[Effect of dihydrostreptomycin on operant behavior of the rat].
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Animals↗
Biomedical subjects
L Molinengo
Publications and source records attributed to L Molinengo.
[Effect of streptomycin on the operant behavior of the rat].
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Animals↗
Action of arecoline on the levels of acetylcholine, norepinephrine and dopamine in the mouse central nervous system.
Modifications caused by arecoline (2 mg/kg and 10 mg/kg injected subcutaneously) in the levels of acetylcholine (ACh), norepinephrine (NE) and dopamine (DA) in the mouse cortex and "subcortex" were studied. The animals were killed by microwave irradiation of the head 15 minutes after drug administration. Arecoline 10 mg/kg caused a reduction in levels of ACh in the cortex and "subcortex" at the limit of statistical significance (p 5-10%) and a statistically significant reduction in levels on NE. A statistically significant increase in DA was observed only in the cortex after 2 mg/kg and 10 mg/kg of arecoline.
Acetylcholine↗
Action of a chronic administration of mescaline in dynamic behavioural situations.
The modifications of the rat behaviour caused by a chronic administration of mescaline were studied in two schedules of operant conditioning. In the "periodic conditioning" test, the schedule of reinforcement was changed from a fixed ratio to a fixed interval schedule. Mescaline (4 mg/kg/day and 10 mg/kg/day) caused no modification of the ability of the rat to adapt its behaviour to the new experimental situation. In the "reversal test" the contingency for food delivery was switched from one lever, where responses were previously reinforced to the other lever where responses had no programmed consequences. A chronic administration of mescaline (4 mg/kg/day) caused a total incapacity of the rat to switch to the lever which became reinforced in the reversal trial. A chronic administration of 9 mg/kg/day of mescaline had an excitatory effect and the number of reinforced responses in the II and III reversals exceeded the unreinforced responses in a measure greater than in the controls.
Animals↗
Mescaline action on "memory decay" and "problem solving" behavior in the rat.
The modifications of behavior caused in the rat by a chronic oral administration of mescaline have been studied in three experimental situations. In the staircase maze mescaline accelerated the spontaneous decay on the conditioned reflex (memory decay) during the period without daily training. Only the results observed at 30 mg/kg/day of mescaline were statistically significant. In a T maze two lateral alleys closed by two swinging doors, 30 mg/kg/day of mescaline increased the time spent in opening the first door. When the two doors of the lateral alleys were closed with a latch, mescaline 30 mg/kg/day, caused an increase in the time spent by the rat in opening the doors. Mescaline caused an increase in food consumption. The increase at 30 mg/kg/day is statistically significant.
Administration, Oral↗
Dose versus survival time curves in the evaluation of 'prompt' and 'delayed' acute toxicities.
The acute toxicity of arecoline, diisopropylfluorophosphate, nicotine and pilocarpine alone or in association with atropine has been evaluated from percentage lethality and from the linear correlation of (doses/(survival time] vs doses. The experimental points obtained with arecoline and diisopropylfluorophosphate, alone or in association with atropine 50 mg kg-1, are apparently ordered according to two straight lines. That at lower doses gave the LD50 values of the compounds studied. The values found are comparable to those found with percentage lethality. The straight line found at high doses may indicate that over certain doses the drugs kill by a different mechanism. It is concluded that the evaluation of the survival time may be a reliable method in identifying and in evaluating quantitatively the two forms of toxicity.
Animals↗
Action of hypo- and hyperthyroidism on the postmortal decay of acetylcholine in the rat spinal cord.
The postmortal decay of acetylcholine (Ach) was studied in the cervical spinal cords of rats in conditions of hyper- and hypothyroidism. The modifications of thyroid function were achieved either by chronic (20-25 days) administration of l-thyroxine or of methimazole. The basal metabolic rate and plasma T4 concentration were measured to estimate the degree of modification of thyroid activity. The levels of Ach at the start of postmortal decay were evaluated by extrapolation to time 0 of the curves of the postmortal decay of Ach and the levels of Ach at stabilization were estimated from the means of all the measures made at lapses of time over 100-200 s from death. In low and high hypothyroidism a reduction (53 and 72%, respectively) of the levels of Ach was found. A similar effect was found in hyperthyroidism: a 73 and 63% reduction of Ach levels in high and low hyperthyroidism, respectively. The level of Ach at stabilization of the postmortal decay increased only in hyperthyroid rats. The process by which Ach is destroyed is not modified in hyper- or hypothyroidism.
Acetylcholine↗
[Changes in the acetylcholine levels of cervical spinal cord of the rat during general anesthesia].
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Acetylcholine↗
The transition from a fixed ratio to a fixed interval schedule of reinforcement in hypo and hyperthyroid rats.
The modification of behavior caused by hypo and hyperthyroidism were studied when the schedule of reinforcement was changed from a fixed ratio to a fixed interval. The conditions of hypo and hyperthyroidism were obtained with a chronic administration of methimazole and of 1-thyroxine. The level of the modifications of thyroid activity was determined by evaluation of the basal metabolic rate and of the plasma levels of T4. Hyperthyroidism caused no modification of the rat behaviour. A difficulty in adapting to the new experimental situation (learning) was found in hypothyroidism. This effect is evident in high hypothyroidism. In low hypothyroidism a depression of the rat behaviour may interfere with the modification of the learning process.
