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I Kitchen

Publications and source records attributed to I Kitchen.

At least 91 records · Page 5Linked to original sources
PubMed1986

Binding characteristics of [D-Ala2-MePhe4-Glyol5] enkephalin and [D-Pen2,D-Pen5] enkephalin in rat brain: inhibition studies with fentanyl-like drugs.

We have investigated the binding characteristics of two tritiated enkephalin analogues [D-Ala2-MePhe4-Glyol5] enkephalin (DAGO) and [D-Pen2, D-Pen5] enkephalin (DPDPE) which are highly selective for mu and delta opioid sites respectively, in homogenates of whole rat brain and of the pons/medulla region. In addition, we have explored the binding profile of four 4-anilinopiperidine drugs (fentanyls) by means of inhibition studies. Our studies show that the delta involvement in pons/medulla of rat is small compared with that in whole brain and with mu binding in both whole brain and pons/medulla. In addition the rank order of affinities of the fentanyl series is the same at the mu and delta site, but the affinities are between 1 and 600-fold greater at the former site.

Animals↗
PubMed1986

Development of delta-opioid receptors in rat brain characterised by [3H]-[D-Pen2,D-Pen5] enkephalin binding.

The development of rat brain delta-opioid receptors has been studied in the postnatal period using the highly selective delta-site ligand [3H]-[D-Pen2, D-Pen5] enkephalin (DPDPE) in binding studies. Between day 10 and day 25 there was a three-fold increase in the number of binding sites (expressed per mg protein) and the KD was constant throughout the postnatal period. Specific binding could not be detected earlier than day 10.

Aging↗
PubMed1985

Determination of proenkephalin products in brain tissue by high-performance liquid chromatography and a modified bioassay procedure.

A method is described for the separation of proenkephalin products using gradient high-performance liquid chromatography preceded by Sep-Pak chromatography. Samples can be assayed simply by use of a modified mouse vas deferens bioassay which is sufficiently sensitive for most applications. The preliminary Sep-Pak chromatography method excludes alpha-neoendorphin and the dynorphins and thus provides a suitable procedure for separation of prodynorphin and proenkephalin products.

Animals↗
PubMed1985

Assessment of the hot-plate antinociceptive test in mice. A new method for the statistical treatment of graded data.

The use of graded data from hot-plate antinociceptive tests is complicated by the problem of how to treat responses that are greater than the cut-off time. This paper describes a statistical procedure for analysis of antinociceptive data that circumvents this problem. The method is based upon the likelihood function and the data is assumed to follow a Weibull distribution. The technique can be implemented with the use of a computer and provides a more comprehensive assessment of antinociceptive data.

Analgesics↗
PubMed1985

Ontogenesis of proenkephalin products in rat striatum and the inhibitory effects of low-level lead exposure.

Certain developmental abnormalities have been associated with environmental exposure to lead and our previous studies have indicated that the endogenous opioid system is disrupted by this metal. In connection with this we report the ontogeny of proenkephalin products in the rat striatum determined by combined HPLC and bioassay and the effects of low-level lead exposure on this ontogeny. The development of Met-enkephalin levels was dissimilar from that of the other proenkephalin products, Met-enkephalyl-Arg6-Phe7, Met-enkephalyl-Arg6-Gly7-Leu8 and Leu-enkephalin. The ratios of Met-enkephalin containing peptides to Leu-enkephalin was less than the 6:1 ratio predicted from the proenkephalin structure. Lead (administered in the maternal drinking water, from conception to weaning at 100, 300 and 1000 ppm) caused a dose-related depression of the levels of proenkephalin products in rat striatum at 10, 21 and 30 days after birth. The most pronounced effects were observed at 10 days and the most persistent effects were seen with Met-enkephalin. Peak blood lead levels were below 45 micrograms/100 ml in the 100 and 300 ppm lead-dosed groups and in all lead-dosed groups at 10 days after birth. It is suggested that lead may have inhibitory effects on proenkephalin-processing enzymes.

Animals↗
PubMed1985

Impairment of ketocyclazocine antinociception in rats by perinatal lead exposure.

The development of ketocyclazocine antinociception has been measured in lead-exposed rats as an indirect determinant of kappa-opioid receptor system development. Perinatal lead administration (at 300 and 1000 ppm) in the maternal drinking water from conception to weaning, impaired the antinociceptive activity of ketocyclazocine (using the paw pressure test) in 10-day-old rats. Lead caused a dose-dependent impairment of ketocyclazocine antinociception, the paw pressure threshold for 0.4 mg/kg being reduced from 207 g to 135 g in the 1000 ppm lead dose-group. Ketocyclazocine antinociception was impaired in the high-lead dose-group at 21 days, but unaffected at 30 days. Blood lead levels in 10-day-old animals were below 35 micrograms/100 ml in the low-lead dose-group and below 50 micrograms/100 ml in the high-lead dose-group. It is suggested that lead may disrupt the development of kappa-opioid receptor systems in the central nervous system and that this disruption occurs early in development.

