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At least 649 records · Page 36Linked to original sources
PubMed1977

Identification by microinjection of TRH-sensitive sites in the cat's brain stem that mediate respiratory, temperature and other autonomic changes.

Cats were prepared with an array of stereotaxically implanted guide tubes, the tips of which rested just above selected structures in the brain stem. Thyrotropin-releasing hormone (TRH) was microinjected in a volume of 0.5 micronl at 347 individual sites scattered throughout the hypothalamus and mesencephalon Polypnea, hypothermia, vocalization, salivation, defecation and vasodilation were evoked by 10-20 ng of TRH injected only at loci in the mesencephalon, principally in the reticular substance. TRH failed to lower body temperature when it was infused at the same sites in the anterior hypothalamus at which norepinephrine produced its characteristic hypothermia. These results suggest that the TRH-induced hypothermia is a secondary effect of tachypnea which results from the action of the tripeptide on the mesencephalic respiratory-autonomic mechanism.

Animals↗
PubMed1981

Secoverine selectively antagonizes muscarinic effects in various in vivo preparations.

Time-activity studies of secoverine and atropine were made with respect to mydriasis and oxotremorine-induced salivation, lacrimation and tremors. Marked differences were found in the anticholinergic activity relation between secoverine and atropine for various tissues. These differences remained present at all time intervals, which excludes a pharmacokinetic explanation. It may be concluded that secoverine possesses a different affinity for various muscarinic receptors.

Animals↗
PubMed1986

Effect of BM-5, a presynaptic antagonist-postsynaptic agonist, on cortical acetylcholine release.

The effect of N-methyl-N-(1-methyl-4-pyrrolidino-2-butynyl) acetamide (BM-5) on acetylcholine release from the cerebral cortex was investigated in unanaesthetized and urethane-anaesthetized rats. BM-5 at doses ranging from 0.3 to 5 mg/kg i.p. enhanced acetylcholine output in both groups of rats. The maximum increase occurred with 0.5 mg/kg in the unanaesthetized and 2 mg/kg in the anaesthetized rats. The effect lasted approximately 60 min. At the largest doses peripheral muscarinic effects including salivation, chromodachryorrhea and rhinorrhea were also seen. These results demonstrate that BM-5 exerts presynaptic antagonistic and postsynaptic agonistic effects on muscarine receptors in vivo also.

Acetylcholine↗
PubMed1990

In vivo characterisation of novel efficacious muscarinic receptor agonists.

Although a number of muscarinic agonists have been used in clinical trials for Alzheimer's Disease, many of these compounds are low in potency and have only limited intrinsic efficacy. The present study describes four non-quaternary oxadiazole based muscarinic agonists from a quinuclidine and a 1-azanorbornane series. These displayed up to 1000 fold higher affinity than arecoline and were efficacious muscarinic agonists at cortical receptors. All four compounds produced peripherally mediated salivation and centrally mediated hypothermia at doses 50-50,000 fold lower than arecoline. The most potent was L-670,548, the methyl oxadiazole in the 1-azanorbornane series, which had an ED50 of 0.0016 mg/kg on the hypothermia model. This derivative was also the most potent compound in ex vivo binding studies (ED50 0.0069 mg/kg) and showed excellent brain penetration (3.8% of the administered dose). These derivatives are the first non quaternary efficacious agonists which show good penetration into the CNS (central nervous system), and will prove useful tools in understanding the role of muscarinic receptors in CNS function.

Animals↗
PubMed1991

(+/-)-Terodiline: an M1-selective muscarinic receptor antagonist. In vivo effects at muscarinic receptors mediating urinary bladder contraction, mydriasis and salivary secretion.

The affinity and selectivity of racemic terodiline (N-tert-butyl-1-methyl-3,3-diphenylpropylamine HCl) for muscarinic receptor subtypes was determined from functional responses of rabbit vas deferens (M1), guinea pig atria (M2) and bladder detrusor muscle (M3). (+/-)-Terodiline was found to be about as potent as pirenzepine in the rabbit vas deferens (Kb = 15 and 31 nM, respectively) and at least as selective for M1 relative to M2 (11-fold) and M3 (19-fold) receptors. Like pirenzepine, (+/-)-terodiline does not distinguish between M2 and M3 receptors in vitro. The peripheral actions of (+/-)-terodiline were evaluated in vivo in terms of its ability to induce mydriasis, and to inhibit salivary secretion and urinary bladder contraction. (+/-)-Terodiline given s.c. was equipotent in inhibiting intravesical bladder pressure and carbachol-induced salivary secretion (ID50 = 24 and 35 mg/kg, respectively), and in increasing pupil diameter (ED50 = 59 mg/kg). These results suggest that the in vivo actions of racemic terodiline at (M3) receptors mediating bladder contraction may not be separable from its actions at receptors mediating mydriasis and salivation. Moreover, its effects on the pupil and salivary glands are apparently not mediated through M1 receptors. Together, these findings help clarify the action of (+/-)-terodiline in the treatment of neurogenic bladder.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1984

Repeated administration of naltrexone and diprenorphine decreases food intake and body weight in squirrel monkeys.

