A CASE FOR TRANSMITTER PLASTICITY AT THE MOLECULAR-LEVEL - AXOTOMY-INDUCED VIP INCREASE IN THE UPPER SPINAL DORSAL HORN IS RELATED TO BLOCKADE OF RETROGRADE AXOPLASMIC-TRANSPORT OF NERVE GROWTH-FACTOR IN THE PERIPHERAL-NERVE
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KNYIHARCSILLIK, E
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机构:ALBERT SZENT GYORGYI MED UNIV,DEPT ANAT,POB 512,H-6701 SZEGED,HUNGARY
KNYIHARCSILLIK, E
KREUTZBERG, GW
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机构:ALBERT SZENT GYORGYI MED UNIV,DEPT ANAT,POB 512,H-6701 SZEGED,HUNGARY
KREUTZBERG, GW
RAIVICH, G
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机构:ALBERT SZENT GYORGYI MED UNIV,DEPT ANAT,POB 512,H-6701 SZEGED,HUNGARY
RAIVICH, G
CSILLIK, B
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机构:ALBERT SZENT GYORGYI MED UNIV,DEPT ANAT,POB 512,H-6701 SZEGED,HUNGARY
CSILLIK, B
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[1] ALBERT SZENT GYORGYI MED UNIV,DEPT ANAT,POB 512,H-6701 SZEGED,HUNGARY
[2] MAX PLANCK INST PSYCHIAT,DEPT NEUROMORPHOL,W-8033 MARTINSRIED,GERMANY
Blockade of retrograde axoplasmic transport in peripheral nerves, by means of perineurally applied microtubule inhibitors, results in an increased vasoactive intestinal polypeptide (VIP) reaction of the segmentally related, ipsilateral upper dorsal horn. Similar effect is elicited by the perineural application of an anti-Nerve Growth Factor (anti-NGF) serum. At the same time, both treatments result in depletion of Substance P from the same region of the spinal cord. It is assumed that this striking example of transmitter plasticity, obviously taking place at the molecular level, is due to a stimulating effect of NGF upon the perikaryal Substance P-synthesizing mechanism in dorsal root ganglion cells, and the inhibitory effect of NGF upon the VIP synthesizing machinery in these same nerve cells.
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
FITZGERALD, M
WALL, PD
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
WALL, PD
GOEDERT, M
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
GOEDERT, M
EMSON, PC
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
FITZGERALD, M
WALL, PD
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
WALL, PD
GOEDERT, M
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND
GOEDERT, M
EMSON, PC
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MED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLANDMED SCH CAMBRIDGE, MED RES COUNCIL CTR, NEUROCHEM PHARMACOL UNIT, CAMBRIDGE CB2 2QH, ENGLAND