Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two molar urea (pH 7.5) and column chromatography on Sepharose 4B were used to separate clathrin (coat protein) from the membrane of coated vesicles from bovine brain. Lytron (polystyrene) particles were used for study of the interaction of clathrin with contractile proteins. Muscle G-actin, F-actin, and alpha-actinin were bound by clathrin-coated Lytron particles, while no interaction was found when muscle tropomyosin and serum albumin were tested. Clathrin molecules dispersed in a solution of 20 mM Tris-HCl (pH 7.5) were found to be elongated. When the pH was adjusted from 7.5 to 6.5, clathrin molecules associated into basketlike or cage structures similar in size and shape to those observed in enriched preparations of coated vesicles. Below pH 6.0, cages or baskets became amorphous aggregates. Raising the pH from 6.5 to 8.0, addition of 5-10 mM ATP or EDTA, or addition of 200 mM KCl resulted in the dissassembly of baskets and the formation of filamentous arrays of various widths. Because of clathrin's biochemical and biophysical properties, its interaction with contractile proteins, and its presence in the membrane of vesicles of various cell types, we classified clathrin in the group of mechanochemical proteins.
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PMID:Mechanochemical properties of brain clathrin: interactions with actin and alpha-actinin and polymerization into basketlike structures or filaments. 3 47

The emotional behavioral aspects and the interaction between the changes of the polyamine contents and muricide response in thiamine deficient rats were investigated. In the thiamine deficient group, there was evidence of muricide and such increased progressively with advanced thiamine deficient feeding. This muricide was characteristic in the following respects; 1) the killer-rats did not eat but only kill a mouse and it was quite difficult to remove a sacrificed animal from the cage. 2) they bit at random into any body region of the mouse. 3) the killer-rats did not bite inanimate objects such as nails nor chalk. 4) the muricide induced by thiamine deficiency could not be suppressed by a single injection of thiamine HCl. On the 30th day of the experimental feeding, both spermidine and spermine levels in the brain of the thiamine deficient group decreased significantly as compared to the control and the pair-fed groups. Both spermidine and spermine levels were reversed to the control levels with a intraperitoneal administration of thiamine. There were no significant differences in spermine and spermidine levels between the killer-rats and non-killer-rats in the thiamine deficient group.
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PMID:[Muricide induced by thiamine deficiency in the rats (author's transl)]. 56

Gravid Sprague-Dawley CD (VAF) rats received 50 mg/kg (d,l)-methamphetamine (MA) HCl (expressed as free base, N = 15) or distilled water (N = 6) by SC injection x 2/day in a 3 ml/kg volume on embryonic (E) days 7-12. Control rats were pair-fed to MA-exposed dams on days E7-18. No control dams failed to deliver; however, of 15 MA-exposed dams 4 did not deliver (2 died and 2 had completely resorbed litters). One additional MA litter had all the offspring die shortly after birth. There was no difference between groups on offspring postnatal (P) body weight. The offspring exposed prenatally to MA had significantly lower olfactory orientation scores (P9, 11, 13) to their home cage scent. In a test of early activity (P10, 12, 14) the MA-exposed progeny were marginally less active than controls. MA-exposed offspring exhibited hyperreactivity and marginally shortened response latency on a test of acoustic startle (P27). Motor activity showed no differential response in MA treated or control offspring to MA (P63) or fluoxetine challenge (P70). However, the MA offspring were more active than controls with respect to central and side activity during the second week of testing. No group differences were found for performance in a straight swimming channel or on the number of errors committed or latency to escape in a complex (Cincinnati) water maze (P84). Prenatal exposure to MA also induced eye defects (i.e., anophthalmia, microphthalmia and folded retina) in 16.7% of the progeny. However, MA did not effect hippocampal or neostriatal monoamine levels when measured on P28.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preliminary evidence for methamphetamine-induced behavioral and ocular effects in rat offspring following exposure during early organogenesis. 136 24

The effect of rearing condition and prenatal exposure to cocaine on maternal behaviors was examined. Sprague-Dawley dams were given SC injections of 40 mg/kg/3cc cocaine HCl (C40) or saline (LC) daily from gestational days 8-20. Maternal behavior was assessed in treated dams rearing their biological pups (LC/LC; C40/C40), treated dams rearing untreated pups (LC/FOS; C40/FOS), and foster dams rearing treated pups (FOS/LC; FOS/C40). All dams were monitored for home cage behavior (time eating, drinking, and with pups) for 2 h during both the light and dark cycle on postnatal day 4 (P4), pup retrieval on P5-P9, and maternal aggression to a female intruder (latency to the first attack, number of attacks, boxing, pins, intruder time spent submissive and motionless) on P10. No differences were observed in nest behavior or in tests of pup retrieval among the six groups. Dams rearing their biological litter (LC/LC and C40/C40) were significantly quicker to initiate the first attack when compared to all other groups. This increased aggression was maintained throughout the test session in the C40/C40 dams who made significantly more intruder attacks than all other groups, with the intruder spending significantly more time in a submissive posture (lying on back). In contrast, LC/LC dams did not exhibit an increased number of attacks during the test, apparently responding to an increased freezing in their intruders with a reduction in aggressive behavior. Taken together these findings suggest that prior cocaine exposure results in alterations in maternal aggression that is evident when these dams rear their own pups.
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PMID:A fostering study of the effects of prenatal cocaine exposure: I. Maternal behaviors. 148 36