Although chronic administration of naloxone has been reported to reduce food intake and body weight in rats, there have been no comparable investigations using a nonhuman primate. We examined the effects of repeated injections of two long acting opiate antagonists - naltrexone and diprenorphine - on the ad libitum intake of a nutritional complete liquid diet and on body weight in squirrel monkeys. Naltrexone binds with highest affinity to the mu opioid receptor whereas diprenorphine binds with equally high affinity to several subtypes of opioid receptor. Diprenorphine (ED50 = 0.01 mg/kg) was 22 times more potent than naltrexone (ED50 = 0.22 mg/kg) in decreasing 2 h food intake, suggesting that more than one opioid receptor subtype may be involved in the anorectic effects of opiate antagonists. A 1.0 mg/kg dose of drug reduced 24 h food intake by 50% and was associated with a weekly reduction in body weight of 4 and 5% for naltrexone and diprenorphine, respectively. Thus, in contrast with shorter time intervals, 24 h food intakes were similar for the two drugs, and this was associated with comparable body weight profiles. The decreases in food intake and body weight remained constant over the period of drug administration. Some monkeys showed profuse salivation and "wet dog shakes" after 4 days of treatment with the 1.0 mg/kg dose but not after 1 day. Therefore, opiate antagonists given chronically to monkeys reduced food intake and body weight in a dose-dependent manner with no evidence of tolerance to these effects.

Animals↗
PubMed1995

Long-term sensitization to the behavioral effects of naltrexone is associated with regionally specific changes in the number of mu and delta opioid receptors in rat brain.

Enhanced sensitivity to some of the behavioral effects of the opioid antagonist naltrexone (NTX) develops following once-weekly injections of cumulative doses of the drug. Rats treated with this regimen of NTX injections show enhanced sensitivity to the operant response rate decreasing effects of NTX and NTX-induced salivation. The enhanced sensitivity is long-lasting and appears to be produced through conditioning processes. We have conducted saturation binding assays to assess possible changes in the number and affinity of mu and delta opioid receptors in cortical, midbrain and hindbrain membrane preparations from Long-Evans rats treated once weekly for 8 weeks with cumulative doses of the drug (1, 3, 10, 30 and 100 mg/kg). 3H-DAMGO (0.5-21 nM) and 3H-pCl-DPDPE (0.04-4 nM) were used to characterize mu and delta receptors, respectively. NTX treatment had no effect on 3H-DAMGO binding in cortex, but decreased binding in midbrain and increased binding in hindbrain relative to saline-treated controls. Saturation analyses revealed that these differences reflected changes in the number, but not the affinity of mu receptors. NTX treatment also increased the amount of 3H-pCl-DPDPE bound to delta receptors in midbrain and hindbrain, but not in cortex. Again, these changes were due to changes in the number of receptors. Thus, chronic NTX differentially affects the number of mu and delta opioid receptors in various brain regions.

Animals↗
PubMed1995

Muscarinic agonists as analgesics. Antinociceptive activity versus M1 activity: SAR of alkylthio-TZTP's and related 1,2,5-thiadiazole analogs.

Alkylthio-TZTPs (3-(3-alkylthio-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1-met hylpyridines) and corresponding azabicyclic analogs were tested for m1 efficacy in cloned human m1 receptors and for antinociceptive activity in the mouse grid shock assay. The m1 (%PI) SAR were distinctly different from the analgesia and the salivation SAR, suggesting that analgesia is mediated by neither m1 nor M3 muscarinic receptors.

Analgesics↗
PubMed1994

Neuropharmacological characterization of SR 140333, a non peptide antagonist of NK1 receptors.

