Wallerian degeneration of the distal stump of a severed peripheral nerve involves invasion by myelomonocytic cells, whose presence is necessary for destruction of myelin and for initiating mitosis in Schwann cells (Beuche and Friede, 1984). Degeneration of the distal ends of the axons themselves is assumed to occur by autolytic mechanisms. We describe a strain of mice (C57BL/6/Ola) in which leucocyte invasion is slow and sparse. In these mice, confirming Beuche and Friede, myelin removal is extremely slow. A new finding is that axon degeneration is also very slow. This is a consequence of lack of recruitment of myelomonocytic cells for if such recruitment is prevented in other mouse strains by a monoclonal antibody against the complement type 3 receptor (Rosen and Gordon, 1987) axon degeneration is again slowed. We have also, surprisingly, found that nerve regeneration in the C57BL/6/Ola mice is not impeded by the presence of largely intact axons in the distal stump and absence of recruited cells, myelin debris and the absence of Schwann cell mitosis.

Injuries to axons in both the central and peripheral nervous systems (CNS and PNS) of mammals result in axonal degeneration distal to the site of the lesion (Wallerian degeneration) and removal of their surrounding myelin sheaths . In the PNS, myelin is rapidly degraded over a few days or weeks, and the axons regenerate but in the CNS the myelin may persist for months (1, 2), and the axons do not regenerate. We have no explanation for this difference, and there is controversy as to which cells are responsible for the rapid removal of myelin in the PNS (3) . Recent evidence suggests that macrophages (MO) may be important in the removal of myelin from the degenerating peripheral nerve (4) . Using the mAb F4/80 (5), specific for mouse M0, we have examined the contribution of Mo to Wallerian degeneration in the CNS and PNS and considered the possible role they may play in subsequent repair. Materials and MethodsWe anesthetized adult mice (CBA/J, BALB/c) with chloral hydrate (0.2 ml per 10 g of 3 .5% chloral hydrate); rats (Long-Evans) with chlornembutal (0.3 ml per 100 g of 4.2% chloral hydrate plus 1 % sodium pentobarbital). Using jewellers forceps, we crushed one sciatic nerve in the upper thigh or one optic nerve a few millimeters behind the optic disk. Animals were killed after 0.5, 1, 3, 4, 5, 7, 10, 14, and 21 d. We removed the nerves unfixed or after perfusion fixation with periodate/lysine/paraformaldehyde (1.5% paraformaldehyde (6) . We rapid-froze the nerves and cut them on a cryostat at 10 um in the transverse or longitudinal plane . We saved sections at 0.25-1 .0-mm intervals along the length of the nerves both distal and proximal to the crush site. Sections of mouse tissue were processed for the localization of M¢ using the mouse M¢-specific mAb F/80 (4) ; rat tissue was stained for leukocytes using the mAbs OX1 and OX30 directed against the leukocyte common antigen (LCA) (7) . Endogenous peroxidase was eliminated using the glucose oxidase method (8) . We incubated the sections with mAbs for 1 h. Binding was revealed by the avidin/biotin complex immunoperoxidase method (9) using reagents supplied by Sera-Laboratories, West Sussex, United Kingdom . We used diaminobenzidine tetrahydrochloride as the chromogen. Some unfixed sections were reacted in diaminobenzidine with hydrogen peroxide to reveal cells with myeloperoxidase . Control sections showed that mAb staining did not result from nonspecific binding . Sections were lightly counterstained with cresyl violet or exposed to 1% osmium tetroxide to intensify the This work was supported by the Medical Research Council of the United Kingdom . V. H. Perry is a Wellcome Senior Research Fellow . 1218J. Exp. MED.

Cochlear outer hair cells (OHCs) express alpha9 nACh receptors and are contacted by descending, predominately cholinergic, efferent fibers originating in the CNS. Mice carrying a null mutation for the nACh alpha9 gene were produced to investigate its role(s) in auditory processing and development of hair cell innervation. In alpha9 knockout mice, most OHCs were innervated by one large terminal instead of multiple smaller terminals as in wild types, suggesting a role for the nACh alpha9 subunit in development of mature synaptic connections. Alpha9 knockout mice also failed to show suppression of cochlear responses (compound action potentials, distortion product otoacoustic emissions) during efferent fiber activation, demonstrating the key role alpha9 receptors play in mediating the only known effects of the olivocochlear system.

SUMMARY1. Longitudinal vibration was applied to the de-efferented soleus muscle of anaesthetized cats while recording the discharge of single afferent fibres from the proprioceptors within the muscle. Conditions were defined under which vibration can be used to excite selectively the primary endings of muscle spindles without exciting the secondary endings of muscle spindles or Golgi tendon organs.2. Frequencies of vibration of 100-500 c/s were used. The maximum amplitude of vibration which the vibrator could produce fell with increasing frequency; it was 250 ,t (peak to peak) for 100 c/s and 20 ,u for 500 c/s.3. Primary endings of muscle spindles were very sensitive to vibration. Most could be 'driven' to discharge one impulse for each cycle of vibration over the whole of the above range of frequencies, provided the initial tension was moderate (20-200 g wt.). The amplitude of vibration required to produce driving usually varied by less than a factor of two over the whole range of frequencies. The most sensitive endings could be driven by vibrations of below 10 t amplitude.4. Stimulation of single fusimotor fibres, whether static or dynamic fusimotor fibres, increased the sensitivity of primary endings to vibration. Contraction of the main muscle, produced by stimulating ac motor fibres, reduced the sensitivity of primary endings even when fusimotor fibres were also being stimulated.5. The secondary endings were very insensitive to longitudinal vibration and with the amplitudes available not one of twenty-five endings could be driven at 150 c/s or above; one ending could be driven at 100 c/s by vibration of 250 t amplitude. Stimulation of single fusimotor fibres, probably all of which were static fusimotor fibres, made them slightly more sensitive to vibration but none of them approached the sensitivity of the primary endings.6. The Golgi tendon organs were as insensitive as the secondary endings * Wellcome-Swedish travelling research fellow. Present address: