Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phencyclidine (PCP) is a dissociative veterinary anesthetic and tranquilizer that at present is being abused as a psychedelic and hallucinogenic agent with increasing frequency. The cases of two young patients suffering from phencyclidine toxicity are reported. In each, central nervous system depression was accompanied by an acute dystonic motor reaction resulting in acute rhabdomyolysis and myoglobinuria. Skeletal muscle injury was felt to be the result of excessive involuntary isometrimc motor activity rather than a direct effect of phencyclidine on skeletal muscle. Patients suffering from phencyclidine intoxication should be screened for acute rhabdomyolysis. Phencyclidine intoxication should be included in the differential of nontraumatic rhabdomyolysis and should be considered among the potential causes of acute myoglobinuric renal failure.
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PMID:Phencyclidine-associated acute rhabdomyolysis. 62 51

delta9-Tetrahydrocannabinol (THC; 2.5, 5.0, 10.0 mg/kg, PO) impaired avoidance and rotarod performance, and caused bradycardia and hypothermia. Phencyclidine (PCP; 1.25, 2.5, 5.0 mg/kg, IP) impaired avoidance and rotarod performance and caused a marked increase in photocell activity. When combined, the depressant properties of each drug were enhanced and the stimulation of photocell activity cg/kg THC and its interactions with PCP followed subacute treatment for six days, whereas many of the effects of PCP were enhanced after subacute treatment with a dose of 2.5 mg/kg. Open-field behavior was affected by each drug alone and in combination in a similar way as photocell activity, but the depression caused by their interaction was greater; both drugs caused an increase in urination. Response rates on an FR-10 schedule of food reinforcement were decreased by 2.5 mg/kg PCP, but not by 5.0 mg/kg THC; the combination caused greater response suppression than either drug alone. The functional interactions between THC and PCP were not related to changes in the concentrations of 14C or 3H in plasma or brain derived from 14C-delta9-THC and 3H-PCP, respectively.
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PMID:Interactions between delta9-tetrahydrocannabinol and phencyclidine hydrochloride in rats. 85 Jun 86

The correlation between the three ischemia indicators angina pectoris (AP), ST-segment depression (ST) and excessive pulmonary wedge pressure rise (PCP) during exercise, and the coronary angiographic findings, were analysed in 293 patients without previous transmural myocardial infarction. This patient material consisted of 253 men and 40 women between the age of 20 and 65 years, the mean age being 48. The exercise tests were performed on a bicycle ergometer in supine position and in relatively steady state conditions. Pulmonary wedge pressure was measured by means of a Swan-Ganz floating catheter. The essential findings were: 1. If all three ischemia indicators were positive, the incidence of a positive angiographic finding i.e. a greater than or equal to 50% stenoses in at least one main coronary artery was 96.3%. 2. If only the two classic ischemia indicators were evaluated and positive, the incidence of a positive angiographic finding was only 86.1% (24). This difference is mainly due to false positive results of AP and ST in women. 3. If all three ischemia indicators were negative, the incidence of a negative angiographic finding was 89.2%. 4. If only the two classic ischemia indicators were evaluated and negative the incidence of a negative angiographic finding was as high (87,6% [24]). This lack of difference is due to the fact that patients with a previous intramural infarcion can be free not only of AP and ST but also of PCP during exercise. 5. The combination of AP and PCP, or ST and PCP, is equally reliable in predicting coronary morphology as the classic combination of AP and ST. It follows that PCP measurement is recommended, if one of the classic ischemia indicators cannot be properly evaluated.
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PMID:[Can predictability of coronary angiographic findings be improved by additional measurement of pulmonary wedge pressure during exercise? (author's transl)]. 91 74

The present study examined the behavioural effects of sigma agonists and PCP-like non-competitive N-methyl-D-aspartate (NMDA) antagonists in guinea-pigs. Subcutaneous (SC) injection of the putative sigma agonist (+)NANM (1 and 10 mg/kg SC) and (-)NANM (1 and 10 mg/kg SC) produced a behavioural response in guinea-pigs which was characterized by sedation and exophthalmos, with locomotor depression, flattened posture and flaccidity, whereas the sigma ligand pentazocine induced sedation but no flattened posture. Ketamine (20 mg/kg SC) and (+)dizocilpine (0.025, 0.1 and 1 mg/kg SC) produced similar effects to those of (+) and (-)NANM. However, the putative sigma receptor ligand DTG (1 and 10 mg/kg SC) had no observable effect on behaviours in guinea-pigs, similar to results for other species. The behavioural effects produced by (+) and (-)NANM were not reversed by injection 1 h later of naloxone hydrochloride (15 mg/kg SC), haloperidol (10 mg/kg SC) or DTG (10 and 30 mg/kg SC), but the effects of all drugs were reversed by the selective dopamine D-2 agonist quinpirole (3 mg/kg IP). Moreover, injection of naloxone (15 mg/kg SC), DTG (10 and 30 mg/kg SC) or haloperidol (1 and 10 mg/kg SC) 10 min before, did not reverse the behaviour induced by (+)NANM (10 mg/kg SC). These data indicate that sigma and PCP-like drugs have a similar gross behavioural effect in guinea-pigs, possibly mediated by non-competitive antagonism of the NMDA subtype of glutamate receptors. The results demonstrating behavioural depression were in contrast to the stimulatory effects of these drugs at similar doses in other rodent species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Similar behavioural effects of sigma agonists and PCP-like non-competitive NMDA antagonists in guinea-pigs. 168 18

Dipalmitoylphosphatidylcholine (DPPC) vesicles acquire negative surface charge on adsorption of negatively charged pentachlorophenolate (PCP-), and lipophilic ions tetraphenylborate (TPhB-), and dipicrylamine (DPA-). We have obtained (a) zeta-potential isotherms from the measurements of electrophoretic mobility of DPPC vesicles as a function of concentration of the adsorbing ions at different temperatures (25-42 degrees C), and (b) studied the effect of PCP- on gel-to-fluid phase transition by measuring the temperature dependence of zeta-potential at different PCP- concentrations. The zeta-potential isotherms of PCP- at 25, 32, and 34 degrees C correspond to adsorption to membrane in its gel phase. At 42 degrees C the zeta-potential isotherm corresponds to membrane in its fluid phase. These isotherms are well described by a Langmuir-Stern-Grahame adsorption model proposed by McLaughlin and Harary (1977. Biochemistry. 15:1941-1948). The zeta-potential isotherm at 37 degrees C does not follow the single-phase adsorption model. We have also observed anomalous adsorption isotherms for lipophilic ions TPhB- and DPA- at temperatures as low as 25 degrees C. These isotherms demonstrate a gel-to-fluid phase transition driven by ion adsorption to DPPC membrane during which the membrane changes from weakly to a strongly adsorbing state. The anomalous isotherm of PCP- and the temperature dependence of zeta-potential can be described by a two-phase model based on the combination of (a) Langmuir-Stern-Grahame model for each phase, (b) the coexistence of gel and fluid domains, and (c) depression of gel-to-fluid phase transition temperature by PCP-. Within the anomalous region the magnitude of zeta-potential rapidly increases concentration of adsorbing species, which was characterized in terms of a Esin-Markov coefficient. This effect can be exploited in membrane-based devices. Comments are also made on the possible effect of PCP, as an uncoupler, in energy transducing membranes.
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PMID:Domains and anomalous adsorption isotherms of dipalmitoylphosphatidylcholine membranes and lipophilic ions: pentachlorophenolate, tetraphenylborate, and dipicrylamine. 186 53

Huntington's disease (HD) is an inherited neuropsychiatric degenerative process characterized by movement disorder, dementia, and, often, affective disorder (AfD) (seen in 38% of patients). Depression in HD is not just an understandable reaction to fatal illness: 10% of HD patients develop mania; AfD can occur 20 yr before neurological signs; and mood disorders are not randomly distributed, but occur in a subset of HD families. This evidence suggests that AfD in HD relates to brain pathophysiology. With its clear neuropathology, HD is proposed as one model for biological underpinnings of idiopathic AfD. There is striking atrophy and neuronal loss in HD neostriatum, particularly caudate. Caudate has rich connections to the limbic system. It is hypothesized that AfD in HD relates to dysfunction of the part of the neostriatum damaged earliest, dorsal medial caudate. Preliminary studies on neuropathological differences between HD patients with and without AfD are discussed. HD neurochemistry is reviewed, emphasizing the excitotoxin hypothesis, which involves dysfunction of the glutamate neurotransmitter system in HD (especially the NMDA receptor, which contains a channel with a phencyclidine (PCP) binding site). Based on the HD model, it is suggested that the glutamate system (particularly NMDA receptors) be examined in idiopathic AfD.
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PMID:Huntington's disease as a model for mood disorders. Clues from neuropathology and neurochemistry. 214 28

For the past 5 years there has been an exponential increase in the use of cocaine, phenylcyclidine hydrochloride (PCP), and other central nervous system (CNS) active drugs. A significant amount of this accelerated usage is in sexually active females, resulting in some urban hospitals reporting positive drug screens in over 16% of the infants born on their busy obstetrical service. There is a growing body of data showing that fetal exposure to cocaine, phenylcyclidine hydrochloride (PCP), and other CNS-active drugs results in infants and children with abnormal brain wave patterns, short-term neurologic signs, depression of interactive behavior, and poor organizational responses to environmental stimuli. Whether such neurologic findings will translate into a significant number of children with learning and behavioral problems needs to be the focus of long-term longitudinal studies of children with fetal drug exposure to cocaine, PCP, and other CNS-active drugs.
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PMID:Fetal drug exposure and its possible implications for learning in the preschool and school-age population. 217 42

The actions of phencyclidine [1-(1-phenylcyclohexyl)piperidine, PCP] and its morpholine analog [1-(1-phenylcyclohexyl)morpholine, PCM] on ionic currents of nicotinic acetylcholine receptors were studied at the neuromuscular junction of frog skeletal muscle and on embryonic rat muscle cells in tissue culture. PCP and PCM reduced the peak amplitude and the decay time constant of the endplate current (EPC). PCP produced a voltage-dependent curvature and a time-dependent hysteresis loop at negative potentials (at potentials from -50 to -150 mV). In contrast, PCM caused a depression of EPC peak amplitude, but the current-voltage relationship (+60 to -150 mV) remained linear. When PCP-modified EPCs were elicited in trains at hyperpolarized potentials the amplitudes of successive events were progressively decreased and the magnitude of the decrease was dependent on the level of hyperpolarization. At positive potentials the process was reversed; the amplitude increased with successive stimulations. The EPC decayed exponentially in the presence of PCP and PCM, with a shortened time constant of decay that was less dependent on membrane potential than control. PCP and PCM caused only a 20% decrease of the amplitude of the iontophoretically evoked acetylcholine potential, which was significantly different from that induced by the desensitizing alkaloid perhydrohistrionicotoxin. Both PCP and PCM reduced by 50% the mean channel open time obtained from rat myoballs, giving a potency ratio for PCP to PCM of 2.5. This relative potency was correlated with that obtained for the reduction in the decay time constant of the EPC (ratio = 2.2). The effects of PCP on the peak amplitude of the EPC seem to be related to a conformational change of the acetylcholine receptor occurring before channel activation and not to a receptor desensitization.
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PMID:Voltage- and time-dependent effects of phencyclidines on the endplate current arise from open and closed channel blockade. 242 53

The interaction between phencyclidine (PCP) and the catecholamine precursor L-3,4-dihydroxyphenylalanine (DOPA) was studied in the isolated spinal cord from neonatal rats. PCP decreased the magnitude of the dorsal-ventral reflex and enhanced frequency-dependent depression of the reflex in a concentration-dependent manner. Although DOPA and DL-threo-3,4-dihydroxyphenylserine (a direct precursor for norepinephrine) had no effect on the reflex by themselves, DOPA, but not DL-threo-3,4-dihydroxyphenylserine prevented the depression of the reflex response by PCP in a concentration-dependent manner. Inhibition of aromatic-L-amino-acid decarboxylase (EC 4.1.1.2A) by m-hydroxybenzylhydrazine markedly attenuated the action of DOPA in preventing the depression caused by PCP. The dopamine receptor antagonists haloperidol and chlorpromazine blocked the action of DOPA, but the alpha and beta adrenergic receptor antagonists phentolamine and timolol, respectively, did not. In addition, prior treatment of neonatal rats with 6-hydroxydopamine diminished the ability of DOPA to prevent the depressant effect of PCP whereas partially attenuating the depressant effect of PCP alone. These results suggest that DOPA attenuated PCP-induced depression of spinal cord transmission through its conversion to dopamine rather than norepinephrine.
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PMID:Prevention of phencyclidine-induced depression of the segmental reflex by L-3,4-dihydroxyphenylalanine in the rat spinal cord in vitro. 249 50

1. In electrophysiological experiments in spinalized, alpha-chloralose anaesthetized rats, opioids and anaesthetics were tested intravenously (i.v.) on the responses of individual motoneurones to alternating noxious (heat or pinch) and non-noxious (tap or vibration) stimuli. 2. On cells that were sensitive to low doses of mu-opioids, both fentanyl (0.5-4 micrograms kg-1 i.v.) and morphine (0.5 mg kg-1 i.v.) selectivity reduced reflexes to noxious stimuli to a greater degree than the higher doses required to reduce nociceptive reflexes (fentanyl 8 micrograms kg-1 i.v.; morphine 1-8 mg kg-1 i.v.) depressed non-nociceptive reflexes to a similar degree. 3. A similar spectrum of selectivity was seen with U-50,488 (0.5-16 mg kg-1 i.v.) although statistically significant selective depression of reflexes was only evident at the lowest dose tested (0.5 mg kg-1 i.v.). All effects of U-50,488 were readily reversed by low doses of the opioid antagonist, naloxone (10-100 micrograms kg-1 i.v.). 4. The dissociative anaesthetic/PCP ligand ketamine (0.5-4 mg kg-1 i.v.) was similar in having selective actions at low doses on sensitive cells but non-selective actions when higher doses were required. In contrast, the general anaesthetics methohexitone (4 mg kg-1 i.v.) and alphadolone/alphaxalone (1 mg kg-1 i.v.) were consistently non-selective between reflexes to noxious and non-noxious stimuli. alpha-Chloralose (20-40 mg kg-1 i.v.) had very little effect on reflexes to any of the synaptic inputs tested.
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PMID:On the selectivity of intravenous mu- and kappa-opioids between nociceptive and non-nociceptive reflexes in the spinalized rat. 255 13


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