SR 140333 (1-[2-[3-(3,4-dichlorophenyl)-1-(3-isopropoxyphenylacetyl) piperidin-3-yl]ethyl]-4-phenyl-1-azonia-bicyclo[2.2.2]octane , chloride), a potent non peptide ligand of the substance P (SP) NK1 receptor subtype with high affinity for NK1 receptors from both rat cortical membranes and human IM9 cells (Ki = 0.02 nM and 0.01 nM, respectively) was studied in vivo on various effects induced by NK1 agonists in rats and mice. SR 140333 given intraperitoneally (i.p.) in mice antagonized dose-dependently and in a stereoselective manner the scratching responses induced by intracerebroventricular SP and septide (ID50 = 0.73 and 0.08 mg/kg, respectively) and the turning behavior elicited by intrastriatal SP and septide (ID50 = 0.07 and 0.06 mg/kg, respectively). This compound had little effect on the scratching responses and the turning behavior elicited by [Sar9, Met(O2)11]-SP. When SR 140333 was coadministered with the peptide agonist, the compound reduced the scratching responses elicited by SP, [Sar9, Met(O2)11]-SP and septide injected intrathecally (i.t.) in mice (ID50 = 72.0, 64.3 and 52.5 ng i.t., respectively). SR 140333 antagonized the salivation induced by SP, [Sar9, Met(O2)11]-SP and septide in rats (ID50 = 0.13, 0.18 and 0.09 mg/kg i.p., respectively). SR 140333 abolished the facilitation of the tail-flick reflex induced by noxious heat in rats (total reversal at 0.06 mg/kg, i.p.). This compound was also found to inhibit the turning behavior induced by intrastriatal apomorphine in mice (ID50 = 0.1 mg/kg, i.p.). In conclusion, these results indicate that SR 140333 behaves as a potent, selective and centrally active NK1 receptor antagonist.

Animals↗
PubMed1986

Behavioral effects of intraventricular dibutyryl cyclic AMP in domestic fowl.

Intraventricular administration of dibutyryl cyclic AMP (dbcAMP) to domestic fowl induced behaviors within 60 seconds which persisted for 7-120 minutes. Stereotyped head movements and increases in preening were observed at the lowest dose (50 nmol), while at higher doses (150 and 225 nmol) head movements were interspersed with escape behavior, increases in locomotor activity, salivation and a loss of coordination. Administration also elicited vocalizations, mainly laying and type 1 warning calls. These calls contained many abnormal elements, possibly caused by relaxation of the syringeal musculature. The rate of calling was influenced by testosterone, being greater in hens and capons than in roosters or capons implanted with testosterone propionate. Caponization also intensified escape behavior. No behaviors were induced by administration of the hydrolysis product of dbcAMP, butyric acid. These behavioral effects of dbcAMP are similar to those reported to occur during electrical stimulation of loci in the avian brain.

Animals↗
PubMed1988

Submandibular and parotid salivary secretion after electrolytic lesioning of the brainstem nucleus parvocellularis in the rat.

The present study, in consonance with recent anatomical investigations, demonstrates that activation of the nucleus parvocellularis in the rat evokes a potent hypersecretory effect in the submandibular and sublingual (S-S) salivary glands. Furthermore, electrolytic lesioning of this region in conjunction with peripheral removal of the parotid glands is followed by an increase in the number of drinking responses in the presence of dry food. Such prandial drinking behavior is only observed after total impairment of salivation (i.e., removal of the S-S + parotid glands), thus suggesting that the parvocellularis lesion led to a marked deficit in S-S salivary secretion. On the other hand, the activation of the nucleus parvocellularis was seen to have only a slight effect on parotid salivary secretion. Electrolytic lesions to this zone, when associated with peripheral removal of the S-S glands, failed to induce prandiality, suggesting that the parvocellularis nucleus exerted a low level of control over parotid salivary secretion. These results are interpreted as functional proof of the relationship between the parvocellularis reticular formation and the superior salivatory nucleus in the secretion of S-S saliva.

Animals↗
PubMed1989

Actions of robustoxin, a neurotoxic polypeptide from the venom of the male funnel-web spider (Atrax robustus), in anaesthetized monkeys.

