Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.16.2 (
PCP
)
3,761
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Phencyclidine (
PCP
) and several behaviorally active or inactive structural analogs were administered i.v. to urethane-anesthetized rats in order to determine their effects on CA1 pyramidal cell discharges elicited by contralateral CA3 (cCA3) stimulation.
PCP
and the behaviorally active m-amino derivative (m-NH2
PCP
) depressed, in a dose-dependent manner, the amplitude of the population spike evoked in CA1 by a cCA3 stimulation (ED 50s: 0.9 mg/kg for
PCP
, 0.5 mg/kg for m-NH2
PCP
). However, the behaviorally inactive derivatives m-nitro (m-NO2
PCP
) and
PCP
methyliodide (
PCP
CH3I
) were ineffective up to 10 mg/kg.
PCP
(0.1-0.3 mg/kg i.v.) also decreased the duration of inhibition of CA1 discharges in a paired-stimulus paradigm; this was in contrast to the effects of thiopental and diazepam. In midcollicular-transected, urethane-anesthetized rats, the inhibitory effect of
PCP
on cCA3-CA1 transmission was not observed but the drug was still as effective as in intact rats in the paired-stimulus paradigm. In animals subjected to 6-hydroxydopamine lesions of the hippocampal noradrenergic innervation (average 85%) decrease in NE content), the potency of
PCP
in inhibiting cCA3-CA1 transmission was the same as in a group of sham-operated controls. These results suggest the following conclusions: (i)
PCP
exerts at least 2 separate types of effects in CA1, both of which result from a central action of the drug; (ii)
PCP
decreases the monosynaptic excitation of CA1 pyramidal cells and this action requires the integrity of brainstem afferents; (iii)
PCP
may decrease recurrent inhibition or afterhyperpolarization in CA1 via a mechanism which is independent of these connections and, therefore, could result from a direct action of the drug at the level of the hippocampus; (iv) finally, no evidence was found to suggest that the noradrenergic innervation of the hippocampus is critically involved in the action of
PCP
on CA1 discharges.
...
PMID:Effect of phencyclidines on hippocampal pyramidal cells. 681 48
A rare case of directly observed alkyl halide reductive elimination from rhodium is reported. Treatment of the naphthyl-based
PCP
-type Rh(III) methyl complexes 2a,b [(C10H5(CH2PR2)2)Rh(CH3)(I)] (R = iPr 2a, R = tBu 2b) with CO resulted in facile reductive elimination of methyl iodide in the case of 2b, yielding the Rh(I) carbonyl complex [(C10H5(CH2PR2)2)Rh(CO)] 3b (R = tBu), while the less bulky 2a formed CO adducts and did not undergo reductive elimination, contrary to expectations based on electron density considerations. Moreover, 3b oxidatively added methyl iodide, while 3a did not. CD3I/
CH3I
exchange studies in the absence of CO indicate that reversible formation of (ligated) methyl iodide takes place in both systems. Subsequently, when CO is present, it displaces methyl iodide in the bulkier tBu system, whereas with the iPr system formation of the Rh(III) CO adducts is favored. Iodide dissociation followed by its attack on the rhodium-methyl group is unlikely.
...
PMID:Direct observation of reductive elimination of methyl iodide from a rhodium(III) pincer complex: the importance of sterics. 1698 91
