The mystacial vibrissae or whiskers on the face have a large representation in the rodent central nervous system. In rats and mice the projections arising from each vibrissa can be demonstrated histologically in five separate parts of the central trigeminal pathway. At every location, the pattern of the projections is isomorphic to the pattern of the facial vibrissae. For example, in the somatosensory cortex (SmI), multicellular cytoarchitectonic units in layer IV--termed barrels--correspond anatomically and functionally to the contralateral whiskers. The cortical barrels are absent at birth and their cytoarchitectonic pattern can be altered by neonatal whisker lesions. The effect is graded such that whisker damage on or after postnatal day (PND) 6 does not produce changes in the anatomical somatotopy. We undertook the present study to determine whether similar "critical periods" for susceptibility to vibrissa damage exist in the subcortical trigeminal stations of mice. In particular, we wished to find out whether subcortical projections are susceptible to whisker damage in a sequence which parallels other described developmental sequences, as has been concluded from previous work on the mouse (Woolsey et al., '79), or whether the "critical periods" are related to other aspects of development as has been concluded from work on the rat (Belford and Killackey, '80). Neonatal Swiss Webster mice sustained lesions of a single row of whiskers on PND 1, 2, 3, 4, or 5. The animals survived to adulthood. Their brains were sectioned and stained for the mitochondrial enzyme, succinic dehydrogenase (SDH), which demonstrates whisker somatotopy in all central nervous system (CNS)stations. The whisker representations at each level of the pathway, often in the same individual, were reconstructed from serial sections to assess qualitative and quantitative changes in somatotopy. Histological sections through the faces of the experimental animals were used to determine the extent of whisker damage and to show that few nerve fibers innervate the damaged zone on the face. In the brainstem representations, the zones corresponding to the damaged whiskers are shrunken and pale, regardless of the animal's age at vibrissa damage; this probably reflects the degeneration of the primary afferents. In the thalamus and the cortex, whisker damage at later postnatal times has progressively less effect on the anatomical projections patterns. Based on the changes in the projection patterns related to the damaged vibrissae and the changes in the projection patterns related to the remaining, intact vibrissae,(ABSTRACT TRUNCATED AT 400 WORDS)
We have reviewed a series of experiments which begin to examine the cellular events underlying afferent regulation of neuronal structure. Our initial interest in such experiments stemmed from a desire to understand the cellular nature of experiential influences on brain development. While this remains a long-range goal, it's elusive nature has become increasingly apparent; how will we know when such a goal is achieved? On the other hand, it has become increasingly clear that by approaching this question as a subset of the larger problem of tissue interactions regulating nervous system structure and function, some progress is possible. In this respect, understanding afferent regulation is part and parcel of understanding "competition." Both exemplify the fact that we are dealing with a dynamic system, where changes in the balance of extracellular factors result in a cascade of events defining a new "steady state." Unfortunately, most of our methods are limited to taking "snap-shots" of a few parameters and attempting to reconstruct an epic. Our analyses of the postsynaptic events following cochlea removal have only scratched the surface. They are beginning to reveal myriad cellular processes that are dramatically altered by changing the balance of synaptic activity, or "synaptic drive," in a neuronal system. We have been continually struck by the rapidity of these postsynaptic changes when the manipulations are performed on immature animals. While the kinetics of metabolic and structural events we have studied do not yet match those of ionic events involved in information transmission, the two classes of intercellular communication are coming much closer. Some neuromodulators can alter synaptic currents for up to many seconds, and we have shown that altering afferent activity can cause changes in protein synthesis within a few minutes. The merging of these two classes of phenomena should come as no surprise since our studies and many others have definitively linked a variety of metabolic and structural events to changes in the synaptic drive between two neurons. On the other hand, this progress does highlight the need for increased attention to the short-term changes following manipulations of afferent activity. Hopefully such studies will lead to an understanding of the intracellular chain of events responsible for the regulation of neuronal form. A second area of interest has been the age restrictions on the events we have studied.(ABSTRACT TRUNCATED AT 400 WORDS)
Results suggest that, particularly in young animals, a unilateral CHL may have profound effects on metabolic activity in the central auditory system.
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