Robustoxin, a polypeptide consisting of a chain of 42 amino acid residues in a known sequence, has been isolated by cation exchange chromatography from the crude venom of the male funnel-web spider (Atrax robustus). Physiological activity or toxicity in the venom fractions was detected by production of fasciculation in mouse phrenic nerve-hemidiaphragm preparations and by lethality in new-born mice. In the present experiments in Macaca fascicularis monkeys anaesthetized with pentobarbitone, robustoxin (5-30 micrograms/kg infused i.v. over 5 min) produced immediate disturbances in respiration (including dyspnoea and apnoea), blood pressure and heart rate followed by severe hypotension (mean systemic blood pressure less than 50 mmHg) or death due to respiratory and circulatory failure within 196 min. Robustoxin also produced lachrymation, salivation, generalized skeletal muscle fasciculation and a parallel increase in body temperature, and increased firing in skeletal motor and autonomic nerves. These effects closely resembled those produced by i.v. infusions over 5 min of 50 micrograms/kg of crude venom from male A. robustus spiders. Crude venom from female A. robustus spiders (500 micrograms/kg i.v. over 5 min) produced some of the effects elicited by robustoxin and crude venom from male spiders, but to a much less marked extent. It was concluded that robustoxin is responsible for the neurotoxic and lethal effects of human envenomation by male A. robustus spiders.

Anesthesia↗
PubMed1988

Salivary changes associated with experimental motion sickness condition in man.

The effect of experimental motion sickness condition (rotation) on salivary flow and composition was studied in 34 healthy male volunteers. In most subjects, the flow rate of whole saliva was significantly decreased, while the potassium concentration was markedly increased during rotation. These results contrast with the classic reports of subjectively increased salivation in the first stages of motion sickness and may tentatively be explained in terms of sympathetic activation. The salivary protein concentration and secretion rate observed before and during rotation were consistently higher in those subjects categorized as moderately or severely sick during rotation. The salivary protein levels may perhaps be considered as an additional objective variable in the prediction of susceptibility to motion sickness.

Adolescent↗
PubMed1986

Use of an electronic stimulator for the treatment of dry mouth.

This paper presents an innovative approach to the treatment of xerostomia through normal physiologic mechanisms with a device that provides electrical stimulation to the oral and pharyngeal afferent nervous system; the result is a reflex volley of efferent impulses to the salivary glands, causing salivation. The device has been successful in treating xerostomic patients regardless of the etiology of their dry mouths.

Animals↗
PubMed1987

Subchronic oral toxicity of 4-chloro-alpha, alpha, alpha-trifluorotoluene in Sprague-Dawley rats.

The subchronic oral toxicity of 4-chloro-alpha, alpha, alpha-trifluorotoluene (CTT) was assessed in Sprague-Dawley rats. Four groups of six male and six female rats were treated daily for 28 days, by gavage, with doses of 0, 10, 100 and 1000 mg CTT/kg body weight using olive oil as a vehicle. No clinical signs were observed, other than salivation in the high-dose group in the last week. The males of this group showed a significant decrease in body-weight gain without a concurrent decrease in food consumption. In males, there were significant dose-dependent increases in blood cholesterol and triglycerides, suggestive of alterations in lipid metabolism. The females showed only a small dose-related increase in serum lactate dehydrogenase. Specific histological alterations were found in the males given 1000 mg/kg/day, namely hyaline droplet nephrosis, along with a significant increase in relative kidney weight, and an increase in lipid vacuoles in the adrenal cortex. Slight nephrosis was also observed in males given 100 mg/kg. Both male and female rats showed a significant increase in relative liver weight at a dose of 1000 mg CTT/kg. CTT appears to have a low subchronic oral toxicity. Neither pathological nor biochemical alterations were found at 10 mg/kg body weight/day and this can be defined as the no-observable-effect level (NOEL).

Administration, Oral↗
PubMed1989

Effect of diphenhydramine on organophosphorus insecticide toxicity in mice.

Male mice were treated orally with the organophosphorus insecticides fenamiphos and dichlorvos at 10 and 150 mg/kg, respectively. The insecticides produced signs of toxicosis characteristic of cholinesterase inhibition, and induced death in all treated mice. Pretreatment of mice with diphenhydramine HCl (20 and 30 mg/kg, subcutaneously) 15 min before either insecticide significantly (P less than 0.05) reduced the incidence of toxic manifestations (excessive salivation, Straub tail, and whole body tremor), delayed the onset of death, and increased the percentage of survivors. Doses of diphenhydramine less than 20 mg/kg were not so effective. The data indicated a protective property of diphenhydramine against organophosphorus insecticide-induced toxicosis.

Animals↗
PubMed1980

What does the lemon test measure?

Salivary output to lemon juice was measured on 24 subjects in the morning and afternoon with and without the presentation of noise. It was found that time of day and noise affected salivation output and that these factors interacted such that more saliva was produced by noise in the morning than in the afternoon. Possible reasons for the interaction are discussed.

Arousal↗