1318 Axonaldiameter-based rate of retrograde degeneration in the rat optic nerve

1318 Axonaldiameter-based rate of retrograde degeneration in the rat optic nerve

S139 1318 AXONALDIAMEI'ER-BASEDRATEOF RETROGRADEDEGENERATIONIN THE RAT OPTIC NERVE. MIHO SUGIOKA, HAJIMESAWAIAND YUTAKAFUKUDA, Dept. Physiol., Osaka...

108KB Sizes 2 Downloads 50 Views

S139

1318

AXONALDIAMEI'ER-BASEDRATEOF RETROGRADEDEGENERATIONIN THE RAT OPTIC NERVE. MIHO SUGIOKA, HAJIMESAWAIAND YUTAKAFUKUDA, Dept. Physiol., Osaka Univ. Med. Sch.. Suita 565. Jat~an.

In the rat optic nerve (ON) and optic tract (OT), fast-, medium- and slow-conductingfibers, that is thick-, medium- and thin-fibers ie axonal diameter, have been identified (Sefton and Swinburn,1964; Sumitomo et a1.,1969). Generally, the larger the diameter of the fibers, the faster they were thrown into Wallerian degeneration (C'revelet a1.,t963; Veronesi and Boyes,1988). But the relationship between the fiber diameter and the rate of retrograde degenerationis not fully resolved. In the present study we examined this relationshipafter unilateral OT transectionin adult rats using electrophysiologicaland morphologicaltechniques.The right OT was transectedbetween the optic cbiasm (OX) and the lateral geniculatenucleus, with the left OT serving as a control. Two and four weeks later, compound action potentials (CAPs) were recorded from the ON stump just behind the optic disk in response to the OX stimulation, or the measurements of the diameters of surviving ON axons were carried out by electron microscopy. From the ON ipsilateral to the transected OT, i.e. the control side, three components 6f CAPs were identified; nt, n2 and n3 components corresponding to fast-, medium- and slow-conducting fibers. At two weeks after the OT section, amplitudeof n3 componentreduced significantlyin records from the ON contralateralto the transectedOT, i.e. the cut side, the n2 reduced moderately in amplitude,whereas the n t relativelypersisted. These tendencieswere more marked at four weeks after the OT section;amplitedesof nt and to. components decreased, their latencies were elongated and n3 componentvanished. In electron microscopic examinations, the fiber density reduced and demyelinated axons occured frequently in the ON of cut side. In a quantitative analysis, smaller axons with diamaters of 0.2-0.5,um reduced and medium sized axons with diameters of 0.5-1.1t, m increasedin relative nfimberas compared with those of the control side. From these physiological and morphological results we concluded that thinner axons were initiallyand remarkablythrowninto the retro~-n'adedegenerationafter the OT section.

1319

RECEPTIVEFIELDPROPERTIESOF CAT RETINALGANGLIONCELLS WITHREGENERATEDAXONS INTOTHE AUTOGRAFTED SCIATIC NERVE . TQMQMITSU M1YOSHI1 MIHO SUGIOKA 1 HA~IIF.IESAWAI1 MASAMI WATANABE 2 AND YUTAKA FUKUDAl, lDepartment of. Physiology, Osaka University Medical School, O~aka, Japan, ~n(J 2Det)artment of Phvsioloev. Institute for Develoornental Research. Aiehi Prefeclural (~olonv, Japan,

Retinal ganglion cells (RGCs) regenerate their axons through the sciatic nerve uutografted to the transected slump of the optic nerve in adult cats. Recording single unit activities from regenerated RGC axons we reported previously that these RGCs preserved normal visual responsiveness and could be classified into .Y, X and W cells (Watanabe et al, 1992). Here we collected more than 200 units and studied their receptive field properties in detail. The left optic nerve of adult cats was sectioned in the orbit close to the eyeball and the sciatic nerve was autografted to the stump. At 50-90 days survival we recorded unit activities of regenerated RGC axons with silver wire electrodes from teased fibers of the graft. With a great majority of units we were able to plot their receptive fields on a tangent screen and to classify them into Y, X or W cells. Furthermore, the proportion of Y cells outnumbered those of X and W cells, confirming our previous report. At peripheral retina receptive field sizes of Y and X cells are similar to those of respective types of intact RGC cells reported previously (Stone and Fukuda, 1974). By contrast, within 10 degrees from the area centralis both Y and X cells with regenerated axons showed significantly larger receptive fields than those of intact Y and X cells. In addition, we found a small population of X cells with large receptive field and Y cells with small receptive field. These observations would suggest that some reorganizations have occurred in intraretinal synaptic circuitry, besides previously reported retractions and extensions of dendrites of regenrated RGCs (Watanabe et al., 1993).

1320

D U A L A C T I O N O F N I T R I C OXIDE ON N M D A - I N D U C E D CYTOTOXICITY IN CORTICAL CULTURE. HISAM1TSU UJIHARA, Y U T A K A T A M U R A * * , Y A S U E y A M A D A , MASASHI SASA*, A N D A K I N O R I A K A I K E * * , D e p a r t m e n t o f P h a r m a c o l o g y , Y a m a g n c h i U n i v e r s i t y ,~chool o f Medicine, Ube 755, * D e p a r t m e n t o f P h a r m a c o l o g y , Hiroshima U n i v e r s i t y School of Medicine, Hiroshima 734, and * * D e p a r t m e n t o f N e u r o p h a r m a c o l o g y , Faculty o f Pharmaceutical Sciences, F u k u y a m a U n i v e r s i t y , F u k u y a m a 729-02, Japan A role o f nitric oxide (NO) o n glutamate-induced n e u r o n a l death was e x a m i n e d using the p r i m a r y

c u l t u r e o f rat cortical cells. Cell viability was m a r k e d l y reduced by a b r i e f e x p o r s u r e of cells to N - m e t h y l D-aspartate ( N M D A ) f o l l o w e d by an i n c u b a t i o n with n o r m a l solution for one hour. A low c o n c e n t r a t i o n o f N O - g e n e r a t i n g agents produced a protection against the N M D A cytotb'xicity, and a high c o n c e n t r a t i o n of them induced the n e u r o n a l death.

Electrophysiologieal e x p e r i m e n t s revealed that the whole-cell c u r r e n t s

evoked by N M D A in the presence o f glycine w e r e blocked by the N O - g e n e r a t i n g agents.

These results

suggest that N O synthesized f o l l o w i n g the e x p o s u r e to N M D A prevents N M D A cytotoxicity via a feedback m e c h a n i s m at a low c o n c e n t r a t i o n as well as mediate the cytotoxicity at a high c o n c e n t r a t i o n .