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PubMed1988

Binding of organic cations to brush border membrane from rat small intestine.

The binding of six organic cations (chlorpromazine, promethazine, imipramine, diphenhydramine, methochlorpromazine and propantheline) to the brush border membrane isolated from rat small intestine has been investigated. The cations were bound to the membrane to varying extents, the order of binding being chlorpromazine greater than promethazine greater than methochlorpromazine greater than imipramine greater than propantheline greater than diphenhydramine. There was no relation between binding and the chloroform-water partition coefficient. Chlorpromazine binding was significantly decreased in the presence of imipramine, methochlorpromazine and propantheline. Anionic compounds (indomethacin and xanthene-9-carboxylic acid) did not affect chlorpromazine binding. High and low affinity binding of the cations to the intestinal brush border membrane was demonstrated with Scatchard plots and Hill plots. Imipramine and methochlorpromazine inhibited chlorpromazine binding at both binding sites. From the results, it was suggested that the organic cations tested were specifically bound to common binding sites on the brush border membrane.

Animals↗
PubMed2002

In vitro increase in chloroquine accumulation induced by dihydroethano- and ethenoanthracene derivatives in Plasmodium falciparum-parasitized erythrocytes.

The effects of a series of dihydroethano- and ethenoanthracene derivatives on chloroquine (CQ) accumulation in CQ-susceptible strain 3D7 and CQ-resistant clone W2 were assessed. The levels of CQ accumulation increased little or none in CQ-susceptible strain 3D7 and generally increased markedly in CQ-resistant strain W2. At 10 microM, 28 compounds yielded cellular accumulation ratios (CARs) greater than that observed with CQ alone in W2. At 10 microM, in strain W2, 21 of 31 compounds had CQ CARs two or more times higher than that of CQ alone, 15 of 31 compounds had CQ CARs three or more times higher than that of CQ alone, 13 of 31 compounds had CQ CARs four or more times higher than that of CQ alone, and 9 of 31 compounds had CQ CARs five or more times higher than that of CQ alone. At 1 microM, 17 of 31 compounds had CQ CARs two or more times higher than that of CQ alone, 12 of 31 compounds had CQ CARs three or more times higher than that of CQ alone, 6 of 31 compounds had CQ CARs four or more times higher than that of CQ alone, and 3 of 31 compounds had CQ CARs five or more times higher than that of CQ alone. At 1 microM, 17 of 31 compounds were more potent inducers of CQ accumulation than verapamil and 12 of 31 compounds were more potent inducers of CQ accumulation than promethazine. The nature of the basic group seems to be associated with increases in the levels of CQ accumulation. At 1 and 10 microM, 10 of 14 and 13 of 14 compounds with amino group (amines and diamines), respectively, had CARs >or=3, while at 1 and 10 microM, only 1 of the 13 derivatives with amido groups had CARs >or=3. Among 12 of the 31 compounds which were more active inducers of CQ accumulation than promethazine at 1 microM, 10 had amino groups and 1 had an amido group.

Animals↗
PubMed1978

Factors influencing jaundice in immigrant Greek infants.

A study of 887 consecutively born immigrant Greek and 220 Anglo-Saxon Australian infants has shown that serum bilirubin concentrations are influenced by these factors: breast feeding, delivery with forceps, gestation, birthweight, sex of the infant, presence of hypoxia, presence of blood group incompatibility, a positive direct Coombs's test, maternal sepis, and administration to the mother of promethazine hydrochloride, reserpine, chloral hydrate, barbiturates, narcotic agents, diazepam, oxytocin, aspirin, and phenytoin sodium. Apart from the administration of promethazine hydrochloride, reserpine, chloral hydrate, and quinalbarbitone sodium, only two factors, breast feeding and delivery by forceps, occured with different frequencies in the immigrant Greek and the Australian infants. Among the Greek infants with jaundice, there were few where the cause of the jaundice was inapparent. The immigrant Greek and Australian newborn populations were therefore remarkably similar. Since differences of frequency and severity of jaundice do exist in infants born in Greece, this difference must be lost when the parents emigrate, and therefore an environmental factor must be incriminated as the causative agent for jaundice of unknown origin in Greece.

Australia↗
PubMed1980

Effects of histamine in the isolated kitten heart.

