Record 8358   View: Overview Glossary  HistCite Guide
Author(s): WAXMAN SG; KOCSIS JD; BLACK JA
Title: TYPE-III SODIUM-CHANNEL MESSENGER-RNA IS EXPRESSED IN EMBRYONIC BUT NOT ADULT SPINAL SENSORY NEURONS, AND IS REEXPRESSED FOLLOWING AXOTOMY
Source: JOURNAL OF NEUROPHYSIOLOGY 72 (1): 466-470
Date: 1994 JUL
Document Type: Journal : Note
Language: English
Comment:  
Address: VET ADM MED CTR,PARALYZED VET AMER EASTERN PARALYZED VET ASSOC NE,W HAVEN,CT 06516.
Reprint: WAXMAN, SG, YALE UNIV,SCH MED,DEPT NEUROL,LCI 707,NEW HAVEN,CT 06510.
Abstract: 1. In situ hybridization with subtype-specific probes was used to ask whether there is a change in the types of sodium channels that are expressed in dorsal root ganglion (DRG) neurons after axotomy. 2. Types I and II sodium channel mRNA are expressed at moderate-to-high levels in control DRG neurons of adult rat, but type III sodium channel mRNA is not detectable. 3. When adult rat DRG neurons are examined by in situ hybridization 7-9 days following axotomy, type III sodium channel mRNA is expressed at moderate-to-high levels, in addition to types I and II mRNA that are present at relatively high levels. 4. To determine whether the expression of type III sodium channel mRNA following axotomy represents up-regulation of a gene that had been expressed at earlier developmental stages, we also studied DRG neurons from embryonic (E17) rats. In these embryonic DRG neurons, type I sodium channel mRNA is expressed at low levels, type II mRNA at high levels, and type III at high levels. 5. These results demonstrate altered expression of sodium channel mRNA in DRG neurons following axotomy, and suggest that in at least some DRG neurons, there is a de-differentiation after axotomy that includes a reversion to an embryonic mode of sodium channel expression. Different channel characteristics, as well as an altered spatial distribution of sodium channels, may contribute to the electrophysiological changes that are observed in axotomized neurons.
Cited References:
BAINES D, 1992, MOL BRAIN RES, V16, P330
BARRON KD, 1989, NEURAL REGENERATION, P79
BECKH S, 1989, EMBO J, V8, P3611
BECKH S, 1990, FEBS LETT, V262, P317
BHISITKUL RB, 1990, EXP NEUROL, V109, P273
BLACK JA, 1994, MOL BRAIN RES, V22, P275
BLACK JA, 1994, MOL BRAIN RES, V23, P235
BRYSCH W, 1991, EXP BRAIN RES, V86, P562
CAFFREY JM, 1992, BRAIN RES, V592, P283
DODGE FA, 1973, IBM J RES DEV, V17, P219
ECCLES JC, 1958, J PHYSIOL-LONDON, V143, P11
ELLIOTT AA, 1993, J PHYSIOL-LONDON, V463, P39
FOEHRING RC, 1986, J NEUROPHYSIOL, V55, P947
FOEHRING RC, 1987, J NEUROPHYSIOL, V57, P1227
GALLEGO R, 1987, J PHYSIOL-LONDON, V391, P39
GRAFSTEIN B, 1986, RETINA MODEL CELL 2, P275
GUSTAFSSON B, 1984, J PHYSIOL-LONDON, V356, P433
HONMOU O, 1994, J NEUROPHYSIOL, V71, P1627
JEFTINIJA S, 1994, BRAIN RES, V639, P125
KAYANO T, 1988, FEBS LETT, V228, P187
KOSTYUK PG, 1981, NEUROSCIENCE, V6, P2423
KUNO M, 1970, J PHYSIOL-LONDON, V210, P807
KUNO M, 1974, J PHYSIOL-LONDON, V240, P725
LANGFORD CJ, 1980, J NEUROCHEM, V34, P531
MCLEAN MJ, 1988, MOL CELL BIOCHEM, V80, P95
NEUMCKE B, 1982, J PHYSL, V329, P163
NODA M, 1986, NATURE, V320, P188
OMRI G, 1990, J MEMBRANE BIOL, V115, P12
PURVES D, 1978, NEURONAL PLASTICITY, P27
ROY ML, 1992, J NEUROSCI, V12, P2104
SCHWARTZ A, 1990, J MEMBRANE BIOL, V116, P117
SERNAGOR E, 1986, P NATL ACAD SCI USA, V83, P7966
SHAPAVALOV AI, 1968, BIOPHYSICS-USSR, V13, P308
STYS PK, 1993, P NATL ACAD SCI USA, V90, P6976
TITMUS MJ, 1986, J NEUROPHYSIOL, V55, P1440
TITMUS MJ, 1990, PROG NEUROBIOL, V35, P1
WAXMAN SG, 1982, CELL TISSUE RES, V223, P487
WELLS MR, 1987, EXP NEUROL, V95, P313
YOSHIDA S, 1978, J NEUROPHYSIOL, V41, P1096