Acetylcholinesterase in the ventrobasal thalamus: transience and patterning during ontogenesis

In this study, maturational alterations in acetylcholinesterase-dependent staining of the thalamic ventrobasal complex of rat and mouse were examined. The study was undertaken to address the question of whether this nucleus exhibits transient acetylcholinesterase positivity during its development and whether the enzyme is likely to be synthesized by its immature intrinsic neurons. Also, the patterning due to acetylcholinesterase staining of cells and fibers, and the developmental changes in these patterns, have not been described in earlier work. In contrast to surrounding thalamic nuclei, the ventrobasal complex is acetylcholinesterase-positive at birth. In rat, acetylcholinesterase staining of the ventrobasal thalamus is still more intense than in adjacent nuclei at the end of the first week postnatally. Virtually all somata in the nucleus are filled with dense reaction product at this time. Ultrastructurally, reaction product is associated with the granular endoplasmic reticulum. At this stage, there is a marked difference in intensity of staining between the medial and lateral subdivisions of the nucleus, and patterned clustering of somata within each subdivision is readily appreciated in acetylcholinesterase-stained material. In the second postnatal week, intrinsic acetylcholinesterase activity is progressively lost. By the end of the third postnatal week, the nucleus is quite pale except for one area. In the posterior portion of the lateral subdivision, adjacent to the nucleus reticularis, interconnecting bundles of acetylcholinesterase-positive fibers enter the nucleus. They course medially in the lateral subdivision and break up into a plexus of fine fibers. The development of acetylcholinesterase-dependent staining patterns in the mouse is quite similar, except that histochemically detectable levels of enzyme are substantially lower in the neonatal period. It is concluded that the ventrobasal complex can be distinguished from other thalamic nuclei in regard to earlier onset and/or transience of acetylcholinesterase staining. Ultrastructural observations suggest that virtually all immature ventrobasal neurons are synthesizing acetylcholinesterase. It is suggested that the transient staining for enzyme is due primarily to alteration in synthesis and/or turnover in neurons of the ventrobasal complex. In addition, the acetylcholinesterase staining reveals a patterning of fibers and cells that also undergoes developmental alteration. Evidence is discussed suggesting that axons in the barrels of somatosensory cortex (SmI) are derived from these transiently acetylcholinesterase-positive somata. Consequently, the loss of acetylcholinesterase fiber staining in the barrels, during the third postnatal week (noted previously), may be related to a decrease in synthesis of enzyme in the neuronal somata of the ventrobasal complex.