The effects of histamine and 4-methylhistamine (4-MH) in isolated kitten heart preparations were examined. Histamine and 4-MH produced dose-dependent increases in the rate of spontaneously beating right atria. The positive chronotropic effect of histamine and 4-MH was unaffected by promethazine but was antagonized by both cimetidine and propranolol. The positive inotropic effects of histamine and 4-MH were studied in the kitten right ventricle strip, right papillary muscle, and left atrium. In all three tissues the positive inotropic effect of histamine and 4-MH was blocked by propranolol and not by either promethazine or cimetidine. In tissues from reserpine-pretreated kittens, histamine caused only a modest increase in rate. The inotropic effects of histamine in the left atrium, right ventricle strip, and right papillary muscle were abolished following reserpine pretreatment. The results of this study indicate two components to the effects of histamine and 4-MH on the kitten heart. The majority of the chronotropic response, and all of the inotropic response, is due to indirect activation of beta adrenoceptors through release of catecholamines. Part of the chronotropic response to both histamine and 4-MH is due to histamine H2-receptor stimulation. Based on the results from reserpine-pretreated animals, it is possible that the release of catecholamines by histamine in the kitten right atrium is through H2-receptor stimulation.

Animals↗
PubMed2003

Histamine alters E-cadherin cell adhesion to increase human airway epithelial permeability.

During the immediate response to an inhaled allergen, there is an increase in the paracellular permeability of the airway epithelium.1 Histamine is an important agonist released during the immediate response to inhaled allergen. We hypothesized that histamine would increase human airway epithelial paracellular permeability and that it would do this by interrupting E-cadherin-based cell adhesion. Histamine, applied to the basolateral surface, increased the paracellular permeability of cultured human airway epithelia, and this effect of histamine was blocked by the histamine receptor antagonist promethazine. ECV304 cells express a histamine receptor, N-cadherin, and elements of the tight junction, including claudins, but they do not express E-cadherin. Histamine increased the paracellular permeability of ECV304 cells transfected with a vector and expressing E-cadherin but not ECV304 cells expressing lac-Z in the same vector. L cells do not express the histamine receptor, cadherins, or claudins. Histamine decreased adhesion of L cells expressing the human histamine receptor and E-cadherin to an E-cadherin-Fc fusion protein. Histamine did not alter the adhesion to the E-cadherin fusion protein of L cells expressing either the histamine receptor or E-cadherin alone. When applied to the apical surface, adenovirus poorly infects airway epithelial cells because its receptor, CAR, is restricted to the basolateral surface of the cells. When histamine was applied to the basolateral surface of airway epithelial cells, infection of the cells by adenovirus increased by approximately one log. This effect of histamine was also blocked by promethazine. Histamine increases airway paracellular permeability and increases susceptibility of airway epithelial cells to infection by adenovirus by interrupting E-cadherin adhesion.

Adenoviridae↗
PubMed2003

In vitro human plasma leucine(5)-enkephalin degradation is inhibited by a select number of drugs with the phenothiazine molecule in their chemical structure.

