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Biomedical subjects

A Maiti

Publications and source records attributed to A Maiti.

At least 37 records · Page 2Linked to original sources
PubMed1989

Synthesis and reactivity of the oxovanadium(IV) complexes of two N-O donors and potentiation of the antituberculosis activity of one of them on chelation to metal ions: Part IV.

A new series of oxovanadium(IV) complexes of two aromatic acidhydrazides (BH and AH) have been reported. Of these two donors, AH is known to possess considerable in vitro antitubercular activity. At pH 2-4, oxometal complexes of the type [VO(BH/AH)2SO4].nH2O (n = 1, 0) and [VO(BH/AH)(C2O4)H2O].H2O (BH = C6H5CONHNH2 and AH = (2-NH2)C6H4.CO.NHNH2) were obtained. Reactions of [VO(BH/AH)(C2O4)H2O].H2O with a monodentate Lewis base lead to the isolation of metal-ligand complexes [VO(BH/AH)(C2O4)L].nH2O (L = NH3, n = 1, L = py, n = 2). Disposition of the bonding sites of donor molecules around the oxometal acceptor center and status of the metal-oxygen multiple bond have been established. A monomeric and distorted octahedral donor environment for the oxovanadium(IV) ion has been proposed on the basis of the electron paramagnetic resonance (EPR) spectra and magnetic susceptibility measurements. Antitubercular activities, in vitro, of the oxovanadium(IV) complexes of AH have also been evaluated towards tuberculosis mycobacteria such as Mycobacterium flae, Mycobacterium smegmatis and Mycobacterium H37Rv.

Antitubercular Agents↗
PubMed1988

Structure-activity studies of carbamate and other esters: agonists and antagonists to nicotine.

A number of aromatic, cycloalkyl, and heterocyclic carbamic acid esters, thiocarbamic acid esters, and carboxylic acid esters of di- and trial-kylaminoalkyl and heterocyclic amino alcohols have been synthesized and tested for their pharmacologic and receptor binding characteristics at the nicotine receptor. Receptor binding was measured in rat brain membranes using (-)-3H-nicotine or 3H-methylcarbamylcholine as radioligands. The compounds were tested for their ability to produce seizures and prostration and to antagonize the nicotine-induced prostration and seizures as well as the hypertensive action of nicotine in rats. Among the potent agonists were the N-methylcarbamyl and N-methylthiocarbamyl esters of choline (trimethylaminoethanol), with the tertiary amino derivatives between considerably less potent than the quaternary. Potent antagonists included trimethylaminoethyl benzoate, 3-quinuclidinyl benzoate, and trimethylaminoethyl esters of phenyl and phenylthiocarbamic acids. One of the most potent antagonists to nicotine was alpha-lobeline.

Animals↗
PubMed1988

Ligational behavior of two biologically active N-S donors toward oxovanadium(IV) ion and potentiation of their antibacterial activities by chelation to metal ions. Part III.

Chelating behavior of two biologically active ligands, pyridine-2-carboxaldehyde thiosemicarbazone (PT) and pyridine-2-carboxaldehyde-(4-phenyl)thiosemicarbazone (PPT), toward oxovanadium(IV) ion has been studied. The ligands are found to react in the thioketo form (pH 2-4), yielding the complexes [VO(PT)X2](X = Cl-, Br-, ClO4-), [VO(PT)(SO4)H2O], [VO(PPT)2X]X (X = Cl-, Br-, ClO4-) and [VO(PPT)2SO4]. Reactions of [VO(PT)(SO4)H2O] and [VO(PPT)2X]X (X = Cl-, Br-, ClO4-) with a monodenate Lewis base (B) like pyridine lead to the formation of [VO(PT)(SO4)Py]H2O and [VO(PPT)2py]X2 respectively. Bonding sites of the donor molecules around the oxometal cation have been located. Nature of the EPR spectra and magnetic moment values point to the monomeric character of the complexes and suggest a distorted octahedral donor environment for the oxovanadium(IV) ion. Status of the metal-oxygen multiple bond in all the complexes has been computed in terms of the V-O(1) stretching force constant. The ligands themselves and most of their oxovanadium(IV) complexes are found to exert powerful in vitro antibacterial activities towards E. coli.

Anions↗
PubMed1986

Barrel rotation and prostration by vasopressin and nicotine in the vestibular cerebellum.

The aim of this study was to determine whether the primary sites for the action of vasopressin and nicotine in producing barrel rotation and prostration in rats were located in the modular cerebellum, i.e., lobule X. When arginine vasopressin was administered into either the fourth ventricles or directly into the nodular cerebellum via chronically implanted cannulae, the rats displayed intermittent barrel rotation and clonic convulsions. The administration of nicotine into the same areas resulted in prostration, atonia and, occasionally, clonic convulsions. A few days after the nodular cerebellum was lesioned with kainic acid, the motor disturbances resulting from either agent were virtually abolished. Histologic studies revealed that kainic acid had destroyed Purkinje and other large neurons, but had left the granular neurons relatively intact. The administration of procaine into either the fourth ventricles or nodular cerebellum blocked the behavioral responses of either vasopressin or nicotine given into the fourth ventricles. It was concluded that the nodular cerebellum is a primary site for the motor disturbances produced by vasopressin and nicotine.

Animals↗
PubMed1986

Behavior and receptor changes after kainate lesioning of nodular cerebellum.

