Biomedical subjects

R Gadamski

Publications and source records attributed to R Gadamski.

At least 37 records · Page 2Linked to original sources

PubMed1994

Effects of MK-801 and ganglioside GM1 on postischemic prostanoid release and hippocampal lesion in gerbil brain.

In this study Mongolian gerbils were submitted to a normothermic bilateral carotid ligation lasting 5 min. A noncompetitive antagonist of NMDA receptors, MK-801, 0.8 mg/kg, was injected i.p. 30 min before ischemia, or the ganglioside GM1, 30 mg/kg, was given i.p. for 3 days, twice a day. The morphology of the hippocampal CA1 neurones and the brain content of cyclooxygenase metabolites of arachidonic acid: prostaglandin 6-keto PGF1 alpha and thromboxane Tx B2 were studied. Untreated ischemia induced the accumulation in brain of the 6-keto PGF1 alpha and Tx B2 immunoreactive materials, and resulted in a lesion of 70% of CA1 neurones. In the MK-801- and GM1-pretreated groups the postischemic levels of Tx B2 were significantly decreased. However MK-801 and GM1 did not prevent damage to the CA1 neurones in gerbils normothermic after ischemia, whereas a partial neuroprotection was observed in hypothermic, MK-801 treated gerbils. The results of this study indicate that NMDA receptors may participate in the mechanism of postischemic release of eicosanoids in brain. They also confirm a potential modulatory role of gangliosides. These results are discussed in terms of the involvement of cyclooxygenase metabolites of arachidonic acid in the mechanism of a selective delayed neuronal damage to the hippocampus CA1 after ischemia.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Comparative morphometric analysis of terminal vascularization of hippocampal CA1 and CA3 sectors in Mongolian gerbils.

Comparative morphometric analysis of terminal vascularization (vessels with a diameter lower than 12.5 microns) in the ischemia-sensitive sector CA1 and the ischemia-resistant sector CA3 of Ammon's horn in Mongolian gerbils was performed. Basing on numerous computer-counted parameters characterizing the terminal vascular network in both hippocampal sectors and its relationship to the surrounding tissue, it was shown that a number of capillary vessels, their average diameter, and exchange and flow surfaces were to a statistically significant degree lower in the pyramidal layer of the CA1 sector as compared with those in CA3 sector. The number of pyramidal neurons in the pyramidal layer, counted per surface unit was in sector CA1 higher than in sector CA3. The obtained data indicate clearly an angioarchitectonically dependent lower microvascular capacity of sector CA1. However, these differences do not indicate per se a leading role of the vascular factor in the pathomechanism of selective vulnerability to ischemia. They may be a factor facilitating neuronal damage evoked by the excitotoxic action of glutamate, observed in CA1 sector as a result of forebrain ischemia.

Animals↗

PubMed1994

Immunoreactivity of astroglia after brief ischemia resulting in asymmetrical damage to the hippocampal CA1 sector in the Mongolian gerbil.

The study was performed on 98 Mongolian gerbils. Cerebral ischemia was evoked by ligation of both common carotid arteries for 5 min. After five postischemic days the animals were decapitated, brains fixed, paraffin section stained with histological methods and for GFAP with ABC method. The investigated animals (ca 18%) presented asymmetrical morphological lesions of the CA1 hippocampal sector showing irregular loss of neurons in both cerebral hemispheres. GFAP immunostaining demonstrated various astroglial proliferation in asymmetrical lesions of CA1 sector. In partial injury to CA1 neurons the astrocytes in stratum (s) pyramidale were single but their number still increased when total loss of pyramidal neurons occurred. Except s. lacunosum moleculare the number of GFAP-positive astrocytes in the remaining layers of dorsal hippocampus presented a direct relationship with the intensity of morphological changes and was highest when 70% loss of pyramidal cells was observed.

Animals↗

PubMed1993

Changes of the Na/K ATPase activity in the cerebral cortical microvessels of rat after single intraperitoneal administration of mercuric chloride: histochemical demonstration with light and electron microscopy.

