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M P Stryker

Publications and source records attributed to M P Stryker.

At least 19 recordsLinked to original sources

Development of orientation preference maps in ferret primary visual cortex.

The development of orientation preference maps was studied in ferret primary visual cortex using chronic optical imaging of intrinsic signals. The emergence and maturation of the maps were examined over time in single animals. The earliest age at which cortical domains selectively responsive to particular stimulus orientations were observed varied considerably between individuals, from postnatal day 31 to 36. In all cases, the earliest maps seen were low-contrast, with regions of orientation-specific activity that were difficult to distinguish from noise. These early maps matured over a period of several days into the high-contrast, patchy maps typical of adult animals. The structure of the orientation maps was remarkably constant over time. The indistinct features in the earliest maps were always patches of the same sizes and shapes and at the same locations as in the maps obtained in subsequent recording sessions. Details of the more mature maps, including the relative intensities of individual iso-orientation domains, were also constant from one recording session to another over periods of several weeks. The patterning of iso-orientation domains in ferret primary visual cortex thus is established early in development and remains stable over time, unaffected by either normal visual experience or the anatomical rearrangements of geniculocortical afferents into eye-specific domains.

Age Distribution

Inhibition of nitric oxide synthase does not prevent ocular dominance plasticity in kitten visual cortex.

1. The neural messenger molecule nitric oxide (NO) has been shown to be involved in several forms of plasticity including hippocampal long-term potentiation. We examined the effects of chronic intracortical infusion of inhibitors of NO synthase (NOS) activity on the plasticity of visual cortical responses following monocular lid suture during the critical period. 2. Single unit recordings (618 cells) made in both the NOS inhibitor-treated (30 mM NG-methyl-L-arginine (L-NMMA), or 22 or 2 mM nitro-L-arginine (L-NOArg)) and saline-treated control hemispheres of barbiturate-anaesthetized, critical-period kittens (n = 8) revealed a profound shift in favour of the non-deprived eye. Shifts were of similar magnitude in hemispheres in which NOS was inhibited and in saline control hemispheres. 3. Subsequent analysis of NOS activity in the same cortical tissue in which recordings had been made showed a pronounced decrease in NOS activity in inhibitor-treated hemispheres. In the region in which all the single unit recordings were made (< 3 mm from the infusion cannula), 22 mM L-NOArg resulted in a reduction of NOS activity to 5.55 +/- 5.33% of control hemisphere NOS activity levels. L-NOArg (2 mM) and L-NMMA (30 mM) also produced clear, but smaller, inhibition of NOS activity. 4. These findings demonstrate that NOS activity is not essential for ocular dominance plasticity in visual cortex.

Animals

Plasticity of geniculocortical afferents following brief or prolonged monocular occlusion in the cat.

During a critical period in early life, physiological studies reveal that either prolonged or brief periods of monocular occlusion induce similar plastic changes in the primary visual cortex (area 17) of the cat, leading to a nearly complete loss of visual responses from the deprived eye (Hubel and Wiesel [1970], J. Physiol. (London) 160: 106-154). However, the recovery of function is markedly different in the two conditions, being complete and thorough only after a brief period of monocular occlusion (Movshon [1976] J. Physiol. (London) 261: 125-174). In search for anatomical correlates that distinguish between these two experimental conditions, we compared the geniculocortical connectivity in normal kittens with that following brief (4 days and 6-7 days) or prolonged (> 5 weeks) periods of occlusion of vision in one eye. Transneuronal labeling of the geniculocortical pathway revealed changes in both cases, and single afferent arbors reconstructed in serial sections were similarly shrunken after short or long periods of deprivation. However, a significant expansion of the geniculocortical afferents serving the nondeprived eye was evident mainly after prolonged deprivation. These findings provide further evidence for rapid, activity-dependent remodeling of afferents during development.

Afferent Pathways

Experience-dependent plasticity of binocular responses in the primary visual cortex of the mouse.

An activity-dependent form of synaptic plasticity underlies the fine tuning of connections in the developing primary visual cortex of mammals such as the cat and monkey. Studies of the effects of manipulations of visual experience during a critical period have demonstrated that a correlation-based competitive process governs this plasticity. The cellular mechanisms underlying this competition, however, are poorly understood. Transgenic and gene-targeting technologies have led to the development of a new category of reagents that have the potential to help answer questions of cellular mechanism, provided that the questions can be studied in a mouse model. The current study attempts to characterize a developmental plasticity in the mouse primary visual cortex and to demonstrate its relevance to that found in higher mammals. We found that 4 d of monocular lid suture at postnatal day 28 (P28) induced a maximal loss of responsiveness of cortical neurons to the deprived eye. These ocular dominance shifts occurred during a well-defined critical period, between P19 and P32. Furthermore, binocular deprivation during this critical period did not decrease visual cortical responses, and alternating monocular deprivation resulted in a decrease in the number of binocularly responsive neurons. Finally, a laminar analysis demonstrated plasticity of both geniculocortical and intracortical connections. These results demonstrate that an activity-dependent, competitive form of synaptic plasticity that obeys correlation-based rules operates in the developing primary visual cortex of the mouse.

