The advent of transgenic mice has made the developing retinogeniculate
pathway a model system for targeting potential mechanisms that underlie
the refinement of sensory connections. However, a detailed
characterization of the form and function of this pathway is lacking. Here
we use a variety of anatomical and electrophysiological techniques to
delineate the structural and functional changes occurring in the lateral
geniculate nucleus (LGN) of dorsal thalamus of the C57/BL6 mouse.
During the first two postnatal weeks there is an age-related recession in
the amount of terminal space occupied by retinal axons arising from the
two eyes. During the first postnatal week, crossed and uncrossed axons
show substantial overlap throughout most of the LGN. Between the first and
second week retinal arbors show significant pruning, so that by the time
of natural eye opening (P12–14) segregation is complete and retinal
projections are organized into distinct eye-specific domains. During this
time of rapid anatomical rearrangement, LGN cells could be readily
distinguished using immunocytochemical markers that stain for NMDA
receptors, GABA receptors, L-type Ca2+ channels, and the
neurofilament protein SMI-32. Moreover, the membrane properties and
synaptic responses of developing LGN cells are remarkably stable and
resemble those of mature neurons. However, there are some notable
developmental changes in synaptic connectivity. At early ages, LGN cells
are binocularly responsive and receive input from as many as 11 different
retinal ganglion cells. Optic tract stimulation also evokes plateau-like
depolarizations that are mediated by the activation of L-type
Ca2+ channels. As retinal inputs from the two eyes segregate
into nonoverlapping territories, there is a loss of binocular
responsiveness, a decrease in retinal convergence, and a reduction in the
incidence of plateau potentials. These data serve as a working framework
for the assessment of phenotypes of genetically altered strains as well as
provide some insight as to the molecular mechanisms underlying the
refinement of retinogeniculate connections.