Search PubMed⌕ Search

Biomedical subjects

S Yehuda

Publications and source records attributed to S Yehuda.

At least 73 records · Page 4Linked to original sources
PubMed1981

Iron deficiency-induced circadian rhythm reversal of dopaminergic-mediated behaviours and thermoregulation in rats.

An iron-free diet for 28 days caused a reduced level of iron in the blood. Iron deficient rats exhibited a lower level of motor activity and reversed circadian rhythms of thermoregulation and motor activity. The hypothermic effect of d-amphetamine was significantly reduced in iron deficient rats, and the magnitude of this effect was correlated with the decrease in the blood and brain. The hypermotility effect of d-amphetamine was also significantly reduced. Apomorphine-induced stereotyped behaviour was greater during the light period in contrast to that of control rats. The results of this study indicate that iron plays a major role in the normal function of the monoaminergic system in the brain, particularly in the dopaminergic system, via modification of dopaminergic receptors.

Animals↗
PubMed1981

Effects of TRH and PS-24 on colonic temperature and motor activity of rats: possible role of dopamine.

TRH and PS-24 (a TRH peptidase resistant analogue) induce different effects on body temperature and motor activity in rats kept at 4 degrees C. PS-24 induced hypothermia, but TRH did not. PS-24 induced hypermotility, while TRH induced slight hypomotility. The thermal effect of TRH in hypophysectomized rats was similar to its effect in control intact rats, but PS-24 induced marked hypothermia in hypophysectomized rats. While TRH partially blocked d-amphetamine-induced hypothermia, PS-24 induced marked hypothermia in hypophysectomized rats. While TRH partially blocked d-amphetamine-induced hypothermia were blocked in olfactory tubercle-lesioned rats. The data indicate that the thermal effects of PS-24 are mediated by the dopaminergic neurons in the nucleus accumbens and are reversible by pretreatment with haloperidol in hypophysectomized rats. In addition, no correlation between the effects of the treatments on thermoregulation and motor activity was found.

Animals↗
PubMed1981

Vasoconstriction and d-amphetamine-induced hypothermia.

The hypothermic effect of d-amphetamine was investigated in rats in which vasoconstriction or vasodilation was induced by pharmacological agents: aramine as vasoconstrictor and neprasol as vasodilator. The d-amphetamine-induced hypothermia was enhanced by both drugs among rats kept at 4 degrees C, and both drugs were unable to modify the d-amphetamine-induced hypothermia. These results indicate that although vasoconstriction and vasodilation play a major role in thermoregulation, d-amphetamine-induced hypothermia is not mediated peripherally by vasoconstriction. Since changes in basal metabolic rate, motor activity, food intake and vasoconstriction are not the peripheral mechanisms by which d-amphetamine induced hypothermia, the mechanisms is still unknown.

Animals↗
PubMed1981

Physiological evidence (hypothermia) for central effects of beta-blocker agents.

In recent studies carried out during the last decade, it has been found that beta-blocker agents have many central effects. These findings raise the question how beta-blocker agents act when they influence central effects. In spite of intensive research efforts on this subject, no answer has been offered so far. Several studies indicate that the effect of beta-blocker agents on the dopaminergic receptors in the brain is very similar to their effect on beta-adrenergic receptors. In a set of experiments we checked the effect of two beta-blocker agents: oxprenolol and dl-propranolol, and the effect of d-propranolol on hypothermia induced by d-amphetamine and apomorphine at an ambient temperature of 4 degrees C. It was found that the two beta-blockers and the d-propranolol significantly potentiated the effect of hypothermia induced by d-amphetamine and apomorphine, an effect which is mediated by the central dopaminergic system. However, the activity of the beta-blockers was agonistic. Furthermore, the influence of d-propranolol on hypothermia shows that this dopaminergic agonistic activity of the beta-blockers is not related to peripheral or central beta-receptor blockage.

Animals↗
PubMed1981

Effects of d-amphetamine on colonic and skin temperatures of rats kept at various ambient temperatures.

d-Amphetamine-treated rats (15 mg/kg) were compared with untreated controls at various ambient temperatures. Colonic and skin temperatures were recorded and their ratio analyzed as a function of ambient temperature. The interaction of the peripheral receptor system (skin) with the central thermoregulatory mechanisms is discussed. The possible utility of this index as a simpler expression of the functional relationship which neither requires nor contradicts the concept of a "set point" is proposed.

Animals↗
PubMed1981

Personality type, life events and sudden cerebrovascular attack.

The severity of cerebrovascular attack (CVA) in patients having no known history of cardiovascular problems tends to be influenced by two factors: (a) recent life events; and (b) "type A" personality. It was found that the higher the frequency of life events reported by the CVA patients, the more severe were the CVAs. The percentage of CVA patients having no known history of cardiovascular disorders who were of type A personality was much higher among the more severe CVA patients. The results of this study indicate the importance of these factors in precipitating CVA.

