No abstract

Seventeen callosally projecting axons originating near the border between areas 17 and 18 in adult cats were anterogradely labelled with biocytin and reconstructed in 3-D from serial sections. All axons terminated near the contralateral 17/18 border. However, they differed in their diameter, tangential and radial distributions, and overall geometry of terminal arbors. Diameters of reconstructed axons ranged between 0.45 and 2.25 microns. Most of the axons terminated in multiple terminal columns scattered over several square millimetres of cortex. Thus in general callosal connections are not organized according to simple, point-to-point spatial mapping rules. Usually terminal boutons were more numerous in supragranular layers; some were also found in infragranular layers, none in layer IV. However, a few axons were distributed only or mainly in layer IV, others included this layer in their termination. Thus, different callosal axons may selectively activate distinct cell populations. The geometry of terminal arbors defined two types of architecture, which were sometimes represented in the same axon: parallel architecture was characterized by branches of considerable length which supplied different columns or converged onto the same column; serial architecture was characterized by a tangentially running trunk or main branch with radial collaterals to the cortex. These architectures may relate to temporal aspects of inter-hemispheric interactions. In conclusion, communication between corresponding areas of the two hemispheres appears to use channels with different morphological and probably functional properties.

Strabismus is a frequent ocular disorder that develops early in life in humans. As a general rule, it is characterized by a misalignment of the visual axes which most often appears during the critical period of visual development. However other characteristics of strabismus may vary greatly among subjects, for example, being convergent or divergent, horizontal or vertical, with variable angles of deviation. Binocular vision may also vary greatly. Our main goal here is to develop the idea that such “polymorphy” reflects a wide variety in the possible origins of strabismus. We propose that strabismus must be considered as possibly resulting from abnormal genetic and/or acquired factors, anatomical and/or functional abnormalities, in the sensory and/or the motor systems, both peripherally and/or in the brain itself. We shall particularly develop the possible “central” origins of strabismus. Indeed, we are convinced that it is time now to open this “black box” in order to move forward. All of this will be developed on the basis of both presently available data in literature (including most recent data) and our own experience. Both data in biology and medicine will be referred to. Our conclusions will hopefully help ophthalmologists to better understand strabismus and to develop new therapeutic strategies in the future. Presently, physicians eliminate or limit the negative effects of such pathology both on the development of the visual system and visual perception through the use of optical correction and, in some cases, extraocular muscle surgery. To better circumscribe the problem of the origins of strabismus, including at a cerebral level, may improve its management, in particular with respect to binocular vision, through innovating tools by treating the pathology at the source.

Brain postnatal development is characterized by critical periods of experience-dependent remodeling of neuronal circuits. Failure to end these periods results in neurodevelopmental disorders. The cellular processes defining critical-period timing remain unclear. Here, we show that in the mouse visual cortex, astrocytes control critical-period closure. We uncover the underlying pathway, which involves astrocytic regulation of the extracellular matrix, allowing interneuron maturation. Unconventional astrocyte connexin signaling hinders expression of extracellular matrix–degrading enzyme matrix metalloproteinase 9 (MMP9) through RhoA–guanosine triphosphatase activation. Thus, astrocytes not only influence the activity of single synapses but also are key elements in the experience-dependent wiring of brain circuits.