Lappuse 1 no 19 rezultātiem
Harmaline and other beta-carbolines act as an inverse agonist for GABA-A receptors and cause central nervous system stimulation and anxiety; thus, it may act hypothetically as a potential seizure augmenter. To examine the hypothesis, the effect of harmaline during the seizures induced The present behavioral study was undertaken to investigate whether neuronal nitric oxide (NO) synthase mediates the abnormal consequences of increased NMDA receptor-mediated synaptic transmission in models of postural tremor, Parkinson's disease and epilepsy. We used 7-nitroindazole, a selective
Cerebrovascular permeability to protein (CVP-p) was assessed in rats following the systemic injection of either kainic acid (KA) or harmaline. The extravasation of a foreign (horseradish peroxidase, HRP) or an endogenous (rat immunoglobulin G, IgG) tracer protein was determined using
The benzodiazepine antagonists Ro 15-1788 and CGS 8216 blocked the clonic and tonic convulsions elicited by 3-carbomethoxy-beta-carboline (beta-CCM). The PD50 values for Ro 15-1788, CGS 8216, and diazepam were: 2.0, 0.6, and 2.0 mg/kg, respectively. Neither Ro 15-1788 nor CGS 8216 potentiated the
The neuropharmacologic profile of harmala alkaloids has been studied and found to have central effects like convulsions, catalepsy, or altered startle response. In number of studies the effects of diazepam, on harmaline and other beta carboline containing compounds-induced tremors were investigated.
Increased CNS activity in the form of electrically or chemically induced seizures is known to alter the properties of GABA(A) receptors. The tremorgen, harmaline, causes a bursting pattern of activity in inferior olivary neurons, the effects of which are transmitted throughout the olivocerebellar
Several lines of clinical evidence suggest that myoclonus is caused by a reduction of serotonin in the brain and hyperactivity of the inferior olive. We determined whether a change in serotonin content within the olivocerebellar system accompanied a predisposition to myoclonus and investigated the
Compounds from both the beta-carboline (BC) and xanthine groups have been suggested to be the natural ligands for benzodiazepine (BZ) receptors. In this study we examined the effects of several BC's and caffeine, 1,3,7-trimethylxanthine, on the binding of 3H-flunitrazepam (3H-FZ) and
Harmaline, an alcaloid of Paganum Armala, induces tremors of central origin and increases cerebellar cGMP without affecting cortical and cerebellar prostaglandin levels. 16(S)-16-methyl PGE2 protects the animals against the seizures induced by the alcaloid and prevents the concomitant rise in
Tofizopam, an anxiolytic 3,4-benzodiazepine, increases the affinity of benzodiazepine receptors for 1,4-benzodiazepines. In this study we investigated whether this increased affinity of the receptors alters the sensitivity of mice to tremor and to convulsions. Convulsions induced by harmane were not
The neuropharmacologic profile of intraperitoneally injected harmala alkaloids and related beta-carbolines was evaluated in the rat. All drugs induced central effects (convulsions, catalepsy, or altered startle), but only harmaline and harmine were tremorogenic at low doses. Methoxylation of the
MDL 105,519, (E)-3-(2-phenyl-2-carboxyethenyl)-4,6-dichloro-1 H-indole-2-carboxylic acid, is a potent and selective inhibitor of [3H]glycine binding to the NMDA receptor. MDL 105,519 inhibits NMDA (N-methyl-D-aspartate)-dependent responses including elevations of
CGS 19755 (cis-4-phosphonomethyl-2-piperidine carboxylic acid) was found to be a potent, stereospecific inhibitor of N-methyl-D-aspartate (NMDA)-evoked, but not KCl-evoked, [3H] acetylcholine release from slices of the rat striatum. The concentration-response curve to NMDA was shifted to the right
The N-Methyl-D-aspartate (NMDA)-type receptor blocking properties of CGS 19755, a novel, rigid analog of 2-amino-5-phosphonopentanoate, were demonstrated in vitro by the ability of the compound to block NMDA-evoked [3H]acetylcholine release (pA2 = 5.93). CGS 19755 (0.045 and 0.224 mmol/kg i.p.) was
Excessive release of glutamate, a potent excitatory neurotransmitter, is thought to play an important role in a variety of acute and chronic neurological disorders, suggesting that excitatory amino acid antagonists may have broad therapeutic potential in neurology. Here, we describe the synthesis,