Animals↗
PubMed1985

Different effects of di-isopropylfluorophosphate on the entry of opioids into mouse brain.

Di-isopropylfluorophosphate (DFP) potentiates the antinociceptive activity of alfentanil but has no effect on the activity of morphine or fentanyl. We have studied the effect of DFP on the distribution of these three opioids in the brain. Distribution studies were carried out using 3H-labelled opioids administered subcutaneously to mice. Animals were killed at times of peak antinociceptive activity and 3H-opioid measured in plasma and in eight brain regions. DFP pretreatment (1 mg kg-1) caused a significant increase in the brain:plasma ratio of alfentanil in all brain regions but had no effect on brain:plasma ratios for morphine or fentanyl. The enhanced entry of alfentanil into the brain of DFP-treated mice probably accounts for the increased antinociception observed with this opioid. This drug interaction appears to be opioid specific.

Alfentanil↗
PubMed1984

Differences in the effects of mu- and delta-opioid receptor antagonists upon plasma corticosterone levels in stressed mice.

The effects of intraperitoneal injections of two opioid antagonists on plasma corticosterone levels in stressed mice was investigated. The effects of the mu-opioid receptor antagonist naloxone was dependent on the dose used. Low doses (0.5 and 1 mg/kg) potentiated the elevation of plasma corticosterone observed in saline treated or ether stressed mice, whereas a higher dose (10 mg/kg) produced the opposite effect. The delta-opioid receptor antagonist ICI 154,129 had no significant effect on corticosterone levels. The findings suggest that mu- rather than delta-opioid receptors are important in modifying corticosterone responses to stress and raise the question as to specificity of naloxone at doses above 1 mg/kg.

Animals↗
PubMed1984

The effect of perinatal lead administration on the ontogeny of striatal enkephalin levels in the rat.

The effect of administration of lead in the maternal drinking water from conception to weaning on enkephalin levels in the developing rat striatum was studied between 10 and 100 days after birth. Concentrations of 300 and 1000 ppm Pb produced no overt toxicity in terms of effects on body and brain weight. However, marked differences in striatal enkephalins were observed. In lead-dosed animals enkephalin content was up to 50% lower at 10 and 21 days postpartum, and in addition lead appeared to delay the attainment of adult levels of this opioid neurotransmitter. Measures at later time points indicated that the effects of lead on enkephalin are reversible. The results suggest that lead depresses and delays the ontogeny of the enkephalinergic system within the striatum.

Animals↗
PubMed1984

Low-level lead exposure alters morphine antinociception in neonatal rats.

Administration of lead (at 300 and 1000 ppm) in the maternal drinking water from conception to weaning impaired the antinociceptive activity of morphine in 10-day-old neonatal rats. Blood lead levels in these animals were below 50 microgram/100 ml in the high lead dose group and below 35 microgram/100 ml in the low lead dose group. The differences in the antinociceptive potency of morphine between normal and lead-exposed animals were not observed at later time points (21 and 30 days). It is suggested that lead disrupts the development of opioid receptor systems in the central nervous system and that this disruption occurs early in development.

Analgesia↗
PubMed1983

Differential effects of di-isopropylfluorophosphate poisoning and its treatment on opioid antinociception in the mouse.

Compounds which enhance cholinergic activity have been reported to interact with opioid drugs. We have shown, using the hot-plate test in mice that di-isopropylfluorophosphate potentiates the antinociceptive activity of alfentanil but has no effect on the activity of morphine or fentanyl. Administration of atropine and pralidoxime as a treatment for DFP poisoning does not reverse this effect, and itself potentiates morphine antinociception. The results suggest that a cholinergic/opioid interaction is dependent on the opioid studied, and may have clinical importance when opioid drugs are required in patients poisoned by irreversible anticholinesterases.

Animals↗
PubMed1981

Differential loss of biological activity of the enkephalins induced by current.

Passage of current across solutions of enkephalins caused loss of biological activity of the peptides, this loss increasing as current strength was increased. The presence of a vas deferens tissue prevented the current-induced loss of activity of Leu-enkephalin but had no effect on the loss of activity of Met-enkephalin. These results provide a possible explanation for the differential potency of the enkephalins on the vas and provide a reason for the inability of several laboratories to show electrically induced enkephalin release.

Animals↗