sincalide has been researched along with Blepharoptosis* in 5 studies
5 other study(ies) available for sincalide and Blepharoptosis
Article | Year |
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Clonidine and yohimbine separate the sedation and the ptosis caused by cholecystokinin octapeptide and ceruletide.
The central depressant effects of ceruletide (CER, 0.04 mg/kg s.c.) and cholecystokinin octapeptide (CCK-8, 0.25 mg/kg s.c.) were compared with those of clonidine (0.04 mg/kg s.c.). At doses that were nearly equipotent with respect to motor inhibition (catalepsy, reduction in ambulation and exploratory rearing), only the peptides produced ptosis. Yohimbine (1 mg/kg s.c., 30 min) antagonized the effect of clonidine but not of the peptides. Clonidine (0.07-0.2 mg/kg s.c., 30 min) antagonised the ptotic action of the peptides, and this effect was abolished by yohimbine (0.2-1 mg/kg i.p.) but resistant to haloperidol (0.05 and 0.15 mg/kg i.p.). These results separate the behavioural effects of the peptides from those of clonidine and also the ptotic effect of the peptides from their effect on motor activity. The antiptotic effect of clonidine may originate from activated adrenergic autoreceptors. Topics: Animals; Apomorphine; Blepharoptosis; Catalepsy; Ceruletide; Clonidine; Drug Antagonism; Haloperidol; Humans; Hypnotics and Sedatives; Male; Mice; Motor Activity; Sincalide; Yohimbine | 1984 |
Neuroleptic-like effects of ceruletide and cholecystokinin octapeptide: interactions with apomorphine, methylphenidate and picrotoxin.
Haloperidol in low doses antagonized the apomorphine-induced cage-climbing behaviour of mice, whereas ceruletide (CER) and its analogue, Nle8-CER-(4-10) had very weak anticlimbing efficacy; Nle8-CER and diazepam were inactive. The ptosis caused by CER and cholecystokinin octapeptide (CCK-8) was antagonized by apomorphine in doses 27 times smaller than those effective against the haloperidol-induced ptosis. No such differences occurred when either methylphenidate or picrotoxin replaced apomorphine. Low-dose haloperidol was an antagonist to the antiptotic effect of apomorphine versus both CER and CCK-8. The rearing inhibiting effect of CER and haloperidol, in contrast to that of clonazepam, was very resistant to apomorphine. Methylphenidate was weakly effective against clonazepam and haloperidol but inactive versus CER. Picrotoxin was no antagonist to either rearing inhibiting agent. The results taken together suggest presynaptic sites of the dopaminergic system as important for the production of ptosis by CCK-like peptides. Topics: Animals; Antipsychotic Agents; Apomorphine; Behavior, Animal; Blepharoptosis; Body Temperature; Ceruletide; Clonazepam; Drug Antagonism; Haloperidol; Male; Methylphenidate; Mice; Peptide Fragments; Picrotoxin; Sincalide | 1983 |
Caerulein and cholecystokinin octapeptide (CCK-8): sedative and anticonvulsive effects in mice unaffected by the benzodiazepine antagonist Ro 15-1788.
Cholecystokinin octapeptide (CCK-8), caerulein and diazepam inhibited exploratory rearing activity and harman-induced convulsions in mice. Pretreatment with the selective benzodiazepine receptor antagonist Ro 15-1788, reduced or abolished the sedative and anticonvulsive effects of diazepam, but left the same effects of both peptides unaffected. The peptide-induced ptosis was even increased by Ro 15-1788. The results suggest that the CCK-like peptides do not directly interact with the benzodiazepine receptor. Topics: Animals; Anticonvulsants; Benzodiazepinones; Blepharoptosis; Body Temperature; Ceruletide; Cholecystokinin; Diazepam; Flumazenil; Harmine; Hypnotics and Sedatives; Male; Mice; Peptide Fragments; Seizures; Sincalide | 1982 |
Central effects of ceruletide analogues.
Ten ceruletide analogues and cholecystokinin octapeptide (CCK-8) were compared with ceruletide regarding neuropharmacological effects in mice after peripheral administration. The effects under study were inhibition of motor response to noxious stimulation (hot plate), production of ptosis, inhibition of exploratory rearing activity, elevation of threshold for picrotoxin-induced convulsions, and antagonism of methylphenidate-induced gnawing. Desulfation, deamidation and shortening of the peptide chain by five amino acids destroyed all pharmacological activities of ceruletide. Other modifications were of unequal consequences for the pharmacological profile of a given analogue, decreasing some effects while increasing others. Hence, structural changes of the ceruletide molecule resulted in modulations of both potency and selectivity. Topics: Analgesia; Animals; Anticonvulsants; Behavior, Animal; Blepharoptosis; Brain; Ceruletide; Cholecystokinin; Dose-Response Relationship, Drug; Humans; Hypnotics and Sedatives; Male; Mice; Peptide Fragments; Sincalide; Stereotyped Behavior; Structure-Activity Relationship | 1981 |
Analgesia and ptosis caused by caerulein and cholecystokinin octapeptide (CCK-8).
Topics: Analgesics; Animals; Blepharoptosis; Catalepsy; Ceruletide; Cholecystokinin; Dose-Response Relationship, Drug; Drug Tolerance; Humans; Male; Mice; Pentagastrin; Reaction Time; Sincalide; Time Factors | 1980 |