A number of drugs with the phenothiazine molecule in their chemical structure inhibit in a dose-dependent manner human plasmatic aminopeptidase leucine(5)-enkephalin (LEU) metabolism. Half-life peptide degradation was significantly increased by thioridazine > fluphenazine > As-1397 [10-(alpha-diethylaminopropionyl)phenothiazine] >/= promethazine >/= chlorpromazine (final drug conc. 10(-4) M); t1/2 (+/- SD) 21.2 +/- 1.1, 19.6 +/- 1.0, 17.2 +/- 0.9, 17.1 +/- 1.0, and 17.1 +/- 1.1 min, respectively. Control and bacitracin (known aminopeptidase inhibitor) values were 11.8 +/- 1.0 and 31.3 +/- 1.7 min, respectively. These drugs significantly decreased (listed in the same order) LEU degradation initial velocity; Iv (+/- SD) 0.77 +/- 0.2, 0.82 +/- 0.2, 0.92 +/- 0.3, 0.93 +/- 0.2, 0.94 +/- 0.3 pg LEU/min, respectively. Control and bacitracin 1.10 +/- 0.3 and 0.20 +/- 0.1 pg LEU/min, respectively. Values represent results from 5 samples, each obtained by pooling 6 individual plasmas (4 male and 2 female; n = 30 healthy, drug-free volunteers). However, neither the phenothiazines ethopropazine, methotrimeprazine, prochlorperazine and trifluoperazine nor the various commonly used heterocyclic antipsychotics tested, e.g., molindone, loxapine, clozapine, haloperidol, sulpiride and thiothixene inhibited plasma LEU degradation kinetics. Our results failed to show correlations between chemical structure, antipsychotic properties and ability to inhibit plasmatic aminopeptidase LEU degradation. Whereas, presence of the phenothiazine molecule appears to be necessary for enzyme inhibition, only five out of nine substituted phenothiazines tested exhibited this effect. Furthermore, there was a lack of correlation between phenothiazines antipsychotic properties and their capacity to inhibit aminopeptidase activity, a property shown by promethazine (antihistaminic) and As-1397 (selective butyrylcholinesterase inhibitor) but lacking in prochlorperazine and trifluoperazine. Our results provide information which could lead to the rational design of agents capable to modulate the bioavailability of enkephalin and other endogenous aminopeptidase-degraded peptides believed to be involved in the etiology and/or pathophysiology associated with various disease conditions. Whether their development could find useful pharmacological applications remains to be explored.

Adult↗
PubMed1985

Droperidol as an antiemetic in cis-platinum-induced nausea and vomiting.

23 patients received cis-platinum, doxorubicin and cyclophosphamide for gynecologic malignancy between December 1, 1980 and December 1, 1982. Each patient was randomized with each course of chemotherapy to receive intravenous droperidol or the combination of promethazine and chlorpromazine rectal suppositories as an antiemetic regimen. Both the rate and duration of emesis were significantly lower when droperidol was used as the antiemetic regimen. There were no major side effects with either regimen. Droperidol seems to be superior to the combination of promethazine and chlorpromazine rectal suppositories in alleviating cis-platinum-induced nausea and vomiting.

Adult↗
PubMed1999

Slow wave sleep-inducing effects of first generation H1-antagonists.

The present study was performed to see if first-generation histamine H1-antagonists are useful sedative-hypnotic drugs. Increases in electroencephalogram (EEG) power spectra of the delta band (0-4 Hz) at the frontal cortex and theta band (4-8 Hz) at the hippocampus in rats were used as an indexes of sleep. The H1-antagonists used in this study resulted in a decrease in sleep latency and an increase in sleep duration (slow wave sleep). The rate of REM (rapid eye movement) sleep during slow wave sleep was decreased by H1-antagonists and brotizolam. The order of potency of H1-antagonists for the reduction in sleep latency (from greatest to least) was promethazine>chlorpheniramine>diphenhydramine and pyrilamine, and that for the increase in sleep duration was chlorpheniramine>promethazine>diphenhydramine and pyrilamine. Brotizolam was more potent than these H1-antagonists, with 14-18-fold and 4-14-fold greater effects on sleep latency and duration, respectively. These results clearly show that H1-antagonists are effective in mild to moderate insomnia as sedative-hypnotic drugs.

Animals↗
PubMed1989

Potentiation of cisplatin-induced lipid peroxidation in kidney cortical slices by glutathione depletion.

Effects of cis-diamminedichloroplatinum II (cisplatin), an antitumor agent with a dose-limiting effect of nephrotoxicity, on lipid peroxides and glutathione (GSH) were examined in rat kidney cortical slices treated with or without diethylmaleate (DEM), a GSH depletor, in vitro. DEM (3 mM) decreased the GSH level to about 16% of the control with a concomitant increase in lipid peroxides after 90 min of incubation. The same effects were obtained with 1 mM cisplatin 90 min later. Cisplatin (1 mM) with DEM (2 mM) stimulated both the decrease in GSH and the increase in lipid peroxides 90 min after incubation. However, cisplatin with DEM markedly stimulated lipid peroxidation with a small effect on the GSH decrease by cisplatin alone 30 min after incubation, while each drug by itself did not affect lipid peroxidation. The antioxidants N,N'-diphenyl-p-phenylene-diamine (DPPD), promethazine, and ascorbic acid abolished cisplatin-induced lipid peroxidation in the presence of DEM. DPPD had no effect on the depletion of GSH caused by cisplatin and DEM. Ascorbic acid and promethazine caused only a slight return towards the control level. The results suggested that cisplatin-induced lipid peroxidation is due to another mechanism in addition to the GSH depletion caused by the antitumor drug.

