Effects Of Neurotropic Drugs Research Articles

Effect of neurotropic drugs in movement stopping in health and disease

Background: Number of disorders slows the ability of movement-stopping. Estimation of movement-stopping is possible through - Stop Signal Reaction Time (SSRT). The effect of neurotropic drugs on SSRT is elusive till now.

Quantitative imaging of neuroreceptors in the living human brain

Positron emission tomography (PET) makes it possible for the first time to examine in living humans the chemistry of the brain, which relates the structures of the brain to the functions of the mind. PET scans make it possible to assess the state of neurotransmitter receptors, such as the dopamine, serotonin, muscarinic cholinergic, opiate, and benzodiazepine receptors, in different regions in normal persons and patients with neuropsychiatric diseases. One of the most striking findings to date is that dopamine receptors fall significantly between the ages of 19 and 73 years, to a greater degree in men than in women. The effects of neurotropic drugs, such as haloperidol and methadone, can be assessed in an individual patient, providing for the first time an objective indicator of the specific desired effects of such drugs in the treatment of nervous or mental disease. Studies of patients with diseases such as Parkinson's disease, Huntington's disease, Alzheimer's disease, bipolar disease, and schizophrenia are in progress. At present, the patients are being examined as part of research protocols, but it is likely that clinical trials will not be far off.

Effect of neurotropic drugs on sleep disturbance caused by electrical stimulation of the hypothalamus in cats

A state of stress induced in cats by electrical stimulation of the hypothalamus was shown to reduce the total duration of sleep at the expense of its paradoxical phase. Haloperidol (1, 2, or 3 mg/kg), diazepam (0.5 or 1 mg/kg), nitrazepam (1 or 6 mg/kg), Noxyron (glutethimide) (10, 30, and 60 mg/kg), and pentobarbital (5, 15, and 30 mg/kg) did not restore the structure of sleep when disturbed by stress, and lithium hydroxybutyrate (100 and 150 mg/kg), dimedrol (diphenhydramine) (1, 5, and 6 mg/kg), and imipramine (1, 3, and 6 mg/kg) increased the total duration of sleep on account of the slow-wave phase. Sodium hydroxybutyrate (100 mg/kg) restored the normal electrophysiological pattern of sleep, reduced the latent period, and increased the total duration and number of episodes of the paradoxical phase, and also reduced the number of awakenings.

Effects of neurotropic drugs on hypothalamic self-stimulation

Imipromine-like antidepressants (10(-7)--10(-5) M) significantly inhibited the uptake of serotonin by the human blood platelets. Among the neuroleptics haloperidol alone depressed the uptake of serotonin in the concentration of 10(-5) M. Amphetamine and cholinolytics failed to affect the uptake of serotonin even in a concentration of 10(-4) M. The data obtained supported the hypothesis on mediation of the thymoanaleptic action through the intensification of the central serotoninergic processes. Serotonin uptake by the human blood platelets can be used for screening the antidepressants.

Effect of neurotropic drugs on motor hyperactivity induced in dogs by benactyzine

Quantitative recording of motor activity in dogs showed that benactyzine (2 mg/kg intramuscularly) led to an increase in this activity which persisted for 2–3 h. The effect of benactyzine was abolished by intramuscular injection of galanthamine in a dose of 3 mg/kg. The most effective of the neuroleptics and tranquilizers studied was perphenazine. Chlorpromazine and diazepam not only did not abolish the hyperactivity induced by benactyzine, but they also caused the animals' condition to worsen. A further increase in hyperactivity was observed after diazepam and haloperidol. Levomepromazine abolished hyperactivity in some animals but potentiated other symptoms induced by benactyzine. It is postulated that motor hyperactivity produced by benactyzine is connected with anticholinergic mechanisms; the use of the drug for blocking the action of neuroleptics with marked cholinolytic properties is thus contraindicated.