Since inorganic mercury salts only poorly penetrate the cerebral microvascular endothelial cells comprising the blood-brain barrier (BBB), their neurotoxicity may be predicted to result from interference with BBB transport enzymes. In the present study, we tested the effect of mercuric chloride (HgCl2) on Na+/K+ ATPase activity, a key enzyme involved in the ion transport in and out of the brain. Routine histochemical staining in conjunction with light and electron microscopy was used to evaluate the changes in the Na+/K+ ATPase activity in cerebral cortical microvessels of rats who received a single intraperitoneal injection of 6 mg/kg HgCl2. At 1 h after HgCl2 administration, light microscopy revealed uniform reduction of the Na+/K+ ATPase reaction in all cortical layers. Electron microscopy confirmed the enzyme reaction to be very weak to completely absent in both the luminal and abluminal endothelial cell membranes, and the luminal plasmalemma showed invaginations and pinocytic vesicles indicative of changes in its transport functions. The enzyme inhibition coincided with, and was likely to contribute to, profound perivascular swelling, involving mainly the astrocytic endfeet. The enzyme activity showed a partial recovery 18 h after HgCl2 treatment, mainly in cortical layers II and III. After 5 days, the recovery of the enzyme activity appeared complete as observed by light and electron microscopy. The recovery of the microvascular Na+/K+ ATPase coincided with the appearance of a strongly positive Na+/K+ ATPase reaction in the adjacent astrocytic processes and with the diminution of perivascular swelling.

Animals↗

PubMed1992

Lectin histochemistry and alkaline phosphatase activity in the pia mater vessels of spontaneously hypertensive rats (SHR).

Some lectins were used to study the localization of sugar residues on the endothelial cell surface in the pia mater blood vessels of control (WKY) and hypertensive rats (SHR). The lectins tested recognized the following residues: beta-D-galactosyl (Ricinus communis agglutinin 120, RCA-1), alpha-L-fucosyl (Ulex europaeus agglutinin, UEA-1), N-acetylglucosaminyl and sialyl (Wheat germ agglutinin, WGA), N-glycolyl-neuraminic acid (Limax flavus agglutinin, LFA), and N-acetyl-D-galactosaminyl (Helix pomatia agglutinin, HPA). Several differences were revealed in the presence of sugar receptors on the surface of endothelial cells between the control and the hypertensive rats. Our studies showed also differences in the localization of the tested glycoconjugates between pial capillaries, small, medium-size and large pial arteries. The histochemical evaluation of alkaline phosphatase revealed an increased activity of the enzyme in the pial vessels of SHRs as compared with control rats with a similar localization of the enzyme activity. Some differences in the distribution of lectin binding sites and alkaline phosphatase activity could be associated with the different functions of particular segments of the pial vascular network.

Alkaline Phosphatase↗

PubMed1992

Asymmetric damage of the CA1 sector of Ammon's horn after short-term forebrain ischemia in Mongolian gerbils.

The studies were carried out on 98 three-month-old Mongolian gerbils, submitted to short-term (5 or 7.5 min) forebrain ischemia induced by bilateral ligation of common carotid artery. After 5-day survival animals were sacrificed by transcardiac perfusion with 10% formaldehyde. Paraffin brain sections were stained with cresyl violet and according to Klüver-Barrera method. Pickworth benzidine method was also applied to evaluate hippocampal vascular network. Varying susceptibility of individual animals to the ischemic incident was found. This was expressed by differences in the intensity and extent of structural lesions of CA1 pyramidal neurons. No abnormalities were found in 41.7% of animals, total neuronal loss in the CA1 sector was observed in 33.3% of cases, while the partial neuronal loss appeared in the remaining 25% of animals. Asymmetric distribution of the neuronal changes observed in 18.4% of cases was a very striking feature. Differences of the angioarchitectonics of CA1 sector as compared with neighbouring parts of Ammon's horn were found. In the pyramidal cell layer very scarce fragments of the blood vessels were present. In adjacent cortical layers (stratum oriens and stratum radiatum) relatively dense capillary network was characterized by appearance of specific vascular loops and tangles localized on the border of stratum pyramidale. It is supposed that particular spatial arrangement of the vascular network in pyramidal layer of CA1 sector, favouring appearance of local hemodynamic and rheologic abnormalities after temporary brain ischemia, may play an essential pathogenic role in both, selective vulnerability of this neuronal population and individual variations in the intensity and distribution of the neuronal changes.

Animals↗

PubMed1992

Immunoreactivity of astroglia in the hippocampus of the Mongolian gerbil during short survival following brief ischemia.

