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P D Butler

Publications and source records attributed to P D Butler.

At least 37 records · Page 2Linked to original sources
PubMed1990

Corticotropin-releasing factor produces fear-enhancing and behavioral activating effects following infusion into the locus coeruleus.

The present series of experiments tested the hypothesis that the behavioral activating and anxiogenic effects produced by intraventricular administration of corticotropin-releasing factor (CRF) may be mediated by noradrenergic neurons in the brain-stem locus coeruleus (LC). Results showed that infusion of CRF into the LC (100 ng) significantly increased nonambulatory spontaneous motor activity measured in photocell cages; ambulatory (i.e., locomotor) activity was not altered. In the modified Porsolt swim test, which examines arousal and agitation in a stressful situation, significant behavioral activation (i.e., decreased floating) was seen following infusion of CRF (10 ng) into the LC; a 500 ng dose of CRF was necessary to produce similar effects following infusion into the lateral ventricle. The results of these 2 tests suggest that the behavioral activating effects of CRF in the LC may be related to arousing or stress-related effects, rather than to increased locomotor activity per se. Anxiogenic activity was assessed in animals placed in an open field containing a small, darkened compartment. Infusion or CRF into the LC (1-100 ng) significantly increased the time spent in the compartment and decreased the amount of time spent exploring the outside of the compartment or venturing into the inner squares of the open field, all indices of anxiogenic behavior. Biochemical studies showed that bilateral infusion of CRF into the LC produced significant increases in the concentration of the norepinephrine metabolite 3,4-dihydroxyphenylglycol in such forebrain projection areas of the LC as the amygdala and posterior hypothalamus. These data, taken together, suggest that CRF produces its behavioral activating and anxiogenic effects, at least in part, by increasing the activity of LC noradrenergic neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Imipramine and tetrabenazine: effects on monoamine receptor binding sites and phosphoinositide hydrolysis.

Treatment of rats for 21 days with tetrabenazine, a drug which depletes monoamines and is used behaviorally to screen for antidepressants, significantly decreased 5-HT2 receptor density, increased alpha 1-adrenoceptor density but did not alter beta-adrenoceptor density in homogenates of frontal cortices labeled with [3H]ketanserin, [3H]prazosin and [3H]dihydroalprenolol, respectively. These effects were not opposite to those of the antidepressant drug imipramine which decreased both 5-HT2 and beta-adrenoceptor density and did not alter alpha 1-adrenoceptor density. Some evidence for antagonistic interactions between the two drugs was found in that imipramine partially prevented the tetrabenazine-induced increase in alpha 1-adrenoceptor density and tetrabenazine partially prevented the imipramine-induced decrease in beta-adrenoceptor density. Neither drug altered phosphoinositide hydrolysis coupled to alpha 1-adrenoceptors. While the effects of tetrabenazine are frequently attributed to its reserpine-like action of depleting monoamines, these results provide the first indication that tetrabenazine alters 5-HT2 and beta-adrenoceptor density in a manner different from that of reserpine.

Animals↗
PubMed1987

Agonist-stimulation of cerebral phosphoinositide turnover following long-term treatment with antidepressants.

Receptor-mediated stimulation of the formation of inositol phosphates (IP) in cerebral tissue may serve as a useful tool for studying long-term changes in the function of serotonin-2 (5-HT2), alpha-1-adrenergic (al), and muscarinic-cholinergic (musc) receptors. In this study we have evaluated the effects of chronic treatment with various antidepressants on receptor-mediated formation of IP in rat brain. Imipramine (IMI: 10 mg/kg/day; 14 days), Bupropion (BUPR: 40 mg/kg/day; 14 days), Lithium (Li: 0.5% in diet; 7 days) and electroshock treatment (EST: 20-30 mA/day; 7 days) were investigated. Cross-chopped slices of cerebral cortex from control and treated rats were prelabelled with myo-3H-inositol in HEPES buffer containing 11.1 mM LiCl. Accumulation of IP was measured in the presence and absence of serotonin (5-HT, 10 uM), norepinepherine (NE, 5 uM), and carbamylcholine (CCH, 100 uM). Values for agonist-stimulated IP formation in control rats were: 5-HT = 123 +/- 5%; NE = 268 +/- 16%; CCh = 205 +/- 21% of the basal level. The IP response to 5-HT was significantly lower following BUPR and higher following EST. Responses to NE and CCH were significantly lower following BUPR treatment but were not affected by the other antidepressant treatments. These observations are consistent with results of receptor-binding studies indicating up-regulation of 5-HT2 receptors by EST but are not consistent with studies showing down-regulation of 5-HT2 receptors by IMI and a lack of effect on 5-HT2 receptors by BUPR. Our results are not supportive of the notion, based mainly on [3H]prazosin binding studies, that al receptors are up-regulated by EST as well as by different antidepressant drugs.