In order to clarify the effects of ethanol (EtOH) on metabolism of methamphetamine hydrochloride (MA-HCl), the plasma and urine samples were taken from three groups of three male crab-eating monkeys (Macaca fascicularis). MA-HCl was given to the first group, both MA-HCl and EtOH were given once to the second group, the after consecutive administration of EtOH for four weeks, both MA-HCl and EtOH were given to the third group. Comparisons were made of the sequential change in the concentration of unchanged methamphetamine (MA) and its supposed metabolites, amphetamine (AP), p-hydroxymethamphetamine (p-HOMA), and p-hydroxyamphetamine (p-HOAP). Additional hematological and plasma-biochemical tests were performed to monitor the influences under the administration of MA-HCl and EtOH on the animals. For the extraction of MA and its metabolites from blood and urine, a solid phase extraction was carried out with which an excellent recovery was achieved. Gas chromatography mass spectrometry (GC-MS) was used to measure the metabolites after changing them to the form of TFA derivative, producing good results. EtOH concentration in the blood was measured by GC using a head-space method. The biological half-life (t1/2) of MA tended to be shortened slightly in the plasma when EtOH was given consecutively. The maximum concentration of AP obtained by administration of EtOH was half that obtained by single administration of MA-HCl and the detectable time was shortened. A high concentration of p-hydroxy metabolites that the been almost undetectable when both MA-HCl and EtOH were administered once, was detected when EtOH was administered consecutively, compared with that when only MA-HCl was administered. Particularly, considerable amounts of p-HOAP was detected even after 72 hours. The trends seen in the excretion of MA and its metabolites into the urine were the same as seen in their plasma concentrations, although there was a difference in the detectable time. The urine collected in a metabolic cage for the monkey was contaminated with drinking water, so that the total amounts of metabolites, rather than sequential change as in the case of plasma, were considered to be of greater significance. When EtOH was administered consecutively, the excreted amounts of p-HOAP in the urine increased saliently and characteristically.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The effect of ethanol on the metabolism of methamphetamine]. 159 31

Male spiny mice (Acomys cahirinus) were challenged with several putative dipsogenic stimulus conditions: hypertonic sodium chloride (NaCl), 24-h water deprivation, d,l-isoproterenol HCl, angiotensin II (AII) and polyethylene glycol (PEG), or control conditions, in within-subjects designs. Water intake and drinking pattern were monitored electronically in the home cage over a 2--6-h test period without food present, during the light portion of the L/D cycle. In addition, hematocrits were measured following several treatments and mean arterial blood pressure was monitored in response to several doses of AII. As expected, both water deprivation and hypertonic NaCl led to robust drinking with short latencies. PEG was also an effective dipsogen; while quite variable, latencies were often shorter than are typically reported for the rat. Isoproterenol induced a modest, but significant, dose-related drinking. Interference by AII's prominent pressor action might account, at least in part, for its relative ineffectiveness as a dipsogen. Comparisons are made with other rodent species similarly challenged.
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PMID:Drinking behavior in the spiny mouse (Acomys cahirinus) following putative dipsogenic challenges. 187 Dec 4

The domains on clathrin responsible for interaction with the plasma membrane-associated assembly protein AP-2 have been studied using a novel cage binding assay. AP-2 bound to pure clathrin cages but not to coat structures already containing AP that had been prepared by coassembly. Binding to preassembled cages also occurred in the presence of elevated Tris-HCl concentrations (greater than or equal to 200 mM) which block AP-2 interactions with free clathrin. AP-2 interactions with assembled cages could also be distinguished from AP-2 binding to clathrin trimers by sodium tripolyphosphate (NaPPPi), which binds to the alpha subunit of AP-2 (Beck, K., and Keen, J. H. (1991) J. Biol. Chem. 266, 4442-4447). At concentrations of 1-5 mM, NaPPPi blocked clathrin-triskelion binding; in contrast, interactions with cages persisted in the presence of 25 mM NaPPPi. To begin to identify the region(s) of the clathrin molecule important in recognition by AP-2, clathrin cages were proteolyzed to remove heavy chain terminal domains and portions of the distal leg as well as all of the light chains. AP-2 bound to these "clipped cages"; however, unlike the interaction with native cages, binding of AP-2 to clipped cages was sensitive to the lower concentrations of both Tris-HCl and NaPPPi which disrupt interactions of AP-2 with clathrin trimers. Reconstitution of the clipped cages with clathrin light chains did not restore resistance of AP-2 binding to Tris-HCl. We conclude that one binding site for AP-2 resides on the hub and/or proximal part of the clathrin triskelion whereas a second site is likely to involve the terminal domain and/or distal leg; the second site is manifested only in the assembled lattice structure. We suggest that these two distinct binding interactions may be mediated by the two unique large subunits within the AP-2 complex, acting sequentially during assembly.
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PMID:Clathrin domains involved in recognition by assembly protein AP-2. 190 33

