Reduced levels of acetylcholine receptor expression in chick ciliary ganglion neurons developing in the absence of innervation.

Chick ciliary ganglion neurons receive innervation from a single source, the accessory oculomotor nucleus (AON), and nicotinic ACh receptors (AChRs) mediate chemical synaptic transmission through the ganglion. Previous experiments examining the developmental expression of AChRs in embryonic chick ciliary ganglion neurons in situ have shown that AChR levels increase substantially in the neurons at the time of innervation. Prior to synapse formation, few AChRs are detected in the neurons. In the present experiments, the role of presynaptic inputs in inducing an increase in AChRs was established by examining AChR levels in ciliary ganglion neurons that have been deprived of innervation by surgical ablation of the AON prior to synapse formation. AChR levels were dramatically reduced in neurons of input-deprived ganglia as compared to control innervated neurons at all developmental stages examined from embryonic day (ED) 5 to ED 12 as determined by indirect immunocytochemical labeling of frozen ganglion sections with the anti-AChR monoclonal antibody mAb 35, and light microscopy. In contrast, neuronal somata of input-deprived and control ganglia had equivalent levels of immunolabeling for three other components, a transmembrane glycoprotein of synaptic vesicles, SV2, and two microtubule-associated proteins, MAP 1B and MAP 2, from ED 5 up to ED 10. The results demonstrate that presynaptic inputs specifically increase the levels of AChR expression in developing neurons. In addition, changes in the levels of immunolabeling for AChRs, SV2, MAP 1B, and MAP 2 in neuronal somata after ED 10 demonstrate that other major developmental events also influence the levels of these components in neurons. Declines in the intensity of AChR, SV2, MAP 1B, and MAP 2 immunolabeling within a subset of neuronal somata in both operated and control ganglia at ED 10 and 12 coincide with the period of neuronal cell death. Increases in AChR labeling in the rest of the neuronal population of input-deprived ganglia at ED 12 suggest that, in addition to innervation, synapse formation with the peripheral target tissue influences AChR levels in developing neurons in situ.

Mature oligodendrocytes. Division following experimental demyelination in adult animals.

Primary demyelination can be caused by injury to oligodendrocytes or to the myelin sheaths that these cells maintain. Although remyelination does take place in multiple sclerosis (MS), its possible role in the recovery from MS attacks has been inadequately considered, partly because of the belief that oligodendrocytes, once destroyed, cannot be replaced in the adult. The injection of lysolecithin into the mouse spinal cord causes primary demyelination, followed by the generation of new oligodendrocytes and remyelination. By using a pulse label of tritiated thymidine, this electron-microscopic autoradiographic study demonstrated a source of these regenerated oligodendrocytes. The replacement of oligodendrocytes can occur through the division of preexisting oligodendrocytes. This is the first demonstration that mature oligodendrocytes are capable of dividing in older animals. These results lend support to recent observations of an apparent proliferation of these cells in an active MS lesion. We believe that the ability of mature oligodendrocytes to divide and to remyelinate axons in the adult may play an important role in the recovery from MS attacks.