽  
Author(s):  
C. J. Beaver ◽  
Q.-H. Ji ◽  
N. W. Daw

Group II metabotropic glutamate receptors (mGluR 2/3) are distributed differentially across the layers of cat visual cortex, and this distribution varies with age. At 3–4 wk, mGluR 2/3 receptor immunoreactivity is present in all layers. By 6–8 wk of age, it is still present in extragranular layers (2, 3, 5, and 6) but has disappeared from layer 4, and dark-rearing postpones the disappearance of Group II receptors from layer 4. We examined the physiological effects of Group II activation, to see if these effects varied similarly. The responses of single neurons in cat primary visual cortex were recorded to visual stimulation, then the effect of iontophoresis of 2R,4R-4 aminopyrrolidine-2,4-decarboxylate (2R,4R-APDC), a Group II specific agonist, was observed in animals between 3 wk and adulthood. The effect of 2R,4R-APDC was generally suppressive, reducing both the visual response and spontaneous activity of single neurons. The developmental changes were in agreement with the immunohistochemical results: 2R,4R-APDC had effects on cells in all layers in animals of 3–4 wk but not in layer 4 of animals >6 wk old. Moreover, the effect of 2R,4R-APDC was reduced in the cortex of older animals (>22 wk). Dark-rearing animals to 47–54 days maintained the effects of 2R,4R-APDC in layer 4. The disappearance of Group II mGluRs from layer 4 between 3 and 6 wk of age is correlated with the segregation of ocular dominance columns in that layer, raising the possibility that mGluRs 2/3 are involved in this process.


1996 ◽  
Vol 13 (3) ◽  
pp. 585-590 ◽  
Author(s):  
Ivan Suner ◽  
Pasko Rakic

AbstractWe examined the numerical correlation between total populations of neurons in the lateral geniculate nucleus (LGN) and the primary visual cortex (area 17 of Brodmann) in ten cerebral hemispheres of five normal rhesus monkeys using an unbiased three-dimensional counting method. There were 1.4 ± 0.2 million and 341 ±54 million neurons in the LGN and area 17, respectively. In each animal, a larger LGN on one side was in register with a larger area 17 of the cortex on the same side. Furthermore, asymmetry in the number of neurons in both the LGN and area 17 favored the right side. However, because of small variations across subjects, correlation between the total neuron number in LGN and area 17 was weak (r = 0.29). These results suggest that the final numbers of neurons in these visual centers may be established independently or by multiple factors controlling elimination of initially overproduced neurons.


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