Animals↗
PubMed1991

Participation of histamine in the step-through active avoidance response and its inhibition by H1-blockers.

The effects of intravenous and intracerebroventricular administrations of certain H1-blockers on the active avoidance response in rats were studied. Among the classic H1-blockers used in this study: pyrilamine, diphenydramine, promethazine and chlorpheniramine, promethazine was the most effective and chlorpheniramine the least in inhibiting the active avoidance response; namely, a variation of prolongation in the response latency of the avoidance response. Meanwhile, ketotifen most potently inhibited the active avoidance response when the drugs were administered intracerebroventricularly. Mequitazine, astemizole and oxatomide were weak depressants when administered by either route. Azelastine was less effective than the classic H1-blockers by intravenous injection, while by intracerebroventricular injection, the inhibition was almost identical to those induced by the classic H1-blockers. Intracerebroventricular injection of histamine was antagonized the prolonged latency in the avoidance response induced by pyrilamine or diphenhydramine. A similar effect was also produced by 2-methylhistamine, but 4-methylhistamine had no effect. Intracerebroventricular injection of acetylcholine was restored the retarded avoidance response induced by pyrilamine, but a dose 20 times greater than that of histamine was required. From these findings, it can be concluded that inhibition of the active avoidance response induced by H1-blockers may be exerted through interaction with H1-receptors in the brain.

Analysis of Variance↗
PubMed2003

Sensing phenothiazine drugs at a gold electrode co-modified with DNA and gold nanoparticles.

DNA and gold nanoparticles are co-immobilized at a gold electrode through elaborate self-assembly processes. This configuration has proven to be useful as a sensor for phenothiazine drugs, taking advantage of the well-known, relatively large surface area of gold nanoparticles and the strong intercalation between dsDNA and phenothiazine drugs. This modified electrode has demonstrated good sensitivity and stability towards the oxidation of two model phenothiazine drugs: promethazine and chlorpromazine. A linear dependence between the concentration of phenothiazine drugs and the peak current is observed, with a concentration range of 2.0 x 10(-5)-1.6 x 10(-4) M and 1.0 x 10(-5)-1.2 x 10(-4) M, and a detection limit of 1.0 x 10(-5) M and 7.0 x 10(-6) M, for promethazine and chlorpromazine, respectively.

Animals↗
PubMed1978

Dose-related response of mouse mamma to some phenothiazine drugs.

The dose-related response of the mammary growth was studied in immature ICR-JCL female mice given 0.03 micrograms of estradiol per animal subcutaneously, and 0.005-1.0mg of either of the following phenothiazines (chlorpromazine, levometh iomeprazine, promethazine, perphenazine, thioridazine and propericiazine) per 10g of body weight was given orally once a day for 9 days starting on the 5th day after ovariectomy. The right second mamma of the chest was used to compare the hypertrophic affects. All the phenothiazines used produced mammary growth in the intensity sequence of thioridazine greater than chlorpromazine greater than promethazine greater than propericiazine greater than perphenazine greater than levomethiomeprazine. An optimal dose of each of the phenothiazines required to produce the maximum hypetrophy of the mammary gland was examined. From the results obtained, the relationship between the side-chain moiety of the compounds and the mammary growth activity could not be revealed.

Animals↗
PubMed1978

Neurotensin hyperglycemia:evidence for histamine mediation and the assessment of a possible physiologic role.