A study was undertaken on the effects of kainic acid lesioning on the nodulus of the rat cerebellum on behavior and various brain receptors in conscious, freely moving rats. The basis for the study was the observation that barrel rotation and other motor effects induced by intraventricular administration of vasopressin and nicotine could be elicited by their administration into the nodular area of the cerebellum. Histology revealed a marked destruction of Purkinje, stellate, and Golgi cells in the area surrounding the site of kainate administration, with little effect on the granular cells. Immediately after administering 4-12 ng of kainic acid into the nodular cerebellum, rats exhibited circling movements, barrel rotation, and clonic convulsions accompanied by stereotypic head movements, aggressiveness, and gnawing-biting; effects gradually diminishing over 3 days. Receptor binding studies 4-14 days after kainate lesioning revealed a marked increase in 3H-nicotine and 3H-QNB binding in the surrounding cerebellar region, caudate nucleus, and hypothalamus, with no change in 3H-dihydromorphine binding. The findings are consistent with the hypothesis that nicotinic and muscarinic pathways in the vestibular cerebellum, along with its connection to nigrostriatal dopaminergic systems, are involved in the mediation of barrel rotation, ataxia, and other motor disturbances resulting from administration of vasopressin on nicotine intraventricularly.

Animals↗
PubMed1979

Stimulation of gastric secretion by prostaglandin F2 alpha in rats.

In rats with chronic gastric fistulas, prostaglandin F2 alpha stimulated the gastric acid secretion in graded doses of 50, 100, 200 and 400 microgram/kg b.wt, while higher doses above 1 mg/kg b.wt tended to inhibit significantly. The gastric antisecretory effect of prostaglandin E1 could not be altered or modified by subsequent treatment of prostaglandin F2 alpha, while the latter alone without any prior treatment of the former, stimulated output of gastric juice, HCl and pepsin without significantly affecting the concentration of these components.

Animals↗
PubMed1976

Cerebellar contributions to the Papez circuit.

Cerebellar influences on the various substructures in the Papez Circuit are indicated by the following. 1. Anatomical studies indicate that the major midbrain areas to which this circuit projects are : 1) ventral tegmental area; 2) interpeduncular area; and 3) periaqueductal gray areas; and these same areas project back to the limbic system. There are projections to these regions from the cerebellar nuclei, as indicated by terminal degeneration studies which show that cerebellar nuclei connect, mostly by fine fibers, with a continuum of cells located on either side of the midline in the ventral tegmentum of the midbrain. Observations that the cerebellum also projects to the locus ceruleus (NA system) and VTA (DA system) indicate that cerebellar influences can also reach the limbic areas via the catecholamine fiber bundles. 2. Electrophysiological studies indicate that vermiam and fastigial stimulation induce evoked responses in the basolateral amygdala, the hippocampus, and the septum, with latencies to the peak of first wave ranging from 4 to 8 msec and to the second wave of 16-29 msec. Citations from the physiological literature indicate that electrical stimulation of the cerebellum, especially the vermis, can modify a wide range of responses which involve functional activities of either the sympathetic or parasympathetic nervous systems. 3. Studies on electrically induced afterdischarges in the septum, hippocampus, and amygdala indicate that cerebellar stimulation can shorten the duration of or terminate the afterdischarges, and the site of lowest threshold is the midline cortex. Focal cooling of the vermis promotes prolongation of the afterdischarges as does pretreatment of animals with 6-OH dopamine. Chemical lesions in the catecholamine system induced by 6-OH dopamine reduce the effectiveness of the cerebellar stimulation, as do lesions of nucleus fastigii. These data are interpreted to indicate that the cerebellum can exert a tonic suppressor (inhibitory?) influence on substructures within the Papez Circuit. 4. Citations from animal behavioral studies indicate that electrical stimulation of the anterior cerebellum can induce responses such as arousal, predatory attack, and feeding which mimic those obtained by amygdaloid stimulation. Fastigial stimulation can produce drowsiness and EEG changes which resemble the sleep patterns resulting from stimulation of the ventral amygdala.

Afferent Pathways↗
PubMed1975

Cerebellar control of basal forebrain seizures: amygdala and hippocampus.

Electroamygdalagrams and electrohippocampalgrams of the cat and monkey were studied before, during, and after electrically induced afterdischarges. Cerebellar stimulation, particularly of midline cortex, shortened or terminated afterdischarges. Prestimulation of the vermis suppressed afterdischarges for as long as 5 min. Excitation of nucleus fastigii prolonged afterdischarges, and legions of n. fastigii abolished the effects of stimulation of the vermis. Cooling of the vermis prolonged afterdischarges, an effect reversed by warming. Pretreatment with 6-OH dopamine to induce chemical lesions in the catecholamine system reduced the effectiveness of cerebellar stimulation. The findings indicate that the cerebellar cortex can exert a tonic suppressor (inhibitory?) INFLUENCE ON THE AMYgdala and hippocampus by way of n. fastigii. Evoked responses demonstrated cerebellar projection to the amygdala and the hippocampus. The evoked potentials were small with a short latency (4 to 10 msec to peak) and larger with a long latency (20 to 30 msec to peak) wave. Return projection to the cerebellum was shown, the small evoked potential having a latency of 6 to 12 msec and the larger one of 20 to 30 msec.

Amygdala↗