Effects of neuropharmacological agents on in vitro formation of complexes between nucleic acids and proteins

Effects of neurotropic drugs on the formation of sodium dodecyl sulphate (SDS)—insoluble complexes between proteins and nucleic acids were investigated. Several drugs interfered with this reaction, either increasing or decreasing the final yield. Certain regularities in the interference patterns were observed. The neuropharmacological agents were found to inhibit binding of DNA to methyl-esterified bovine serum albumin (MBSA) and RNA to calf thymus histone. The less toxic drugs tend to be active predominantly under conditions when the compound is pre-incubated with either the protein or the nucleic acid tested. While the relevance of the observed phenomena to the in vivo effects remains to be established, the available data suggest that this simple and reproducible technique may be utilized for drug screening.

Control of synthesis and release of radioactive acetylcholine in brain slices from the rat. Effects of neurotropic drugs

1. Studies of the synthesis and release of radioactive acetylcholine in rat brain-cortex slices incubated in Locke-bicarbonate-[U-(14)C]glucose media, containing paraoxon as cholinesterase inhibitor, revealed the following phenomena: (a) dependence of K(+)-or protoveratrine-stimulated acetylcholine synthesis and release on the presence of Na(+) and Ca(2+) in the incubation medium, (b) enhanced release of radioactive acetylcholine by substances that promote depolarization at the nerve cell membrane (e.g. high K(+), ouabain, protoveratrine, sodium l-glutamate, high concentration of acetylcholine), (c) failure of acetylcholine synthesis to keep pace with acetylcholine release under certain conditions (e.g. the presence of ouabain or lack of Na(+)). 2. Stimulation by K(+) of radioactive acetylcholine synthesis was directly proportional to the external concentration of Na(+), but some synthesis and release of radioactive acetylcholine occurred in the absence of Na(+) as well as in the absence of Ca(2+). 3. The Na(+) dependence of K(+)-stimulated acetylcholine synthesis was partly due to suppression of choline transport, as addition of small concentrations of choline partly neutralized the effect of Na(+) lack, and partly due to the suppression of the activity of the Na(+) pump. 4. Protoveratrine caused a greatly increased release of radioactive acetylcholine without stimulating total radioactive acetylcholine synthesis. Protoveratrine was ineffective in the absence of Ca(2+) from the incubation medium. It completely blocked K(+) stimulation of acetylcholine synthesis and release. 5. Tetrodotoxin abolished the effects of protoveratrine on acetylcholine release. It had blocking effects (partial or complete) on the action of high K(+), sodium l-glutamate and lack of Ca(2+) on acetylcholine synthesis and release. 6. Unlabelled exogenous acetylcholine did not diminish the content of labelled tissue acetylcholine, derived from labelled glucose, suggesting that no exchange with vesicular acetylcholine took place. In the presence of 4mm-KCl it caused some increase in the release of labelled acetylcholine. 7. The barbiturates (Amytal, pentothal), whilst having no significant effects on labelled acetylcholine synthesis in unstimulated brain except at high concentration (1mm), diminished or abolished (at 0.25 or 0.5mm) the enhanced release of acetylcholine, due to high K(+) or lack of Ca(2+). The fall in tissue content of acetylcholine, due to lack of Ca(2+), was diminished or abolished by pentothal (0.25 or 0.5mm) or Amytal (0.25mm).

Effect of neurotropic drugs on cortical evoked potentials

In acute experiments on unanesthetized, curarized cats and rabbits and also on animals anesthetized with chloralose, recordings were made of direct cortical and transcallosal responses, responses in the pyramids of the medulla to peripheral stimulation and stimulation of the motor cortex, primary responses in area S-I, and interzonal somatomotor responses. The effect of narcotics on these cortical responses was shown to persist under conditions partially or completely excluding effects mediated through the reticular formation and other subcortical structures (intracarotid injection of the drugs or their local application to the cortex, experiments after premesencephalic section or on the isolated cortex). Neuroleptics have only a slight effect on these cortical evoked responses, mainly due to their blocking action on the reticular formation. Tranquilizers of the benzodiazepine series are active against the cortical responses studied, and this effect is due to their direct action on the cortex.