The hyperglycemic and hyperglucagonemic effects of systemically administered neurotensin in rats were investigated to explore the possibility that they are mediated by histamine and to determine whether neurotensin might have a role in the mediation of the responses to central nervous system glucopenia. The hyperglycemic response to neurotensin was partially blocked by the histamine H-1 receptor blockers, diphenhydramine and promethazine, and by the H-2 receptor blocker, cimetidine. The hyperglucagonemic response was completely blocked by diphenhydramine and promethazine and only partially blocked by cimetidine. The effects of histamine on glucose, glucagon, and insulin secretion were similar to those of neurotensin, and the inhibitory effects of both H-1 and H-2 blockers were comparable. The stimulatory effect of histamine on insulin secretion observed after adrenal autotransplantation was also similar to that previously reported for neurotensin. Neither antineurotensin serum nor diphenhydramine, however, was effective in blocking the hyperglycemic and hyperglucagonemic responses to the central administration of 2-deoxyglucose. The results are consistent with a histamine mediation of the effects of exogenously administered neurotensin but do not support a proposed role for neurotensin or histamine in the mediation of the hyperglycemic and hyperglucagonemic responses to central glucopenia.

Animals↗
PubMed1991

N(+)-glucuronidation of aliphatic tertiary amines, a general phenomenon in the metabolism of H1-antihistamines in humans.

1. Representative drugs of the various structural classes of H1 antihistamines were chosen for study. The drugs chosen (class name in parentheses) were chlorpheniramine maleate and pheniramine maleate (alkylamines), diphenhydramine hydrochloride and doxylamine succinate (ethanolamines), pyrilamine maleate and tripelennamine hydrochloride (ethylenediamines), promethazine hydrochloride (phenothiazine), cyclizine lactate (piperazine) and terfenadine (miscellaneous). In each case oral dose(s) were administered over no more than 6 h to two healthy volunteers and the total urine collected for 36 h. 2. Metabolites from urine were separated by h.p.l.c. and individually collected prior to mass spectrometric analysis in the fast atom bombardment mode. The structure of each metabolite identified as a quaternary ammonium-linked glucuronide metabolite was confirmed by direct comparison of its mass spectrum and chromatographic behaviour with that of a synthetic authentic compound. 3. For eight of the nine drugs studied, metabolism by the N(+)-glucuronidation pathway was observed in each of the volunteers. Terfenadine was the exception. 4. The amount of each N(+)-glucuronide in the urine was estimated by h.p.l.c. analysis. The mean proportion of dose excreted as the metabolite was 14.3%, 6.5% and 4.0% for cyclizine, tripelennamine and diphenhydramine, respectively. Promethazine was the only case where the N(+)-glucuronide accounted for less than 1.0% of the administered dose in both volunteers examined.

Adult↗
PubMed2001

Antagonists of calcium fluxes and calmodulin block activation of the p21-activated protein kinases in neutrophils.

Neutrophils stimulated with fMLP or a variety of other chemoattractants that bind to serpentine receptors coupled to heterotrimeric G proteins exhibit rapid activation of two p21-activated protein kinases (Paks) with molecular masses of approximately 63 and 69 kDa (gamma- and alpha-Pak). Previous studies have shown that products of phosphatidylinositol 3-kinase and tyrosine kinases are required for the activation of Paks. We now report that a variety of structurally distinct compounds which interrupt different stages in calcium/calmodulin (CaM) signaling block activation of the 63- and 69-kDa Paks in fMLP-stimulated neutrophils. These antagonists included selective inhibitors of phospholipase C (1-[6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione), the intracellular Ca(2+) channel (8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate), CaM (N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide; N-(4-aminobutyl)-5-chloro-1-naphthalenesulfonamide; trifluoperazine), and CaM-activated protein kinases (N-[2-(N-(chlorocinnamyl)-N:-methylaminomethyl)phenyl]-N-[2-hydroxyethyl]-4-methoxybenzenesulfonamide). This inhibition was dose-dependent with IC(50) values very similar to those that interrupt CaM-dependent reactions in vitro. In contrast, less active analogues of these compounds (1-[6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-2,5-pyrrolidinedione; N-(6-aminohexyl)-1-naphthalenesulfonamide; N-(4-aminobutyl)-1-naphthalenesulfonamide; promethazine; 2-[N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzyl-amine]) did not affect activation of Paks in these cells. CaM antagonists (N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide; trifluoperazine), but not their less-active analogues (N-(6-aminohexyl)-1-naphthalenesulfonamide; promethazine), were also found to block activation of the small GTPases Ras and Rac in stimulated neutrophils along with the extracellular signal-regulated kinases. These data strongly suggest that the Ca(2+)/CaM complex plays a major role in the activation of a number of enzyme systems in neutrophils that are regulated by small GTPases.

