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Journal of Neuroscience, Vol 14, 3588-3602, Copyright © 1994 by Society for Neuroscience
Independent control of dendritic and axonal form in the developing lateral geniculate nucleus
MB Dalva, A Ghosh and CJ Shatz
Department of Neurobiology, Stanford University School of Medicine, California 94305.
To identify mechanisms that regulate neuronal form in the mammalian CNS, we
have examined dendritic development in the lateral geniculate nucleus (LGN)
during the period of segregation of retinal ganglion cell axons. The tracer
Dil was used to label retrogradely LGN neurons that send their axons to
primary visual cortex at different ages between embryonic day 36 (E36) and
E60 in the cat. LGN neurons grow extensively during this period, in concert
with the progressive restriction of ganglion cell axons from the two eyes
to their appropriate eye-specific layers. At E36 neurons have simple
bipolar morphology; by E60 all have acquired complex multipolar dendritic
trees. During this period, soma size increases by 190% and total dendritic
length increases 240%. Dendritic complexity, as measured by dendritic
branch points, also increases. As dendrites grow, the number of spines
increases, but their density remains constant at 0.015/micron throughout
this period. Since it is known that blockade of action potential activity
significantly alters the branching pattern and extent of retinal ganglion
cell axonal arbors within the LGN, we also investigated whether the
dendritic development of the postsynaptic LGN neurons is similarly
susceptible. Following 2 weeks of the intracranial minipump infusion of TTX
between E42 and E56, the morphology of LGN neurons was examined.
Surprisingly in view of the striking effect of the treatment on the
morphology of retinal ganglion cell axons, dendritic growth and development
were essentially normal. However, the density of dendritic spines increased
almost threefold, suggesting that this specific feature of dendritic
morphology is highly regulated by action potential activity. These
observations indicate that normally during this period of development, the
previously described changes that occur in the morphology of the
presynaptic inputs to LGN neurons are accompanied by a progressive growth
of post-synaptic dendrites. Because the intracranial TTX infusions have
almost certainly blocked all sodium action potentials, our results suggest
that the basic dendritic framework of LGN neurons can be achieved even in
the absence of this form of neural activity. Moreover, since the same
treatment causes a profound change in the morphology of the presynaptic
axons, at least some aspects of axonal and dendritic form must be
controlled independently during this prenatal period of development.
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