Effects of neurotropic drugs on lannate and atropine toxicity in the western spruce budworm, Choristoneura occidentalis (Lepidoptera: Tortricidae)

By treating sixth instar western spruce budworm with drugs known to alter cholinergic or aminergic neurotransmission in vertebrates, the toxicity of sublethal Lannate and atropine could be abolished or enhanced. Balance between acetylcholine and 5-hydroxytryptamine appeared to be more important than their absolute concentrations. Toxicity effects were maximal under conditions favoring elevation of one of these transmitters and reduction of the other. No toxic effects occurred under conditions favoring the elevation or reduction of both transmitters.

Effect of neurotropic drugs on nucleic acid content of glial and nerve cells in tissue culture and on neuroglial motor activity

Effect of neurotropic drugs on nucleic acid content of glial and nerve cells in tissue culture and on neuroglial motor activity

Effect of neurotropic drugs on the early signs of neurogenic trophic disturbances in the stomach wall

Effect of neurotropic drugs on the early signs of neurogenic trophic disturbances in the stomach wall

Effects of neurotropic drugs on glucose metabolism in rat brain in vivo

The effects of centrally-active drugs on the incorporation of 14C from glucose into rat brain α-keto acids and amino acids were tested in vivo. Chlorpromazine lowered the incorporation into all metabolites tested and nembutal into all except alanine and pyruvate. Morphine lowered the radioactivity of the isolated γ-aminobutyrate and aspartate. No significant effects were observed after treatment with the stimulants iproniazid or amphetamine.

Neurotropic drugs, electroshock, and carbohydrate metabolism in the rat

The effects of neurotropic drugs on the alterations of blood sugar, lactate, and tissue glycogen levels in relation to blood serotonin level in rats were investigated. Among the drugs employed here, chlorpromazine and chlordiazepoxide were found to increase blood sugar and lactate and to deplete liver glycogen levels in intact rat when administered i.p. On the other hand, in electroshock, hypoglycemia, hyperlactacidemia, and liver glycogen depletion were observed in both intact and adrenodemdullated rats. These changes in electroshock were, to some extent, prevented by the treatment of chlorpromazine and chlordiazepoxide. Electroshock increased the serotonin level in the whole blood of rats and serotonin caused hyperlactacidemia and liver glycogen depletion.

126b Contribution to the study of cerebral maturation in animals. Effect of neurotropic drugs

126b Contribution to the study of cerebral maturation in animals. Effect of neurotropic drugs

Effects of neurotropic drugs and cerebellar impulses on cortically stimulated phasic and tonic muscular activity

Investigations were performed on awake cats and rats to study: the type of muscular response to trains of stimuli applied on the motor area at a frequency of 1 to 30 per second; and the influence exerted on this response by iterative stimulation of the paleocerebellum as well as by certain drugs depressing the central nervous system (chloralose, Luminal, chlorpromazine). Cortical stimulation at 1 to 6 per second induced only clonus synchronous with stimulation rhythm, without changing myographic background level. The electromyogram after four to ten stimuli revealed a low-voltage asynchronous tonic activity following each clonic discharge during a period of 100 to 500 msec. At frequencies between 6 and 15 per second, this tonic activity changed the background trace of the myogram, clonus being superimposed on a sustained muscular contraction. The drugs in subanesthetic doses strongly depress tonic without affecting clonic activity. Muscular response consequently maintained its clonic aspect, synchronous with stimulation rhythm up to a frequency of 25 or 30 per second. Iterative stimulation of the paleocerebellum with subliminal stimuli, when simultaneous with cortical stimulation, induced a strong inhibition of clonic, as well as tonic components of muscular response. When cortical stimulation was applied 1 to 50 sec after arresting cerebellar stimulation an important facilitation of muscular response occurred, particularly affecting its tonic component.

The Effects of Neurotropic Drugs Upon the Electrical Activity of the Midbrain Tegmentum

The Effects of Neurotropic Drugs Upon the Electrical Activity of the Midbrain Tegmentum