Antagonism of kainic acid lesions in the mouse hippocampus by U-54494A and U-50488H.

A morphometric study of kainic acid- (KA) induced lesions was designed for the study of the interaction of the diamines U-5449A and U-50488H with excitatory amino acids, and the dose-response relationship thereof. IC50S determined for binding at the kappa receptor and other opioid receptors demonstrated the lack of kappa activity of U-54494A, a structurally related analog of U-50488H. Both opiate kappa receptor related anticonvulsant diamines were tested for their ability to protect the mouse hippocampus from the cytopathological changes induced by KA in neurons and glia. The damage observed with i.c.v. KA in mouse was restricted to neurons of the CA3 pyramidal region and glia of the hippocampus. It involved massive cell loss and shrunken neurons with dark cytoplasm and nuclei. Groups treated with combinations of KA and U-54494A or U-50488H showed scarce damage, but patches of necrotic changes were still observed. Control animals treated with saline (i.c.v.) and U-54494A (s.c.) or U-50488H (s.c.) did not suffer any noticeable alterations of the polymorphic layers of the hippocampal formation. Image analysis of the CA3 area of the hippocampus was used to quantitate the vacuolization induced by KA lesions in the control and treated groups. By this method, both U-54494A and U-50488H were shown to protect this area in a dose-related fashion as evidenced by reduced vacuolization. The anticonvulsant properties of these compounds may result in the antagonism of the excitotoxic lesions. More specifically, the ability of these diamines to block depolarization-induced influxes of Ca++ may protect the CA3 cells from the cytotoxic effects of persistent depolarization.     

Antidiabetic and Anticoagulant Properties of Heparin–Glutamic Acid Complex

Natural heparin complexes proved to activate the anticoagulation system. The obtained experimental data convincingly confirm that glutamic acid alone, and particularly in a complex with heparin, has a considerable preventive potential and efficiently protects experimental animals with induced diabetes mellitus.     

Cytokinesis inMicrasterias rotata problems of directed primary wall deposition

Summary The ultrastructure of cytokinesis inM. rotata is described with particular attention to the early stages. At prophase a girdle of primary wall material is deposited at the cell isthmus. The girdle thickens medially, a septum is established and grows inward to separate the daughter semicells by telophase. It is argued that the wall microtubules present at the isthmus are not responsible for delimiting the area over which the girdle is initially deposited, but may participate in girdle deposition and thickening. An important role is ascribed to the secondary wall which, at the isthmus, is devoid of pore bodies and slime. The inner wall surface could, at the isthmus, provide the substratum required for unitial girdle deposition. Though microtubules may be associated with septum initiation, they appear to play no part in subsequent septum growth.