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B Oderfeld-Nowak

Publications and source records attributed to B Oderfeld-Nowak.

50 records · Page 3Linked to original sources
PubMed1977

Relationship between changes in the content of acetylcholine and the activities of acetylcholinesterase and choline acetyltransferase in the hippocampus of the rat after septal lesions.

Changes in acetylcholine (ACh) content and acetylcholinesterase (AChE) and choline acetyltransferase (ChAc) activity in the hippocampus were compared after various septal lesions. With the use of a multiple regression model it was shown that the time course of the ACh and enzymic level changes is concordant after total destruction of the septum, but not always after partial damage. Septal lesions produced an effect mainly on bound ACh. The results suggest that the activity of AChE and ChAc is not the rate-limiting factor of the ACh level in the hippocampus. The involvement of other hippocampal neurotransmitters acting through the high-affinity uptake of choline is supposed to play an important role in ACh content regulation.

Acetylcholine↗
PubMed1976

Alterations in acetylcholinesterase isoenzyme pattern of hippocampus after septal lesions in rat brain.

The effect of septal lesions upon the AChE (EC 3.1.1.7) isoenzymic pattern in the hippocampus of the rat brain was studied 1-3 months after surgery by means of polyacrylamide disc electrophoresis. Alterations in the isoenzymic pattern were found in the membrane-bound but not in the soluble fraction of the enzyme. In addition to the two slowly migrating bands seen in the membrane-bound AChE fraction of the normal hippocampus, the fast-migrating isoenzyme becomes visible.

Acetylcholinesterase↗
PubMedDate not supplied

Differential susceptibility of senile and lesion-induced astrogliosis to phosphatidylserine.

The susceptibility of age- and lesion-induced astrogliosis to the treatment with phosphatidylserine was investigated with the use of GFAP immunoblotting. The existence of age-induced upregulation of GFAP content was confirmed in the hippocampus, septum, and corpus callosum of the rat. The Ptd-Ser treatment of the aged rats further increased the GFAP content in the hippocampus and corpus callosum. The GFAP content increase in the corpus callosum was additionally illustrated by the upregulation in GFAP immunostaining. In the septum no further elevation of GFAP was observed after Ptd-Ser treatment, and in the striatum the compound elicited significant GFAP content increase, absent in the untreated aged rat brain striatum. In the intact adult rat brain no effect of Ptd-Ser on GFAP content was observed; neither did the compound elicit any modulation of the astrogliosis related to the mechanical lesion of the brain in the septum, hippocampus, cortex, and striatum. In the corpus callosum, Ptd-Ser potentiated the GFAP content increase related to the mechanical lesion, pointing to the structure-related heterogeneity of astrocytic population. Because it has been previously found that Ptd-Ser partly reverses one of the aspects of rodent brain aging, the aging-induced decrease of the acetylcholine release, the possibility exists that the effects of Ptd-Ser administration on glia and neurons in the aged brain may be related.

Aging↗