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Abstract
ATP, the energy source for axoplasmic transport, is indispensable for the transport of nerve growth factor (NGF). NGF regulates the regeneration of central processes of the primary sensory neurons, by means of transganglionic regulatory mechanisms. This central regeneration was investigated with the help of the histochemical detection of fluoride-resistant acid phosphatase (FRAP), one of the marker enzymes of the primary nociceptive neurons. Transganglionic degenerative atrophy (TDA) of the central terminals of primary sensory neurons was induced with sciatic nerve crush. Dynamics of central regeneration was studied in rats treated with a cobalt-ATP complex, and with commercially available Na-ATP, respectively, by means of histochemical detection of the restitution of FRAP activity in the Rolando substance. Disappearance of FRAP activity was complete on the 6th postoperative day in the medial two-thirds of the upper dorsal horn in segments L2-L6. The regeneration (i.e. replenishment of FRAP activity) began on the 14th day and was complete by the 31st day in animals treated with cobalt-ATP, while in the animals treated with Na-ATP the replenishment of FRAP activity began on the 20th day and was complete only by the 60th day. It is concluded that the cobalt-ATP-complex significantly enhances central regeneration.
Published Version
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