Schwann cell basal lamina and central nerve regeneration

Schwann cell basal lamina and central nerve regeneration

$131 SCHWANN CELL BASAL LAMINA AND CENTRAL NERVE REGENERATION C H I Z U K A IDE, S A T O R U O N O D E R A ~, K O U J I R O T O H Y A M A *, R...

76KB Sizes 1 Downloads 143 Views

$131 SCHWANN

CELL

BASAL

LAMINA

AND

CENTRAL

NERVE

REGENERATION

C H I Z U K A IDE, S A T O R U O N O D E R A ~, K O U J I R O T O H Y A M A *, R E I K O Y O K O T A ~, T O H R U N I T A T O R I *. Department of Anatomy, Iwate Medical University School of M e d i c i n e , U c h i m a r u , M o r i o k a 020, J a p a n . It h a s b e e n d e m o n s t r a t e d t h a t the b a s a l l a m i n a s c a f f o l d s o f S c h w a n n c e l l s are e f f e c t i v e p a t h w a y s f o r r e g e n e r a t i n g p e r i p h e r a l n e r v e s (Ide, et al, 1983). The p r e s e n t s t u d y w a s c a r r i e d o u t to e x a m i n e w h e t h e r the S e h w a n n c e l l b a s a l l a m i n a e c a n be e f f e c t i v e f o r r e g e n e r a t i n g f i b e r s o f the c e n t r a l n e r v o u s s y s t e m . The r a t sciatic nerve was transected for predegeneration, and after one w e e k a p a r t o f the d i s t a l p o r t i o n o f the t r a n s a c t e d n e r v e w a s e x c i s e d a n d t r e a t e d s e v e r a l t i m e s b y f r e e z i n g a n d t h a w i n g to kill the S c h w a n n c e l l s . The t r e a t e d n e r v e s e g m e n t w a s t h e n i m p l a n t e d i n t o the s p i n a l c o r d of the s a m e a n i m a l . About 7 days after implantation, macrophages phagocytized dead S e h w a n n c e l l s , l e a v i n g b a s a l l a m i n a s c a f f o l d s o f S e h w a n n c e l l s in the i m p l a n t . Regenerating fibers entered such basal lamina s c a f f o l d s , b e i n g a c c o m p a n i e d b y c e l l s r e s e m b l i n g S e h w a n n c e l l s in appearance. A f t e r 20 days, m o s t o f the r e g e n e r a t i n g f i b e r s w e r e myelinated. The cells forming myelin sheaths resembled Schwann cells, b e i n g s u r r o u n d e d w i t h b a s a l l a m i n a e . Some astrocytic p r o c e s s e s w e r e f o u n d w i t h i n the b a s a l l a m i n a s c a f f o l d s , e n c l o s i n g one to s e v e r a l m y e l i n a t e d f i b e r s o f the c e n t r a l n e r v e type. T h e s e f i n d i n g s s u g g e s t at l e a s t the p o s s i b i l i t y o f the e f f e c t i v e ness of Sehwann cell basal laminae for central nerve regeneration.

THE LONG-TE~.! POTENTIATION OF TRANSMITTER RELEASE INDUCED BY PRESYNAPTIC ACTIVITIES IN BULL-FROG S~4PATHETIC NEURONES. SHOICHI IIINOTA, KENJI KUBA and KONOMI KOYANO*, Department of Physiology, Saga Medical School, Nabeshima, Saga 840-01, Japan. The long-term potentiation (l.t.p.) of the fast excitatory post-synaptic potentials (fast e.p.s.p.s) induced by repetitive presynaptic activities was studied intraeellularly in the bull-frog paravertebral sympathetic ganglion. After a brief tetanus to the preganglionic nerve, the amplitude of the fast e.p.s.p, was potentiated for a period from several tens of minutes to more than 2 h. This l.t.p, was accompanied by an increase in quantal content (43% of cells examined), quantal size (19%) or both (38%). The increased quantal content (presynaptic l.t.p.) declined exponentially or decayed to a certain enhanced level which lasted for several hours. In contrast, the increased quantal size grew with a relatively long latency (10-25 min) and remained relatively constant for at least 2h. The magnitude of prcsynaptic l.t.p, increased with increased duration of the presynaptic tetanus (33 Hz) from 2 to 5 s. No l.t.p, was elicited by a 1 s-tetanus. The time course of presynaptic l.t.p, appeared to be independent of the tetanus duration and the ~agnitude of l.t.p. There was a positive correlation between the magnitude of 3resynaptic l.t.p, and the pre-tetanic quantal content up to m=3; but the former deviated from linear regression when the value of the latter exceeded 3. Io 1.t.p. occurred when the quantal content was less than 0.5. A tetanus ~pphed zn Ca -free solution elicited no presynaptic l.t.p., while the same tetanus in normal Ringer solution produced a large presynaptic l.t.p. Pre~ynaptic l.t.p, was enhanced in magnitude at low temperature (8-10 °C). These results demonstrate the existence of a use-dependent, long-term potentiation of transmitter release, which is activated by an increased intracellular ~aL+ without consuming much metabolic energy, in bull-frog sympathetic ganglia.