Animals↗
PubMed1987

Nucleotide sequence of the sporulation operon, spoIIIE, of Bacillus subtilis.

A fragment of Bacillus subtilis DNA 3490 bp long, capable of complementing spoIIIE mutations, was sequenced. The region of the fragment that encodes functions required for sporulation was delimited using integrational plasmids. Sequencing showed that this region contained an operon with two open reading frames together with associated ribosome-binding sites. The deduced translation products would be polypeptides of 518 and 252 amino acid residues. Several sequences resembling promoters recognized by RNA polymerase containing sigma 29 occur in the region preceding the larger open reading frame. Although no transcription-termination signal was identified downstream of the smaller coding region, analysis with integrational plasmids and determination of the size of spoIIIE messenger RNA suggest that the locus does not contain a third gene.

Bacillus subtilis↗
PubMed1985

The location of a mutation affecting ribosomal protein synthesis by Escherichia coli.

A mutation in a strain of Escherichia coli 15 produced ribosomes by an abnormal pathway that caused the accumulation of 47S ribonucleoprotein particles. The mutation was transferred to strains of E. coli K12 by transductions with bacteriophage P1cam and was at about 82 min, between cysE and pyrE and rather closer to the latter. The location and the physiological properties of the mutant suggested that the mutation was in the rpmB,G transcription unit and affected the synthesis of ribosomal proteins L28 and L33.

Centrifugation, Density Gradient↗
PubMed1985

Interactions between mutations affecting ribosome synthesis in Escherichia coli.

RNA synthesis was followed during amino acid starvation of strains of Escherichia coli that contained both the relaxed (relA) mutation and a mutation affecting ribosome assembly that results in oversynthesis of RNA. The ribosome mutation did not by itself lead to relaxedness. The relaxed mutation could be expressed in organisms that contained the ribosome mutation.

Amino Acids↗
PubMed1984

Ribosomal protein synthesis by a mutant of Escherichia coli.

The mutant strain of Escherichia coli, TP28, synthesises ribosomes by an abnormal pathway and accumulates large quantities of 47S ribonucleoprotein particles. The protein complement of mutant 70S ribosomes is normal but 47S particles contain only traces of proteins L28 and L33 and have a significantly reduced content of four other proteins. The mutation reduces the rates of synthesis of L28 and L33 by about half but other widespread alterations ensue. In particular, ribosomal protein synthesis in the mutant strain becomes less well balanced than in its parent: some proteins, particularly those from promoter-proximal genes, are oversynthesized and their excess then degraded.

Escherichia coli↗
PubMed1984

Monosodium glutamate and analgesia induced by morphine. Test-specific effects.

Neonatal administration of monosodium glutamate (MSG) destroyed perikarya in the arcuate nucleus and median eminence, including those that contain met-enkephalin and beta-endorphin and it increased the density of opiate receptors in the midbrain. Treatment with glutamate decreased the analgesic response on the jump test following a 10 mg/kg dose of morphine, yet increased the analgesic response on the hot-plate test following 1 mg/kg dose of morphine. The present study demonstrated that changes in morphine-induced analgesia induced by glutamate varied as functions of the pain test and of gender. While males treated with glutamate displayed attenuated analgesia induced by morphine (2.5-15 mg/kg) on the jump test, jump thresholds of females treated with glutamate were potentiated after a 10 mg/kg dose of morphine and attenuated after a 15 mg/kg dose of morphine, relative to controls. In contrast, analgesia on the hot-plate test was potentiated in animals of both genders treated with glutamate after all doses of morphine. Changes in tolerance to morphine induced by glutamate also depended on the pain test and gender. While the peak analgesic response on the jump test did not occur until the fifth injection of morphine in all rats treated with glutamate, tolerance on the jump test was subsequently retarded in males treated with glutamate and accelerated in glutamate-treated females. Tolerance on the hot-palate test appeared not to be consistently affected by treatment with glutamate. Morphine-induced hyperthermia was initially decreased in rats treated with glutamate, but subsequently decreased in glutamate-treated males and increased in glutamate-treated females.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Impairments in analgesic, hypothermic, and glucoprivic stress responses following neonatal monosodium glutamate.

