Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity.
2. Eleven colour coded units were investigated. They all gave on responses to blue light in the centre of their receptive field and off responses to green light in the periphery of their receptive field. The blue pigment had a spectral sensitivity peaking at about 465 nm. The other pigment peaked near 500 nm, like the rods, but gave a response at high mesopic and probably photopic levels. In some cases there was evidence for an excitatory input from the green receptors to the centre ofthe receptive field. All the colour coded cells had rapidly conducting axons and were on centre X cells by all criteria.3. Eighty-five cells of various types other than colour coded were tested for their thresholds at 420 nm and 590 nm. In all cases the results were explained by a pigment peaking close to 500 nm, even at high mesopic and low photopic levels, which suggests the existence of cones with a cyan pigment in them.
1. Cats were monocularly deprived for 3 mo starting at 8-9 mo, 12 mo, 15 mo, and several years of age. Single cells were recorded in both visual cortexes of each cat, and the ocular dominance and layer determined for each cell. Ocular dominance histograms were then constructed for layers II/III, IV, and V/VI for each group of animals. 2. There was a statistically significant shift in the ocular dominance for cells in layers II/III and V/VI for the animals deprived between 8-9 and 11-12 mo of age. There was a small but not statistically significant shift for cells in layer IV from the animals deprived between 8-9 and 11-12 mo of age, and for cells in layers V/VI from the animals deprived between 15 and 18 mo of age. There was no noticeable shift in ocular dominance for any other layers in any other group of animals. 3. We conclude that the critical period for monocular deprivation is finally over at approximately 1 yr of age for extragranular layers (layers II, III, V, and VI) in visual cortex of the cat.
SUMMARY1. The effects of picrotoxin and strychnine were tested on the receptive fields of direction sensitive cells, orientation sensitive cells, local edge detectors, uniformity detectors and large field units in the rabbit retina.2. Picrotoxin eliminated the direction specificity and size specificity of 'on-off' and 'on' directionally sensitive cells for both black and white objects. Picrotoxin also made 'on' directionally sensitive cells responsive to faster velocities.3. Picrotoxin eliminated the orientation specificity of orientation sensitive cells, and changed the bar-flank arrangement of the receptive field into a centre surround arrangement. Thus, the orientation specificity is due to inhibitory rather than excitatory mechanisms.4. Picrotoxin altered the speed sensitivity of large field units so that they responded to slow speeds as well as fast ones, like centre surround Y cells.5. Strychnine abolished the size specificity of local edge detectors and changed their speed specificity so that they responded to faster speeds.6. Picrotoxin changed a uniformity detector into a sustained on centre cell. 7. Strychnine did not affect the direction specificity of directionally sensitive cells, the orientation specificity of orientation sensitive cells, or the speed specificity of large field units. Picrotoxin did not affect the size specificity of local edge detectors.8. Picrotoxin and strychnine usually had opposing effects on the transient responses of these units to spots and annuli. In general picrotoxin prolonged and enhanced these responses at both on and off, and strychnine shortened them.9. The effect of these drugs for every type of ganglion cell with complex receptive field properties was to make the receptive field more simple. The orientation selective cells, large field cells, 'on' direction selective cells and uniformity detectors seem to be centre surround cells with special properties that are abolished by these drugs. The 'on-off' direction selective cells and local edge detectors still have on-off receptive fields, but in each case one of the drugs abolished the feature that was the basis for the cell's name.
The role of N-methyl-D-aspartate (NMDA) receptors in cat visual cortex was studied as a function of both layer and age by iontophoresis of the NMDA antagonist (D)-2-amino-5-phosphonovaleric acid (APV). Effects on both visual responses and spontaneous activity were observed. In superficial layers (II and III), D-APV reduced visual responses substantially at all ages. Iontophoresis of D-APV with 10 nA of ejecting current for 2-3 min was sufficient to reduce the response to approximately one third of control levels. The magnitude of the reduction did not vary with age. In granular and deep layers (IV, V, and VI), D-APV affected the visual response in young animals but only spontaneous activity in older animals. On average, visual responses were reduced to about half at 20-23 days of age and to about 75% at 4 weeks of age but in most cases were not significantly affected in adults. The rapid change in the functional effect of NMDA receptors over the third and fourth week in granular and deep layers suggests a role in development. There was a reasonable age correlation between the change in effect and the period of geniculocortical afferent segregation. Further experiments will be necessary to determine whether NMDA receptors are necessary for segregation to occur. The presence of an NMDA component to the visual response in the adult in layers II and III argues either that these layers retain some form of plasticity in the adult or that NMDA receptors play a role in the transmission of normal visual input to these layers.
uring the past 20 years, basic science has shown that there are different critical periods for different visual functions during the development of the visual system. Visual functions processed at higher anatomical levels within the system have a later critical period than functions processed at lower levels. This general principle suggests that treatments for amblyopia should be followed in a logical sequence, with treatment for each visual function to be started before its critical period is over. However, critical periods for some visual functions, such as stereopsis, are not yet fully determined, and the optimal treatment is, therefore, unknown. This article summarizes the current extent of our knowledge and points to the gaps that need to be filled.
In this review, we have concentrated on the parallels between the cellular properties of the NMDA receptor and a variety of functional properties within sensory and motor systems. Of course, the NMDA channel exists within the cell in conjunction with a variety of other channels, including non-NMDA channels. Although the NMDA receptor is unique in a cellular sense--it is the only ligand-gated channel that is also voltage dependent and calcium permeable--it is not unique in a functional sense. A cell that has non-NMDA receptors and voltage-sensitive channels will also exhibit nonlinear behavior. Moreover, Buhrle & Sonnhof (1983) demonstrated some time ago that calcium flows into frog motor neurons through more than one type of calcium channel. The contribution to the inflow of calcium from NMDA channels may vary from cell to cell and could easily be a minor proportion of the total. Many authors have pointed out that the NMDA channel has a low conductance at a resting potential of -70 mV. However, many cells in the nervous system are depolarized from -70 mV by excitatory input. Thus, as pointed out above. NMDA receptors make a contribution to the tonic or spontaneous activity of cells in both visual cortex and spinal cord. In practice, many cells are probably working in a range of membrane potentials where the NMDA channels are always open to some extent. Even in the hippocampal slice where a substantial amount of afferent input is removed, NMDA receptors contribute to spontaneous activity (Sah et al 1989). Does the NMDA receptor act as a switch? Does it act as an AND gate? The suggestion that it may act as a switch comes from work on LTP in the hippocampus, which is readily produced by high-frequency stimulation and is abolished by APV. However, activation of the NMDA receptor is only the first in a sequence of reactions leading to LTP: In theory, switch-like behavior could also be produced by calcium-buffering systems within dendritic spines, or by enzymatic processes (Lisman 1985; Zador et al 1990). Fox & Daw (1992) have modeled the action of NMDA and non-NMDA receptors that are activated in parallel with each other, and shown that the occurrence of switch-like behavior depends on the relative density of NMDA versus non-NMDA receptors. Switch-like behavior is not seen in the visual cortex, but might be seen in the hippocampus if the relative density of NMDA receptors there was higher than in the visual cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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