Cerebrovascular Disorders↗
PubMed1981

Increased serotonin level via augmented tryptophan diet and its effect on escape learning.

Brain serotonin level was increased by supplementing the diet in two groups of rats. They were first exposed to conditions of shock, either escapable or inescapable. They were then placed in a cool water bath, and the response latency to successful escape was noted. Two other groups fed normal diets were similarly examined. Tryptophan effects of hypothermia were shown to interact with the analgesic effects of serotonin and to the tolerance of the noxious water bath. The results are discussed in relation to brain serotonin effects on escape following shock pretreatment ("learned helplessness") and its relevance to clinical depression.

Animals↗
PubMed1981

A comparison of the hypothermic effects of methylphenidate and d-amphetamine.

Methylphenidate is a central nervous system stimulant with a spectrum of action similar to the effects of d-amphetamine. d-Amphetamine-induced hypothermia is mediated via release of dopamine in the DA mesolimbic pathway. Methylphenidate causes hypothermia among rats kept at 4 degrees C, but d-amphetamine is twice as potent as methylphenidate. Dose-response relationship of methylphenidate thermal effects exhibits a U-shape curve. The hypothermic effects of 5-15 mg/kg methylphenidate are mediated by central dopaminergic neurons, as pretreatment with haloperidol inhibits these effects. The hypothermia produced by larger doses of methylphenidate is not blocked by pretreatment with haloperidol and hypothermia induced by d-amphetamine is blocked by pretreatment with haloperidol.

Animals↗
PubMed1980

Thermoregulatory and locomotor effects of DSIP: paradoxical interaction with d-amphetamine.

A low dose (0.1 mg/kg) of peripherally administered delta sleep-inducing peptide (DSIP) caused hypothermia in rats maintained at 4 degrees C but larger doses (1.0 or 3.0 mg/kg) did not. At 22 degrees C all 3 doses of DSIP caused hyperthermia. The interaction of d-amphetamine with DSIP was dependent on ambient temperature; at 4 degrees C DSIP had no effect on d-amphetamine-induced hypothermia, but at 22 degrees C DSIP reversed the usual d-amphetamine-induced effect of hyperthermia to hypothermia. At 4 degrees C, DSIP also potentiated the hypermotility effects of d-amphetamine but blocked it at 22 degrees C. Many rats receiving DSIP (0.1 mg/kg) and d-amphetamine (15.0 mg/kg) at 22 degrees C paradoxically exhibited what appeared to be sleep. This sleep-like effect was not found after several other doses of DSIP and d-amphetamine, chlorpromazine, or at a cold ambient temperature. Sodium methohexital caused apparent sleep in animals treated with DSIP alone or with DSIP and d-amphetamine, but was unable to induce this effect in rats receiving d-amphetamine alone. The results suggest that the effects of peripherally injected DSIP on body temperature are independent from its effects on locomotion and that both effects are dependent upon ambient temperature.

Animals↗
PubMed1980

Peptides and thermoregulation.

Several peptides are now known to affect thermoregulation. These include beta-endorphin, bombesin, MIF-I, alpha-MSH, neurotensin, TRH, and DSIP. Some of these have been found to interact with the thermal effects of d-amphetamine, a drug with well established actions on thermoregulation. The effects of morphine on body temperature provide some notable comparisons with beta-endorphin, as do the similarities between the effects of naloxone and MIF-I. In general, it seems that two of the major variables which interact and modify the thermal effects of peptides are ambient temperature and route of administration.

Animals↗
PubMed1980

Interaction of MIF-I or alpha-MSH with D-amphetamine or chlorpromazine on thermoregulation and motor activity of rats maintained at different ambient temperatures.

Administration of several doses of MIF-I or alpha-MSH did not modify colonic temperature or the level of motor activity of rats in ambient temperatures of 4 degree or 20 degrees C. However, the thermoregulatory but not motor effects of the interaction between MIF-I or alpha-MSH with d-amphetamine were dependent upon ambient temperature. At 4 degree C, 1.0 mg/kg of both peptides enhanced the d-amphetamine-induced hypothermia, but at 20 degrees C both peptides blocked the hyperthermic effects of d-amphetamine. The hypothermic effect of chlorpromazine (CPZ) at 4 degree C and 20 degrees C was blocked by 1.0 mg/kg MIF-I but not by 1.0 mg/kg alpha-MSH. No linear dose response relationships between various doses of MIF-I or alpha-MSH and thermal responses were found. Administration of melanin or the use of hypophysectomized rats did not alter the significant interactions observed after peripheral injections.

Animals↗
PubMed1980

D-Amphetamine-induced hypothermia and hypermotility in rats: changes after systemic administration of beta-endorphin.