Animals

Ocular dominance plasticity under metabotropic glutamate receptor blockade.

Occluding vision through one eye during a critical period in early life nearly abolishes responses to that eye in visual cortex. This phenomenon is mimicked by long-term depression of synaptic transmission in vitro, which may require metabotropic glutamate receptors (mGluRs) and is age-dependent. Peaks in mGluR expression and glutamate-stimulated phosphoinositide turnover during visual cortical development have been proposed as biochemical bases for the critical period. Pharmacological blockade of mGluRs specifically prevented synapse weakening in mouse visual cortical slices but did not alter kitten ocular dominance plasticity in vivo. Thus, a heightened mGluR response does not account for the critical period in development.

Animals

Deficient plasticity in the primary visual cortex of alpha-calcium/calmodulin-dependent protein kinase II mutant mice.

The recent characterization of plasticity in the mouse visual cortex permits the use of mutant mice to investigate the cellular mechanisms underlying activity-dependent development. As calcium-dependent signaling pathways have been implicated in neuronal plasticity, we examined visual cortical plasticity in mice lacking the alpha-isoform of calcium/calmodulin-dependent protein kinase II (alpha CaMKII). In wild-type mice, brief occlusion of vision in one eye during a critical period reduces responses in the visual cortex. In half of the alpha CaMKII-deficient mice, visual cortical responses developed normally, but visual cortical plasticity was greatly diminished. After intensive training, spatial learning in the Morris water maze was severely impaired in a similar fraction of mutant animals. These data indicate that loss of alpha CaMKII results in a severe but variable defect in neuronal plasticity.

Animals

Control of thalamocortical afferent rearrangement by postsynaptic activity in developing visual cortex.

The formation of specific connections in the developing central nervous system is thought to result from mechanisms that increase the strengths of synapses at which pre- and postsynaptic activity are correlated and decrease it otherwise. In the visual cortex, initially widespread inputs normally sort out into eye-specific patches during early life. If only one eye can see during this period, its patches are much larger than normal, and patches from the occluded eye become much smaller. Anatomical experiments here show that closed-eye inputs expand within a region of cortex that is silenced, establishing that inhibition of common target cells gives less active inputs a competitive advantage.

Animals

Rapid remodeling of axonal arbors in the visual cortex.

If vision in one eye is blurred or occluded during a critical period in postnatal development, neurons in the visual cortex lose their responses to stimulation through that eye within a few days. Anatomical changes in the nerve terminals that provide input to the visual cortex have previously been observed only after weeks of deprivation, suggesting that synapses become physiologically ineffective before the branches on which they sit are withdrawn. Reconstruction of single geniculocortical axonal arbors in the cat after either brief or prolonged monocular occlusion revealed striking axonal rearrangements in both instances. Rapid withdrawal of the branches of deprived-eye arbors suggests that axonal branches bearing synapses respond quickly to changing patterns of neuronal activity.

Animals

Amblyopia induced by anisometropia without shrinkage of ocular dominance columns in human striate cortex.

Amblyopia can be induced by opacity of the ocular media (e.g., cataract), misalignment of the ocular axes (strabismus), or unequal refractive error in the eyes (anisometropia). Experiments in monkeys have shown that early monocular eyelid suture, a model of amblyopia caused by cataract, results in shrinkage of the eye's ocular dominance columns in striate cortex. This reduction of the geniculocortical projection from the deprived eye has been thought to explain in part the mechanism of amblyopia. We labeled the ocular dominance columns in monkeys with amblyopia by using cytochrome oxidase histochemistry. In animals rendered amblyopic by early unilateral eyelid suture, no pattern of cytochrome oxidase activity appeared in layer IVc. Outside layer IVc, alternating rows of light and dark patches were present; the pale patches fit in register with the shrunken ocular dominance columns of the deprived eye, which were labeled by autoradiography. Subsequent removal of one eye caused a striking cytochrome oxidase pattern to emerge in layer IVc that correlated precisely with the shrunken (deprived eye) and expanded (normal eye) ocular dominance columns. This correlation was shown by injecting one eye with [3H]proline. It has remained unsettled whether other forms of amblyopia are accompanied by shrinkage of ocular dominance columns. To address this issue, in an analogous clinical case, we examined the pattern of cytochrome oxidase activity in a human subject with a history of anisometropic amblyopia who suffered a lesion of one optic nerve shortly before death. The ocular dominance columns were normal in width, indicating that some forms of amblyopia occur without shrinkage of ocular dominance columns.

