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Chronic administration of antidepressant drugs increases the density of cortical [3H]prazosin binding sites in the rat.
Administration of antidepressants (imipramine, citalopram) or antidepressant neuroleptics (levomepromazine, chlorprothixene) for 14-24 days enhanced by 20-30% the density of [3H]prazosin binding sites in the membranes from the cerebral cortex of the rat, without significant change in their affinity.
[Action of chlorpromazine, prochlorpemazine and levomepromazine on the electroencephalogram and behavior of the rabbit].
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Further studies on the accumulation and disappearance of catecholamines formed from tyrosine-14C in mouse brain. Effect of some phenothiazine analogues.
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Drug action on tail shock-induced vocalization in mice and its relevance to analgesia.
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The relationship between the lipophilic nature of tricyclic neuroleptics and antidepressants, and histamine release.
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Effects of levomepromazine, chlorpromazine and their sulfoxides on isolated rat atria.
The effects of levomepromazine, chlorpromazine and their sulfoxides were studied on spontaneously beating and on electrically driven rat atria in vitro. Levomepromazine, chlorpromazine and levomepromazine sulfoxide produced a dose-dependent decrease in the work index of spontaneously beating atria and in the contractile force of electrically driven atria, while chlorpromazine sulfoxide was relatively inactive in these respects. At higher concentrations, levomepromazine sulfoxide caused a pronounced increase in the threshold for electrical stimulation and the effective refractory period. Compared to chlorpromazine, levomepromazine looses less of its cardio-depressive effect through sulfoxidation.
Anticholinergic and cardiodepressive effects of levomepromazine and two of its metabolites on isolated rat atria.
The effects of monodesmethyl levomepromazine on effective refractory period (ERP) threshold for electrical stimulation and contractile force on isolated rat atria were compared to the effects of levomepromazine and levomepromazine sulfoxide. All agents caused an apparently dose-dependent increase in ERP, and antagonized acetylcholine-induced reductions in ERP. Levomepromazine and monodesmethyl levomepromazine decreased excitability and contractile force to a similar extent.
Increase in rat cortical [3H]naloxone binding site density after chronic administration of antidepressant agents.
Given chronically, the first and second generation antidepressants imipramine and citalopram, and antidepressant neuroleptics levomepromazine and chlorprothixene, elevated moderately but significantly (by 15-30%) the density of [3H]naloxone binding sites in rat cerebral cortical membranes. There were only small non-significant changes in Kd values.
Phenothiazine drug metabolites: dopamine D2 receptor, alpha 1- and alpha 2-adrenoceptor binding.
The in vitro binding affinities of levomepromazine, chlorpromazine, fluphenazine, perphenazine and methoxypromazine and their main metabolites to dopamine D2 receptors, alpha 1- and alpha 2-adrenoceptors in rat brain, were examined using [3H]spiperone, [3H]WB 4101 and [3H]yohimbine binding. All compounds had 10-500 times lower affinities to alpha 2-adrenoceptors than to dopamine D2 receptors and alpha 1-adrenoceptors. Ring-hydroxylated and N-demethylated metabolites had relative potencies for dopamine D2 receptor and alpha 1-adrenoceptor binding ranging from 20 to 70%, compared to that of the parent drugs. The ring sulphoxides of levomepromazine, chlorpromazine and perphenazine, except dextro levomepromazine sulphoxide, were virtually inactive in all binding systems. The results indicate that the metabolites having the highest binding affinities for dopamine D2 receptor and alpha 1-adrenoceptor binding may contribute significantly to the therapeutic effect and side-effects of the drugs, and should be measured together with the parent drugs in blood level-effect studies.
Decreased concentration of high density lipoprotein cholesterol in schizophrenic patients treated with phenothiazines.
In chronic schizophrenic patients treated with phenothiazines (Chlorpromazine, Levomepromazine, Perphenazine) for long periods (average = 8 years), high density lipoprotein cholesterol (HDL-C) levels were significantly lower (P less than 0.001) compared with normal controls. The HDL subfractions showed that HDL3-C was significantly low (P less than 0.005) whereas HDL2-C was not. Both serum apo A-I and apo A-II levels were also low (P less than 0.005 and P less than 0.001, respectively) in schizophrenics treated with phenothiazines. The serum triglycerides (TG) level was significantly higher (P less than 0.05) in patients treated with phenothiazines than in controls. No significant differences in total cholesterol (TC), TG and HDL-C were found between users and nonusers of benzodiazepine in schizophrenic patients receiving phenothiazines. In addition to chronic schizophrenic patients, 8 new patients with schizophrenia and related diseases were studied. The serum HDL-C level decreased by 24% within 1 week following administration of phenothiazines. No significant differences were found in TC and TG levels for 10 weeks after initiation of phenothiazine administration.
Antagonism of presynaptic dopamine receptors by phenothiazine drug metabolites.