Systemically administered beta-endorphin was tested in rats for its ability to modify the hypothermia and hypermotility induced by d-amphetamine. Colonic temperature and motor activity were measured in a cold (4 degrees C) ambient temperature in animals given IP injections of beta-endorphin (0.1, 1.0 or 3.0 mg/kg), naloxone (10 mg/kg), or morphine (30 mg/kg). The same measurements were taken in animals given beta-endorphin (1.0 mg/kg) in combination with naloxone or saline pretreatment and d-amphetamine (15 mg/kg) or saline post-treatment. Morphine alone had a biphasic effect on thermoregulation, but did not affect d-amphetamine-induced hypothermia. Activity scores were decreased by morphine, in both d-amphetamine and saline treated animals. The thermal response of rats to beta-endorphin alone was variable, depending on dosage, but all 3 dosages partially blocked the hypothermic effect of d-amphetamine. Naloxone blocked the thermal effects of both beta-endorphin and d-amphetamine. Motor activity tended to be decreased by naloxone, regardless of amphetamine treatment, but beta-endorphin tended to increase activity in amphetamine-treated animals and reduce it in saline-treated controls. In their action on both thermoregulation and activity, naloxone and beta-endorphin appeared to interact independently with d-amphetamine, often producing effects in the same direction, but in combination, they tended to be mutually inhibitory.

Animals↗
PubMed1980

Antagonistic actions of MIF-I on the hypothermia and hypomotility induced by beta-endorphin or morphine.

Recently it has been suggested that MIF-I can act as an opiate antagonist for analgesia. Therefore, rats kept at 4 degrees C were pretreated with MIF-I in an attempt to extend the observation to a nonanalgesic opiate effect by determining any blockade of the thermal response to beta-endorphin and morphine. MIF-I, at an ip dose of 1.0 mg/kg, was found to block the thermal responses to beta-endorphin injected ip at doses of 0.1 and 1.0 mg/kg. A lower dose (0.1 mg/kg, ip) of MIF-I, or naloxone (10 mg/kg), was also able to block the thermal effects of 30 and 60 mg/kg doses of morphine. However, an ip dose of 1.0 mg/kg MIF-I potentiated the hypothermic effects of morphine but, like naloxone, reduced the magnitude of the decrease in the level of motor activity induced by beta-endorphin or by morphine. The results of this study demonstrate a nonanalgesic situation in which MIF-I can act as an antagonist of opiate effects after peripheral injection.

Animals↗
PubMed1980

Chronic lithium treatment and dopamine-mediated behavior.

The effect of 3--4 weeks of chronic lithium (Li) treatment in food on amphetamine-induced stereotypy, hyperactivity, and hypothermia was examined. The long-term Li treatment failed to inhibit these behaviors and even resulted in small but statistically significant potentiation of stereotypy and hypothermia. The absence of an inhibitory effect of Le on these dopaminergic processes is consistent with Li's lack of antischizophrenic properties. Previous studies reporting conflicting results, including lithium inhibition of amphetamine-induced hyperactivity, used acute or very short-term lithium administration and/or did not verify serum lithium levels to be at therapeutically equivalent levels.

Animals↗
PubMed1979

Clomipramine and amitriptyline in the treatment of severe pain.

Clomipramine is the most potent 5-HT reuptake blockade agent among the antidepressants. A comparison between the effect of clomipramine and a less powerful 5-HT reuptake blockade agent (amitriptyline) could test the hypothesis that brain 5-HT is a mediator of pain sensation. Groups of patients of either sex, with pain indication of trigeminal neuralgia, tension headache or postherpatic neuralgia, received doses of clomipramine or amitriptyline in a single blind clinical experiment. The results after three months of treatment showed that clomipramine: (1) was better than amitriptyline in treating trigeminal neuralgia; (2) tended to be better in the treatment of tension headache; and (3) amitriptyline is better in treating postherpatic neuralgia. Clomipramine was better tolerated. The results support the hypothesis that in certain pain situations, clomipramine exerts a beneficial effect, not only because of its effect on the depression and anxiety level of the patient, but also via its effects on the 5-HT brain system.

Adult↗
PubMed1979

Habituation and transfer during sleep in cats.

In order to test the concept of "sleep learning", cats were exposed to habituation treatment of auditory stimuli during different stages of the sleep-waking cycle. While it was possible to demonstrate that habituation to an auditory stimulus can take place in paradoxical sleep (PS) and slow-wave sleep (SWS) as well as during periods of wakefulness, it was not always possible to demonstrate a transfer of habituation from the training period to other periods. A complete transfer of habituation occurred between the two sleep periods (PS and SWS); a partial transfer of habituation occurred between the waking period and both of the two sleep stages (PS and SWS), but only a minimal transfer of habituation was found between any one of the sleep stages and the waking period. When the cats were able to transfer the habituation, they also were able to discriminate between the habituating tone and a novel tone. The findings that only minimal transfer of habituation could occur between each of the sleep stages and the waking period do not lend support to the concept of "sleep learning".

Animals↗