Cholinergic sprouting in the rat fascia dentata after entorhinal lesion is not linked to early changes in neurotrophin messenger RNA expression.
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Cholinergic sprouting in the rat fascia dentata after entorhinal lesion is not linked to early changes in neurotrophin messenger RNA expression. / Förster, Eckart; Naumann, T; Deller, T; Straube, A; Nitsch, R; Frotscher, M.
in: NEUROSCIENCE, Jahrgang 80, Nr. 3, 3, 1997, S. 731-739.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Cholinergic sprouting in the rat fascia dentata after entorhinal lesion is not linked to early changes in neurotrophin messenger RNA expression.
AU - Förster, Eckart
AU - Naumann, T
AU - Deller, T
AU - Straube, A
AU - Nitsch, R
AU - Frotscher, M
PY - 1997
Y1 - 1997
N2 - After unilateral entorhinal cortex lesion cholinergic septohippocampal fibres sprout in the denervated fascia dentata. This process is dependent on neurotrophin changes following the lesion. Thus, there is an up-regulation of nerve growth factor and brain-derived neurotrophic factor messenger RNA expression in the denervated granule cells which is detectable 4 h postlesion and returns to control levels by 24 h. Here, using a competitive polymerase chain reaction and in situ hybridization, a transient neurotropin messenger RNA increase could be demonstrated bilaterally following unilateral electrolytic entorhinal cortex lesion. Treatment of the animals with the N-methyl-D-aspartate receptor antagonist dizocilpine maleate blocked this messenger RNA increase, suggesting an involvement of this receptor type in the neurotrophin changes. However, in spite of this blockade, the typical cholinergic sprouting response as visualized with acetylcholinesterase histochemistry was present in animals four weeks after entorhinal cortex lesion. These data suggest that brief initial changes in neurotrophin messenger RNA expression in dentate granule cells are not responsible for the induction of the cholinergic sprouting. Changes in neurotrophin messenger RNA expression occurring immediately postlesion may be linked to glutamate release from entorhinal terminals resulting from the electrolytic lesion of the projection cells in the entorhinal cortex. We hypothesize that later changes in neurotrophin expression, for example in glial cells, are more likely to be related to the cholinergic sprouting process.
AB - After unilateral entorhinal cortex lesion cholinergic septohippocampal fibres sprout in the denervated fascia dentata. This process is dependent on neurotrophin changes following the lesion. Thus, there is an up-regulation of nerve growth factor and brain-derived neurotrophic factor messenger RNA expression in the denervated granule cells which is detectable 4 h postlesion and returns to control levels by 24 h. Here, using a competitive polymerase chain reaction and in situ hybridization, a transient neurotropin messenger RNA increase could be demonstrated bilaterally following unilateral electrolytic entorhinal cortex lesion. Treatment of the animals with the N-methyl-D-aspartate receptor antagonist dizocilpine maleate blocked this messenger RNA increase, suggesting an involvement of this receptor type in the neurotrophin changes. However, in spite of this blockade, the typical cholinergic sprouting response as visualized with acetylcholinesterase histochemistry was present in animals four weeks after entorhinal cortex lesion. These data suggest that brief initial changes in neurotrophin messenger RNA expression in dentate granule cells are not responsible for the induction of the cholinergic sprouting. Changes in neurotrophin messenger RNA expression occurring immediately postlesion may be linked to glutamate release from entorhinal terminals resulting from the electrolytic lesion of the projection cells in the entorhinal cortex. We hypothesize that later changes in neurotrophin expression, for example in glial cells, are more likely to be related to the cholinergic sprouting process.
M3 - SCORING: Zeitschriftenaufsatz
VL - 80
SP - 731
EP - 739
JO - NEUROSCIENCE
JF - NEUROSCIENCE
SN - 0306-4522
IS - 3
M1 - 3
ER -