Neonatal administration of monosodium glutamate (MSG) produces in rats neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). The present study examined whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences or properties of a stimulus. To accomplish this, the analgesic, hypothermic, and locomotor responses following CWS and the analgesic, hyperphagic, and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8, and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal's ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. These data indicate the importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated, and synchronous coping response.

Animals↗
PubMed1983

Modulation of deprivation-induced food intake by D-phenylalanine.

D-phenylalanine has been shown to possess opiate-like effects upon pain perception. The present study examined whether it would have similar opiate-like effects upon food intake in deprived rats. The first experiment demonstrated that food intake of rats deprived for 24 h prior to injection was significantly reduced for 2 h following a 250 mg/kg dose of D-phenylalanine. However, intake over a 24 h period following injection was significantly increased following a 125 mg/kg dose of D-phenylalanine. The second experiment revealed that 0.3, 1.0, 3.0 and 10.0 mg/kg doses of naloxone dose-dependently reduced intake for 2 h in deprived rats when paired with a vehicle injection. However, the inhibitory actions of the two lower naloxone doses were significantly attenuated when paired with an injection of a 250 mg/kg dose of D-phenylalanine. These results are discussed in terms of whether D-phenylalanine possesses direct or indirect opiate-like effects upon ingestion.

Animals↗
PubMed1982

Effects of iodoamphenicol on ribosome assembly in two strains of Escherichia coli.

When the growth of Escherichia coli strain 15TP was inhibited by iodoamphenicol, three 'iodoamphenicol particles' accumulated with sedimentation coefficients of 25S, 33S and 45S. The 25S and 33S particles differ in sedimentation properties from equivalent ribosome precursor particles detected during pulse-labelling of exponentially growing cells. Inhibition of a mutant, strain 15-28 (defective in ribosome assembly), by iodoamphenicol resulted in the accumulation of 38S iodoamphenicol particles that are different from the particles made by the parent. The results support the contention that assembly of 50S ribosomal subunits by the mutant is altered at an early stage.

Bacterial Proteins↗
PubMed1980

Intermediates in the assembly of ribosomes by a mutant of Escherichia coli.

Escherichia coli strain 15--28 is a mutant that accumulates ribonucleoprotein ('47 S') particles during exponential growth. These particles contain mature 23 S rRNA, but lack three of the proteins of the larger ribosomal subunit, to which they are a precursor. In organisms growing at 20 degrees C, assembly of 47 S particles involves three intermediates that contain precursor 23 S rRNA, one of which has the same sedimentation properties as 47 S particles. Assembly of 50 S ribosomal subunits in the parent strain is 'normal'. There are three intermediates; each contains precursor 23 S rRNA, and one cannot be distinguished from completed subunits by sedimentation. Synthesis of 30 S ribosomal subunits in parent and mutant strains is qualitatively similar, but quantitatively different. When growth is at 37 degrees C, assembly in the mutant alters. There are now two sequential precursors to 47 S particles. Both contain precursor 23 S rRNA; one has the same sedimentation coefficient as 47 S particles. In some respects, synthesis in the mutant proceeds as though 47 S particles, rather than 50 S ribosomal subunits, are the end-product of assembly.

Centrifugation, Isopycnic↗
PubMed1979

Abnormal ribosome assembly in a mutant of Escherichia coli.

The mutant strain, 15--28, of Escherichia coli accumulates ribonucleoprotein ('47S') particles that were previously shown [Markey, Sims & Wild (1976) Biochem. J. 158, 451--456] to be an unusual intermediate in the assembly of 50S ribosomal subunits...