The effects of the superactive agonist analog D-Trp-6-LH-RH were investigated in several neuropharmacological tests: inhibition of picrotoxin-induced seizures, open-field behavior, hot-plate and tail-flick tests, assessment of catalepsy and apomorphine-induced cage-climbing. In most tests, D-Trp-6-LH-RH was administered subcutaneously (sc.) at the dose of 100 micrograms/kg. The opiate involvement in the peptide action was checked by using naloxone HCl (NX) in a dose of 1 mg/kg intraperitoneally (ip.), with the exception of the analgesic tests where the dose was 0.5 mg/kg. The analog significantly suppressed the open-field parameters of ambulation, rearing and grooming; except for grooming, these actions were fully antagonized by NX. Similarly, NX pretreatment restored to the control levels the latencies of seizure parameters increased by D-Trp-6-LH-RH. The hot-plate latencies did not change after pretreatment with NX but the opiate antagonist was fully able to antagonize the analgesic effect of the peptide in the tail-flick test. The cataleptogenic effect and the inhibition of apomorphine-induced cage-climbing demonstrated after D-Trp-LH-RH were not antagonized by NX.
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PMID:Partial reversal of behavioral action of the agonist D-Trp-6-LH-RH by naloxone in mice. 213 49

Male rats were injected with methadone HCl (METH) at 5 mg/kg s.c. for 4 days prior to mating with drug-free females. Offspring resulting from these matings were compared with offspring of drug-free males. The progeny of METH-treated males gained less weight after weaning and had lighter thymuses as adults (but not in infancy). Gonadal weights did not differ in infancy or adulthood, and adrenal weights were heavier in female offspring in adulthood. In adulthood METH offspring were significantly different from controls on all behavioural tests used (open field activity, activity cage activity, passive avoidance latencies, shuttle box avoidances, and rotarod latencies), with the differences frequently affected by test order, days of testing, or sex of offspring. The effects in progeny of METH-treated males in the absence of differences in litter size or neonatal mortality indicate that paternal drug ingestion prior to mating can produce physiological and behavioural changes in progeny that are not dependent on detectable effects on early viability or growth.
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PMID:Progeny of male rats treated with methadone: physiological and behavioural effects. 232 32

Antihistamines are being increasingly administered in combination with various other agents, with adverse drug reactions the frequent result. The present study consisted of two experiments. Experiment 1 examined the toxicological response of rats to nicotine tartrate (0.0, 2.0, 4.0, and 8.0 mg/kg) in combination with either of two H1-histamine receptor antagonists, the ethylene diamine tripelennamine HCl (0.0, 16.0, 32.0, and 64.0 mg/kg) or the aminoethyl ether diphenhydramine HCl (0.0, 32.0, 64.0, and 96.0 mg/kg). Adult female rats received intraperitoneal injections when housed 12 per cage and toxicological response (number dead per group) was assessed 24 hours post-treatment. The results showed that over the dose ranges employed, and when given alone, nicotine was completely non-lethal, tripelennamine was virtually non-lethal and diphenhydramine was toxic only at the highest dose (5 of 12, at 96.0 mg/kg). However, when nicotine and the antihistamines were delivered in combinations, the toxicological response was markedly altered. Tripelennamine in combination with nicotine yielded supra-additive interaction, with the degree of potentiation being a simple linear function of nicotine within each dose of tripelennamine. The interaction between nicotine and diphenhydramine was more complicated, with certain dose combinations yielding supra-additivity, yet with others yielding antagonism. It was suggested that seizure-precipitated cardiopulmonary collapse was the immediate cause of death, plausibly mediated by central mechanisms. As such, Experiment 2 examined the influence of adding the proconvulsant pentylenetetrazole (PTZ) (0.0, 10.0, and 20.0 mg/kg) to nicotine (0.0, 2.0, 4.0, and 8.0 mg/kg)-tripelennamine (0.0 and 32.0 mg/kg) combination treatments. Effects were assessed both at 1.0 and 24.0 hours post-injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Supra-additive toxic interaction of nicotine with antihistamines, and enhancement by the proconvulsant pentylenetetrazole. 285 8


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