piperidines and 1-(1-phenylcyclohexyl)-3-methylpiperidine

piperidines has been researched along with 1-(1-phenylcyclohexyl)-3-methylpiperidine* in 4 studies

Other Studies

4 other study(ies) available for piperidines and 1-(1-phenylcyclohexyl)-3-methylpiperidine

ArticleYear
Neuroendocrine responses produced by enantiomeric pairs of drugs that interact with phencyclidine and sigma receptors.
    European journal of pharmacology, 1994, Sep-22, Volume: 263, Issue:1-2

    The present study characterized the response of the hypothalamo-pituitary-adrenal axis after the acute administration of enantiomeric pairs of drugs that bind to phencyclidine (PCP) and sigma receptors. Rats were injected with the enantiomers of 1-(1-phenylcyclohexyl)-3-methylpiperidine (PCMP), N-allylnormetazocine (SKF 10,047), dioxadrol (dexoxadrol and levoxadrol) or pentazocine, and plasma levels of adrenocorticotropin (ACTH) and corticosterone were determined by radioimmunoassay. The effects of the enantiomers of PCMP and dioxadrol showed stereospecificity as both (+)-PCMP and dexoxadrol increased plasma levels of ACTH and corticosterone but (-)-PCMP and levoxadrol had no effect. Whereas (-)-pentazocine produced greater responses than (+)-pentazocine, the two enantiomers of SKF 10,047 did not show stereoselectivity. Although the potency of the enantiomers of PCMP and dioxadrol parallel their affinity for binding to PCP receptors, the potency of the enantiomers of pentazocine did not. These results suggest that although the stimulation of the hypothalamo-pituitary-adrenal axis by PCP and drugs with PCP-like activity might be due to interactions with PCP receptors, the effects of pentazocine also involve interactions at other sites.

    Topics: Adrenocorticotropic Hormone; Analgesics; Animals; Corticosterone; Dioxolanes; Drug Interactions; Hypothalamo-Hypophyseal System; Injections, Subcutaneous; Male; Phenazocine; Phencyclidine; Piperidines; Pituitary-Adrenal System; Rats; Rats, Sprague-Dawley; Receptors, sigma; Stereoisomerism; Sympathomimetics

1994
Facilitation of GABA-induced depression with PCP and sigma receptor agonists was mediated through catecholaminergic pathways.
    Life sciences, 1990, Volume: 47, Issue:22

    The purpose of this experiment was to investigate the interactions of norepinephrine with PCP (phencyclidine) and sigma receptor agonists--modulated GABA (gamma aminobutyric acid) response in the cerebellum. Drugs were directly applied to a single cerebellar Purkinje neuron of urethane-anesthesitized rat through a multibarrel pipette. (+)PCMP [1-(-1-phenylcyclohexyl)-3-methyl piperidine], a PCP receptor agonist, and dexoxadrol, a sigma receptor agonist, significantly enhanced GABA induced inhibition. In norepinephrine-depleted animals, however, both (+)PCMP and dexoxadrol did not modulate GABA's effect. In conclusion, our findings indicated that the PCP/sigma-induced facilitation of GABA reactions were mediated through noradrenergic system in the cerebellum.

    Topics: Animals; Cerebellum; Dioxolanes; Electrophysiology; gamma-Aminobutyric Acid; Male; Norepinephrine; Phencyclidine; Piperidines; Purkinje Cells; Rats; Rats, Inbred Strains; Receptors, Opioid; Receptors, sigma

1990
Facilitation of gamma-aminobutyric acid-induced depression by (+)PCMP and dexoxadrol in the cerebellar Purkinje neurons of the rat.
    Neuropharmacology, 1989, Volume: 28, Issue:4

    The purpose of this experiment was to investigate the interaction of GABA (gamma aminobutyric acid) with PCP (phencyclidine) and sigma receptor agonists in the cerebellum. Drugs were applied directly to a single cerebellar Purkinje neuron of urethane-anesthetized rats, through a multibarrel pipette. The PCP receptor agonist, (+)PCMP [1-(-1-phenylcyclohexyl)-3-methyl piperidine], significantly enhanced GABA-induced inhibition. On the other hand, its stereoisomer, (-)PCMP, had no such modulatory effect. Dexoxadrol, a sigma receptor agonist, similar to (+)PCMP, potentiated GABA-induced depression. Its stereoisomer, levoxadrol, although inhibiting the spontaneous firings of Purkinje neurons, did not alter the effect of GABA. In conclusion, the findings indicate that the electrophysiological mechanisms of PCP-induced facilitation of GABA-induced reactions are similar to those triggered by sigma agonists in the cerebellum.

    Topics: Analgesics; Animals; Cerebellum; Depression, Chemical; Dioxolanes; Dioxoles; Electrophysiology; gamma-Aminobutyric Acid; Heart Conduction System; In Vitro Techniques; Male; Neurons; Phencyclidine; Piperidines; Purkinje Fibers; Rats; Rats, Inbred Strains; Stereoisomerism; Sympathomimetics

1989
Phencyclidine selectively blocks the sustained voltage-dependent potassium conductance in PC12 cells.
    Brain research, 1988, Jul-19, Volume: 456, Issue:1

    We investigated the effects of phencyclidine (PCP), a psychotomimetic dissociative anesthetic, and several related drugs on voltage-dependent K+ currents in PC12 cells, a neuron-like clonal cell line derived from a rat pheochromocytoma. Whole-cell voltage clamp recordings demonstrated two kinetically distinct voltage-dependent outward (K+) current components in these cells: a rapidly activating and inactivating component, IA, that was selectively eliminated by 4-aminopyridine (2 mM) and a slowly activating, minimally inactivating (sustained) component, IK, that was specifically blocked by tetraethylammonium (20 mM). PCP (1-100 microM) produced a dose-dependent blockade of both IK and IA, however, at low doses the drug selectively reduced IK with little effect on IA; the IC50s for blockade of IK and IA were 4 and 25 microM, respectively. The blockade of IK was voltage-dependent so that the degree of block decreased with increasing depolarization, indicating that the blocking mechanism is likely one in which the positively charged PCP molecule is drawn into the channel pore. Several PCP related drugs also suppressed IK. Thienyl-PCP (TCP), a drug that is behaviorally more potent than PCP, partially blocked IK at low doses (31% at 1 microM), but even at high doses (25 microM) the degree of block was never as great as that produced by PCP. The optically active PCP congeners (+)-PCMP (1-(1-phenylcyclohexyl)-3-methyl-piperidine) and dexoxadrol were also potent blockers of IK. However, in contrast to the stereospecificity these compounds demonstrate in binding to high-affinity PCP receptors and in eliciting PCP-like behavioral responses, their enantiomers (-)-PCMP and levoxadrol showed similar potencies as the parent compounds in blocking IK. These results demonstrate that PCP and related drugs are powerful, selective blockers of IK in PC12 cells. The structure-activity studies indicate that this effect occurs at a site that is pharmacologically distinct from the behaviorally relevant PCP receptor. Blockade of K+ channels is unlikely to be responsible for the psychotomimetic or anti-convulsant properties of PCP, but could account for the convulsant potential of the drug.

    Topics: Anesthetics; Animals; Dioxolanes; Electric Stimulation; Ion Channels; Membrane Potentials; Phencyclidine; Pheochromocytoma; Piperidines; Potassium; Rats; Tumor Cells, Cultured

1988