Centrifugation, Density Gradient↗
PubMed1978

Binding of chloramphenicol and a fragment of aminoacyl-transfer ribonucleic acid to ribosomes and a ribosome precursor from a mutant of Escherichia coli.

During exponential growth, the mutatn strain Escherichia coli 15-28 accumulates 47S particles, which are unusual precursors to 50S ribosomal subunits. The 47S particles have little ability to bind chloramphenicol, but binding of a fragment of aminoacyl-tRNA is about half that by completed subunits. The 70S (and 50S) ribosomes of strain 15-28 and its parent (strain 15TP) do not differ in chloramphenicol binding. Although ribosomes from the mutant are less able than those from the parent to bind the fragment, this difference is not as marked as was found previously [Sims & Wild (1976) Biochem. J. 160, 721-726] for the binding of an analogue of peptidyl-tRNA and for peptidyltransferase activity. The altered activities may arise because strain 15-28 misassembles 50S subunits of altered conformation and because the few proteins that 47S patricles lack have vital functions in some of the partial reactions of protein synthesis.

Binding Sites↗
PubMed1976

Mammograms on medichrome film.

When medichrome film is vacuum packed and used in combination with a single high definition intensifying screen exposure times of 0.06-0.1 s and a skin radiation dosage 0.5 rad per exposure can be achieved. The diagnostic accuracy of the system is similar to that obtained on conventional black and white film currently used for mammography.

Adult↗
PubMedDate not supplied

Potentiation of foot shock analgesia by thyrotropin releasing hormone.

Thyrotropin releasing hormone (TRH) interacts with both opioid and non-opioid systems in mediating hypothermic, hypoactive, cataleptic, respiratory and analgesic effects. While TRH neither antagonizes opioid analgesia nor alters pain thresholds itself, it blocks neurotensin analgesia. Different forms of pain-inhibition in rats can be activated by selectively altering the parameters of shock: while analgesia induced by 20 inescapable tail-shocks is not reversed by naltrexone, exposure to 60 or 80 shocks does elicit naltrexone-reversible analgesia. The first experiment examined whether intracerebroventricular administration of TRH (0, 10, or 50 micrograms) would alter the elevations in tail-flick latencies in rats induced by 20 or 80 foot shocks and found that TRH significantly lengthened the duration and magnitude of analgesia induced by 20 and 80 foot shocks in a dose-dependent manner. The second experiment extended these findings to the writhing test, a visceral pain test. While the number and duration of writhes of vehicle-treated rats exposed to 80 foot shocks failed to differ from baseline values. TRH (50 micrograms)-treated rats exposed to 80 foot shocks displayed significant decreases in the number and duration of writhes. The third experiment indicated that the differential effects of naltrexone upon analgesia induced by 20 or 80 tail shocks were not apparent when foot shocks were employed, precluding a definitive statement that TRH may be involved in the modulation of both opioid and non-opioid forms of analgesia.

Analgesia↗
PubMedDate not supplied

Neuromodulatory effects of TRH upon swim and cholinergic analgesia.

In addition to short-acting analgesic actions by itself and modulation of analgesic responses induced by endogenous opioids and neurotensin, central administration of thyrotropin-releasing hormone (TRH) potentiates footshock analgesia. The present study evaluated the effects of TRH upon the neurohormonally-mediated though nonopioid analgesia induced by swims in rats. Intracerebroventricular TRH (10 and 50 micrograms) dose-dependently potentiated swim (21, 15, 2 degrees C baths) analgesia on the tail-flick test, an effect which was not due to the hypothermic or basal pain threshold changes. Intravenous (8 mg/kg) TRH potentiated swim (21 degrees C) analgesia; the 600:1 difference in potency between routes strongly suggests central sites of neuromodulatory action. Intracerebroventricular diketopiperazine (50 micrograms), a TRH metabolite, and RX77368 (50 micrograms), a TRH analogue, also potentiated swim (21 degrees C) analgesia, effects also independent of hypothermia and basal reactivity to pain. Finally, given the excitatory interaction between TRH and acetylcholine as well as the cholinergic involvement in swim analgesia, intracerebroventricular TRH potentiated pilocarpine (10 mg/kg, IP) analgesia.

Acetylcholine↗