Mongolian gerbils subjected to 5-min cerebral ischemia by common carotid artery ligation were decapitated after 24, 48, 72 and 96 h of survival to investigate the immunoreactivity of astroglia in the hippocampus. The sections from formalin-fixed, paraffin-embedded brains were stained histologically and with ABC method (Hsu et al. 1981). Control animals (normal and shame-operated) presented positive GFAP immunostaining in corpus callosum, in subventricular regions, in temporal subcortical white matter, in fimbria hipocampi and perivascularly in stratum lacunosum-moleculare. Experimental animals, independently of postischemic survival time showed various individual GFAP reactivity. Differences concerning the number and localization of immunoreactive astrocytes in both cerebral hemispheres of the same animal stressed the asymmetry of the reaction. The authors did not observe any accumulation of reactive astrocytes in the area of synaptic terminals of glutaminergic fibers (mossy fibers, Schaffer's collaterals) or in the neighbourhood of CA1 and CA3 sectors. In particular, there was complete lack or only sporadic reactive astrocytes among pyramidal neurons of CA1 and among granular cells of dentate gyrus in all examined animals.

Animals↗

PubMed1992

Ultrastructural alterations of brain cortex in rat following intraperitoneal administration of mercuric chloride.

Intraperitoneal administration of a single dose (6 mg/kg body weight) of mercuric chloride (HgCl2) results in ultrastructural changes in brain cortex of the rats. 18 hours after administration of HgCl2 the accumulation of dense deposits of mercury in nerve and glial cell cytoplasm was observed. The quantity of microglia in neuropil was also increased in this experimental group. We postulate that these cerebral macrophages can play an important role in the process of intoxication, too. 5 days after administration of mercuric chloride many of these changes reversed.

Animals↗

PubMed1992

Influence of short-term ischemia on the ultrastructure of hippocampal gyrus in Mongolian gerbil. III. Synapses in late stage of the pathological process.

Electron microscope analysis of the CA1 Ammon's horn sector was performed in Mongolian gerbils three days after an incident of short-term ischemia of the forebrain. CA1 pyramidal neurons showed advanced disintegration. Some GABA-ergic interneurons revealed ultrastructural alteration of variable degree. The latter finding contradicts the generally helt view on the relative resistance of CA1 sector interneurons to the ischemic injury. Synapses localized in all cortical layers of the CA1 sector exhibited ultrastructural abnormalities involving both pre- and postsynaptic parts. They consisted in marked swelling and accumulation of unbound electron dense material, considered as calcium deposits. Presynaptic parts revealed additionally reduced number of synaptic vesicles and their abnormal distribution. Contrary to the early postischemic period, the most severe synaptic alterations appeared in stratum pyramidale, radiatum and oriens, involving both small dendritic branchings and their spines as well as large shafts of both basal and apical pyramidal dendrites. Synaptic alterations especially features of the postsynaptic damage correspond to those indicating excitotoxic neuronal lesions. Presynaptic alterations may indicate both cessation of neurotransmission function as well as direct ischemic damage. The presence of calcium deposition seems to favour the former possibility.

Animals↗

PubMed1990

Nimodipine prevents delayed neuronal death of sector CA1 pyramidal cells in short-term forebrain ischemia in Mongolian gerbils.

Delayed death of pyramidal neurons of Ammon's horn CA1 sector after short-term forebrain ischemia in Mongolian gerbils represents a type of ischemic neuronal injury in which calcium influx plays an important role. We evaluated the influence of the calcium channel blocker nimodipine in animals subjected to 7.5 minutes of bilateral carotid artery ligation that were given 1 mg/kg i.p. nimodipine at various periods in relation to the ischemic incident. The control animals were subjected to cerebral ischemia with no medication. Five days after ischemia, the state of CA1 sector neurons was morphometrically evaluated and compared with that in animals not subjected to an experimental procedure. Nimodipine exerted a full protective effect on CA1 pyramidal neurons only after repeated application extending over 24 hours after the ischemia. A less conspicuous effect was obtained with a single dose applied at a late postischemic period, and a double dose given in the peri-ischemic stage remained ineffective. The time-dependent effectiveness of nimodipine is discussed in relation to the characteristics of this model of cerebral ischemia.

Animals↗

PubMed1989

[Adenyl cyclase activity in synapses of the CA1 segment of the horn of Ammon in Mongolian gerbils].

Adenylate cyclase activity, stimulated by dopamine, norepinephrine and forskolin, was demonstrated histochemically in electron microscopy of the CA1 sector of Ammon's horn in Mongolian gerbil. Cobalt and strontium were used as precipitating agents. The reaction product located in the synapses was mostly associated with the postsynaptic membranes. It was also present in the plasma membrane of some nerve fibers. There were no differences in the enzyme activity in particular layers of Ammon's horn as well as between symmetric and asymmetric types of synapses. The intensity of the reaction product depended mostly on the stimulator used.

Animals↗

PubMed1989