Animals↗
PubMed2002

In vitro reversal of chloroquine resistance in Plasmodium falciparum with dihydroethanoanthracene derivatives.

The effects of combining four dihydroethanoanthracenic (DEA) derivatives and chloroquine were assessed in vitro against Plasmodium falciparum chloroquine resistant parasites W2, Palo Alto, FCR3, and Bres1. Like verapamil or promethazine, the four dihydroethanoanthracenic derivatives tested can be added to the growing list of agents that show capability in enhancing the activity of chloroquine against resistant parasites. The structurally related tricyclic antihistaminic compounds examined in this study exerted different intrinsic antimalarial activity, but the same chloroquine-potentiating activity as verapamil or promethazine. They may act both on the rate of chloroquine accumulation and on its access to ferriprotoporphyrin IX. The reversal mechanism would be assumed to result from competition between DEA derivatives and chloroquine for efflux translocation sites, thus causing an increase in steady-state accumulation of chloroquine and a return to susceptibility. Restoration of therapeutic efficacy of chloroquine against resistant parasites by the administration of an additional drug available at relatively low cost may be a more effective strategy than the introduction of another antimalarial drug at the national level.

Animals↗
PubMedDate not supplied

Scombroid poisoning. A report of seven cases involving the Western Australian salmon, Arripis truttaceus.

OBJECTIVE: To present the clinical findings of scombroid poisoning due to ingestion of the Western Australian salmon, Arripis truttaceus, occurring in two separate outbreaks involving seven patients. Both outbreaks occurred in March and the fish had been caught in South Australian waters. CLINICAL FEATURES: Onset of symptoms in all patients occurred within half an hour of ingestion of the affected fish. The clinical syndrome included erythema and urticaria of the skin, facial flushing and sweating, palpitations, hot flushes of the body, headache, nausea, vomiting and dizziness. The fish implicated in one outbreak was noted to have a peppery taste. The diagnosis of scombroid poisoning was confirmed by the presence of the clinical syndrome, and by demonstration of high histamine levels in the cooked fish. INTERVENTION AND OUTCOME: Two patients had minor symptoms which had resolved before seeking medical advice. Another two patients had mild symptoms which disappeared after two hours of observation and required no specific treatment. Three patients had evidence of major toxicity which was successfully treated with parenterally administered promethazine. One of the three patients with major toxicity required overnight admission and repeated doses of promethazine to eradicate her symptoms. No patient had symptoms for longer than 12 hours. CONCLUSION: Scombroid poisoning is caused by ingestion of fish which has accumulated scombrotoxin during spoilage. The toxin is heat stable and has been identified as histamine. The clinical presentation closely resembles an acute allergic reaction. This similarity in symptoms may result in the diagnosis of scombroid poisoning being missed by clinicians. Patients with the symptom complex may be incorrectly informed that they are allergic to the fish species. Diagnosis is clinical and can be confirmed by analysis of the histamine content of the fish. Treatment is with antihistamines, however major toxicity may require the same aggressive management as acute anaphylaxis.

Adult↗
PubMed2000

The mechanism responsible for the drowsiness caused by first generation H1 antagonists on the EEG pattern.

The present study was performed to clarify the mechanism responsible for the drowsiness caused by first generation H1 antagonists according to electroencephalogram activity. All H1 antagonists used in the present study caused the EEG-recorded drowsiness pattern, i.e., increases in EEG power spectra of the delta and theta bands at the frontal cortex in rats. The potency of cyproheptadine was greater than those of diphenhydramine and promethazine, while that of pyrilamine was less than those of the other drugs examined. The increase in EEG power spectra in the delta band induced by H1 antagonists was antagonized by pretreatment with both histidine and physostigmine. The effect of pyrilamine was more potently antagonized by histidine and less potently antagonized by physostigmine as compared to diphenhydramine, promethazine and cyproheptadine. The increases in EEG power spectra induced by H1 antagonists were neither antagonized nor potentiated by 5-hydroxytryptophan. These results clearly indicate that the increases in EEG power spectra in the delta and theta bands at the frontal cortex in rats induced by first generation H1 antagonists are responsible for both histaminergic and cholinergic mechanisms.

5-Hydroxytryptophan↗