Amblyopia

Development of orientation selectivity in ferret visual cortex and effects of deprivation.

The orientation selectivity of cells in ferret primary visual cortex was studied during normal development and in animals deprived of vision or of visual cortical activity. In normal animals from the age when visual responses were first recorded (postnatal day 23) through postnatal week 5, only about 25% of cells showed orientation-selective responses. By postnatal week 7, cortical responses had matured to an adult-like state, with approximately 75% of cells clearly selective for orientation. This development of orientation selectivity was not merely a reflection of the development of cortical cell responsiveness: at all ages studied, there was no correlation between responsiveness and selectivity. Infusion of TTX into visual cortex to silence neuronal activity completely blocked the maturation of orientation selectivity. Visual deprivation by bilateral lid suture impaired but did not completely block the normal development of orientation selectivity. We conclude that the maturation of orientation-selective responses in ferret primary visual cortex requires cortical neuronal activity, and that normal development requires visually driven activity.

Animals

Development of individual geniculocortical arbors in cat striate cortex and effects of binocular impulse blockade.

This study analyzes the morphological changes in geniculocortical axons terminating in the primary visual cortex of the cat, during the period in which, in normal development, the terminals in layer IV undergo an eye-specific segregation. Geniculocortical afferent fibers were filled anterogradely by the Phaseolus lectin (PHA-L) injected into the main laminae of the LGN. After standard immunohistochemical procedures, single axons were serially reconstructed in two or three dimensions. Experiments were performed in normal kittens and in kittens in which retinal activity was continuously blocked by repeated intraocular injections of TTX. In normal kittens, arbors were reconstructed at four different ages (19, 23, 30-31, and 39 days postnatally) spanning the period during which the geniculocortical projection segregates into eye-specific columns in layer IV (LeVay et al., 1978). Results reveal that sparse but widely extending branches characteristic of young arbors are eliminated during normal development at the same time as selected portions of the arbor grow considerably in length and complexity. The terminal arborizations also subdivide into distinct patches of terminals, consistent with the segregation of left and right eye afferents. In TTX-treated animals, axonal arbors reconstructed at postnatal days 23, 29, and 39 show a complexity and extent of terminal arborization similar to that of normal animals, though more variable in size and degree of elaboration. No progressive changes are evident with age. Further, the majority of arbors reconstructed from TTX-treated animals lack the patchy organization typical of normal animals.

Afferent Pathways

Origin of orientation tuning in the visual cortex.

The results of recent experiments have thrown new light on the neuronal connections underlying orientation-selective responses in the primary visual cortex of adult animals. The pattern of afferent input from the lateral geniculate nucleus to the cortex appears to be specific for orientation, while intracortical inhibitory connections appear to be non-specific in this respect. Experimental and theoretical studies have suggested that the development of cortical cell orientation tuning is an activity-dependent process.

Animals

Relation of cortical cell orientation selectivity to alignment of receptive fields of the geniculocortical afferents that arborize within a single orientation column in ferret visual cortex.

Neurons in the primary visual cortex of higher mammals are arranged in columns, and the neurons in each column respond best to light-dark borders of particular orientations. The basis of cortical cell orientation selectivity is not known. One possible mechanism would be for cortical cells to receive input from several lateral geniculate nucleus (LGN) neurons with receptive fields that are aligned in the visual field (Hubel and Wiesel, 1962). We have investigated the relationship between the arrangement of the receptive fields of geniculocortical afferents and the orientation preferences of cortical cells in the orientation columns to which the afferents provide visual input. Radial microelectrode penetrations were made into primary visual cortex of anesthetized adult sable ferrets. Cortical cells were recorded throughout the depth of the cortex, and their orientation preferences were determined. Cortical cell responses were then eliminated by superfusion of the cortex with either kainic acid (Zahs and Stryker, 1988) or muscimol. After the drug treatment, responses from many single units with distinct receptive fields were recorded. These responses were presumed to be those of geniculocortical afferents, because they had the response properties characteristic of LGN neurons, and because they could be recorded only in cortical layers that receive geniculate input. In 16 of 18 cases, the afferent receptive fields recorded in a single penetration covered an elongated region of visual space. In these penetrations, the best-fit line through the centers of the afferent receptive fields generally paralleled the preferred orientation of cortical cells recorded at the same site in cortex. These results are consistent with the Hubel and Wiesel (1962) model for the construction of oriented visual cortical receptive fields from geniculate inputs with aligned receptive fields.

Afferent Pathways