Electrically evoked release of dopamine from the caudate nucleus is reduced by the dopamine receptor agonists, apomorphine and bromocriptine, and facilitated by neuroleptic drugs, which act as dopamine autoreceptor antagonists. The potencies of chlorpromazine, fluphenazine, levomepromazine and their hydroxy-metabolites in modulating electrically evoked release of dopamine were examined by superfusion of rabbit caudate nucleus slices pre-incubated with 3H-dopamine. O-Desmethyl levomepromazine, 3-hydroxy- and 7-hydroxy metabolites of chlorpromazine and levomepromazine facilitated electrically evoked release of 3H-dopamine, having potencies similar to that of the parent compounds. 7-Hydroxy fluphenazine was less active than fluphenazine in this system. These results indicate that phenolic metabolites of chlorpromazine and levomepromazine, but not of fluphenazine, may contribute to effects of the drugs mediated by presynaptic dopamine receptors.
Tardive dyskinesia: an unrecognized cause of orofacial pain.
Tardive dyskinesia has not previously been discussed in the dental literature. It is a drug-induced movement disorder commonly involving the perioral and masticatory muscles. It can sometimes be a cause of orofacial pain. Two brief cases reports are provided as examples. Clinical features of tardive dyskinesia are presented to assist the dental practitioner in recognizing the syndrome. Suggestions for management are included.
Vasopressin receptor blockade in the anterior hypothalamus suppresses aggression in hamsters.
Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.
Antidepressants and endogenous opioid peptide systems.
The influence of antidepressants on the brain and pituitary content of immunoreactive beta-endorphin (ir-beta E) and dynorphin (ir-DYN) was studied in rats. Chronic administration of the first and second generation antidepressants imipramine, citalopram and rolipram, and of the antidepressant neuroleptics levomepromazine and chlorprothixene elevated the level of ir-beta E in the hypothalamus. Imipramine and levomepromazine also increased the level of ir-DYN in this tissue. Imipramine administered chronically potentiated stress-induced as well as morphine analgesia. The results obtained suggest that chronic antidepressants enhance the brain opioid system activity and increase the sensitivity of opiate receptors.
Effects of zopiclone, flunitrazepam, triazolam and levomepromazine on the transient change in sleep-wake schedule: polygraphic study, and the evaluation of sleep and daytime condition.
1. The effects of zopiclone 10mg (ZP), flunitrazepam 1mg (FN), triazolam 0.25mg (TZ) and levomepromazine 5mg (LP) on two models of sleep-wake schedule change-6 hours advanced shift: (A-shift), and 6 hours delayed: (D-shift)--were investigated in 6 healthy volunteers using polysomnography. 2. In A-shift with placebo, TST, SEI, %SR and REM/NREM decreased. ZP, FN and TZ shortened SL. All drugs increased TST and SEI. TZ and LP increased %SR and REM/NREM. 3. In D-shift with placebo, TST decreased, SWSL was prolonged, %S3+4 decreased, and %SR and REM/NREM increased. All drugs increased TST. ZP and LP shortened SWSL. All drugs increased %SWS. ZP, FN and TZ decreased %SR. ZP and FN decreased REM/NREM. 4. Daytime mental and physical conditions were worse than usual on more than half of the days in A- and D-shift. LP and FN caused some inadequate conditions on the following days. Significantly higher REM/NREM was observed in the nights before the days with worse mental conditions in D-shift, and lower REM/NREM in the nights before the days with worse physical conditions in A-shift. 5. It is concluded that TZ and ZP are superior to the others for A-shift and D-shift, respectively.
Time-dependent influence of some sedating agents on basic haematological values in various artio- and perissodactylids.
Basic haematological values in 32 animals of five species were estimated after administration of sedating agents. In all species under investigation, a time-dependent decrease of erythrocyte counts, haematocrit values and haemoglobin content was noted during the first 30 min after sedation, for the following 30 min the lowered values remained essentially without any change in zebras. Derived parameters, mean corpuscular haemoglobin, mean corpuscular Hb concentration and mean corpuscular volume did not change during the period of observation. Only insignificant changes in leukocyte count and in the proportion of lymphocytes and neutrophiles were registered. The shortest possible time between sedation and blood sampling is recommended to minimalize a distortion especially in the red blood picture.
Pain infirmity and psychotropic drugs in oncology.
The treatment of cancer pain by psychotropic drugs is a method which has been employed for a long time [8] and in which the results obtained have appeared very interesting from the beginning: there is a high percentage of success, rapid action, absence of addiction, and although there are sometimes unpleasant side-effects, they are reversible when the treatment is stopped. Even after several years of application, this therapy still sets some unsolved problems. Some consider that psychotropics are not real analgesics, but that they work on the emotional reaction rather than on the pain itself [3]. Still others consider that the results are obtained only at the price of a state of prostration of the patient similar to that obtained after lobectomy. Finally, this procedure is reproached as having unpredictable results and indications difficult to define. We think that what has, up to now, prevented these types of problems from being solved has been the absence of a really objective evaluation of the pain in the patients observed. We have wrestled with this problem for several years [1,2], and offer the following hypothesis: what is important in considering chronic pain is, above all, the infirmity conferred upon the patient. If "pain" in the broad sense of the term lends itself to objective evaluation with difficulty, it is not the same with respect to infirmity. A method of evaluation of the physical disability intended for routine practice in a cancer center has been used on a series of 100 patients. The results obtained in this series have been analyzed and give the answer to questions such as mechanism of action, indications of psychotropic drugs and prognosis of cancer pain.