Animals↗
Postmortal decay of acetylcholine levels in the spinal cord of rat, chicken and frog.
The decay of acetylcholine (ACh) after death of an animal has been estimated in the cervical spinal cord of rat, chicken and frog. The level of ACh in the frog (19.90 nmol/g wet weight) shows no variation from 20 to 500 s after death. In the rat and chicken, there is a decrease in the first 100 s after death to lower values; 4.35 nmol/g wet weight in the rat and 4.60 nmol/g wet weight in the chicken. The levels of ACh in the cervical spinal cord of the rat an chicken at the time of death were estimated by extrapolation to time 0 of the curve of the decay of ACh in the first 100 s. The values obtained were: 121.64 nmol/g wet weight in the chicken and 34.19 nmol/g wet weight in the rat.
Acetylcholine↗
Behavioral interferences modify the acceleration in memory decay caused by diazepam.
A staircase maze has been used to test the modification induced by a chronic administration of different doses of diazepam in the decay of the rat performance caused by an interruption of 20 days in the daily training. The possibility that behavioral interferences modify the diazepam effect has been examined by testing the rat in an open field or in a Y maze during the interruption of the training in the staircase maze. The diazepam effect on the rat behavior in the staircase maze increased linearly with the doses; an intercalated training in the open field increased the diazepam effect, while an intercalated training in a Y maze completely abolished the increase of forgetting caused by diazepam.
Animals↗
Action of antidepressants, stimulants and depressants in the transition from a fixed ratio to a fixed interval schedule of reinforcement.
1. The modifications of rat behaviour caused by imipramine, amitriptyline, doxepin, amphetamine, chlorpromazine, caffeine and diazepam were studied. 2. The schedule of reinforcement was changed from a fixed ratio to a fixed interval schedule. 3. All the studied drugs caused a depression of the rat behaviour but only tricyclic antidepressants and caffeine caused virtually no damage to the ability of the animal to adapt its behaviour to the new experimental situation.
Amitriptyline↗
Action of caffeine, d-amphetamine, diazepam and imipramine in a dynamic behavioural situation.
A study has been made of how the chronic administration of caffeine, d-amphetamine, imipramine and diazepam affect rat behaviour in four successive trials in which the contingency for food delivery was switched from one lever where responses were previously reinforced to the other lever where responses had no programmed consequences (reversal). A complete extinction in the first reversal was obtained with diazepam 0.3 mg/kg/day. Caffeine (6 and 18 mg/kg/day) had no effect in the first reversal and damaged rat performance in the successive reversals. Imipramine (0.6 and 4 mg/kg/day) had the same effect but only in the fourth reversal. Amphetamine (0.16 and 0.7 mg/kg/day) caused a clear damage of rat performance only in the third and fourth reversals.
Animals↗
Drug antagonism studied on frog flexor reflex and on mouse motility.
This study concerns the effects of strychnine and caffeine on ethanol, pentobarbital and atropine-induced depression of mouse motility and of frog spinal reflex. Competitive antagonism was found for the interaction between caffeine and ethanol, caffeine and pentobarbital, strychnine and atropine and strychnine and pentobarbital. The same kind of interaction was found in the mouse motility and in the frog spinal reflex. An attempt is made to interpret the biochemical basis of the competitive antagonisms. The antagonism between strychnine and atropine may be explained taking into account the presynaptic action of atropine and the antagonism between strychnine and pentobarbital is in agreement with a GABAergic action of the barbiturates.
Animals↗
Action of thyroid hormones, diazepam, caffeine and amitriptyline on memory decay ("forgetting").
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Amitriptyline↗
The synergism acetylcholine-eserine in the epinephrine induced ventricular automaticity.
Heart ventricular strips of the rat in Krebs solution were used to test the synergism acetylcholine-eserine. Ventricular automaticity induced by epinephrine 1 10(-6) is inhibited by acetylcholine (a 50% reduction of the automatism is observed with acetylcholine 1,23 10(-8) while four different concentrations of eserine cause an evident potentiation of the effect of acetylcholine (with eserine a 10(-5) the ED50 of acetylcholine is 2,57 10(-14)). It is concluded that the synergism eserine-acetylcholine is a synergism with potentiation and the acetylcholine introduced in the Krebs solution interacts with receptors different from those activated by the acetylcholine which accumulates when cholinesterase is inhibited by eserine.
Acetylcholine↗
Acetylcholine distribution in the spinal cord of the rat.
Spinal cord of male albino rats is cut in four parts: the cervical enlargement (C2-C8) the thoracic cord (T1-T10) the lumbar enlargement (T11-L3) and the sacral extremity (L4-S4). A considerable increase in the acetylcholine levels from the cervical (0,80 g/g +/- 0,15 st.err.) to the sacral section (2,67 g/g +/- 0,48 st.err.) has been observed. It is concluded that the increase of acetylcholine levels in the lower part of spinal cord is the consequence of the relative increase of gray matter at this level.
Acetylcholine↗
The "grasping reflex" in rats with altered thyroid activity.
The "grasping reflex" test was performed in adult rats with altered thyroid function. Any modification of the thyroid activity (hyper or hypothyroidism) caused a prolongation of the grasping time. Our data indicate that the condition of hypo or hyperthyroidism induces behavioural modifications in the adult rats.
Animals↗