Drugs online research references
J Pharmacol Exp Ther. 1991 Jul 1;258(1):118-23.
Anticholinergic drugs potentiate dopamine D1 but not D2 antagonists on a conditioned avoidance task in rats.
Iorio LC, Cohen M, Coffin VL.
CNS Pharmacology, Schering-Plough Research Division, Bloomfield, New Jersey.
The present study investigated whether blockade of conditioned avoidance responding (CAR) in rats by selective D1 and D2 receptor antagonists could be differentially affected by anticholinergics. The results show that atropine and scopolamine dose-relatedly antagonized the effects on CAR of two specific D2 receptor blockers, haloperidol and raclopride, but potentiated the effects of three specific D1 receptor antagonists, SCH 23390, SCH 39166 and NO-01-0756. Of the less specific dopamine receptor antagonists tested, scopolamine blocked the effects of clozapine and cis-flupenthixol, but did not alter the effects of chlorpromazine, thioridazine or cis-piflutixol. Although the mechanisms involved in the differential shifts by the anticholinergics are unknown, the results are consistent with the view that CAR antagonism by the specific D2 vs. D1 receptor antagonists involves unique and separate mechanisms of action. With respect to the less specific dopamine receptor antagonists, the CAR blockade seen with clozapine and cis-flupenthixol might reflect predominant D2 receptor blockade because their effects were blocked by atropine. In contrast, the CAR blockade by chlorpromazine, thioridazine and cis-piflutixol antagonists might be mediated by equal degrees of D1 and D2 receptor blockade inasmuch as they were not blocked or potentiated by atropine. The antagonism of CAR in rats by the D1 receptor antagonists suggests that these drugs have potential antipsychotic activity in humans. However, they do not appear to enhance central cholinergic transmission and therefore may be devoid of the side effects produced by the antipsychotics in clinical use.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1830098&dopt=Abstract
Brain Res. 1983 Nov 28;280(1):127-38.
Blockade of long-term potentiation by phencyclidine and sigma opiates in the hippocampus in vivo and in vitro.
Stringer JL, Greenfield LJ, Hackett JT, Guyenet PG.
Long-term potentiation (LTP) of synaptic transmission in the rat hippocampus in vivo and in vitro, was studied using field potentials. Pretreatment with phencyclidine (PCP) or 'sigma' opiates blocked LTP in vivo while mu and kappa opiates and the antagonist naloxone were ineffective. Scopolamine (20 mg/kg i.p.) neither prevented LTP nor antagonized the LTP-blocking effect of PCP. In vitro, PCP up to 100 microM did not alter synaptic activation of CA1 pyramidal cells by stratum radiatum stimulation but blocked LTP in a dose-dependent manner (ED50: 3 microM). The sigma opiate, cyclazocine, also prevented the induction of LTP in vitro while morphine and procaine were ineffective.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6317141&dopt=Abstract
Jpn J Pharmacol. 1981 Feb;31(1):61-8.
Further studies on the potentiating effect of lithium chloride on methamphetamine-induced stereotypy in mice.
Miyauchi T, Kikuchi K, Satoh S.
To study the mechanism of the potentiating effect of lithium chloride (LiCl) on methamphetamine (MA)-induced stereotypy in mice, effects of various drugs on the action of LiCl on the stereotypy and pharmacokinetics of MA in different brain regions and liver were examined. The potentiating effect of LiCl disappeared in mice pretreated with atropine or scopolamine whereas LiCl potentiated the stereotypy in mice pretreated with p-chlorophenylalanine, alpha-methyl-p-tyrosine, nialamide, physostigmine or butylscopolamine. The concentrations of MA in the striatum, brainstem and liver were increased and the half-life of MA in these tissues was prolonged by LiCl. The effect of LiCl on the kinetics of MA in the brain, but not that in the liver, was blocked by scopolamine. LiCl prolonged the half-life of MA in the brain and liver in mice treated with physostigmine or butylscopolamine. The inhibition of MA elimination from the brain and its blockade by scopolamine seem to explain the potentiating action of LiCl on the stereotypy and the antagonism by scopolamine of the behavioural action of LiCl, respectively.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7195953&dopt=Abstract
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