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Biomedical subjects

M M Morgan

Publications and source records attributed to M M Morgan.

At least 55 records · Page 3Linked to original sources
PubMed1989

Stimulation of the periaqueductal gray matter inhibits nociception at the supraspinal as well as spinal level.

Stimulation of the periaqueductal gray matter (PAG) is known to modulate nociception at the spinal level. Several studies have suggested that nociception may also be modulated via ascending projections from the PAG. To study this hypothesis, the descending pathway was selectively disrupted immediately caudal to the PAG in 28 rats. Twenty-eight additional rats served as non-lesioned controls. All animals were chronically implanted with a stimulating electrode in the PAG, and antinociception was assessed using tests involving spinally and supraspinally mediated responses (tail-flick and hot-plate tests, respectively). Significantly fewer lesioned than non-lesioned rats showed stimulation-produced analgesia (SPA) in the tail-flick test (4 of 28 vs 14 of 28, respectively). In contrast, no significant difference in the incidence of SPA occurred between lesioned and non-lesioned rats in the hot-plate test. These findings demonstrate that nociception can be modulated at the supraspinal, as well as spinal, level.

Animals↗
PubMed1989

Characterization of stimulation-produced analgesia from the nucleus tractus solitarius in the rat.

Electrical stimulation of the commissural region of the nucleus tractus solitarius (NTS) inhibits the tail-flick reflex evoked by noxious heat. This antinociception can be measured in the awake or pentobarbital anesthetized rat at current intensities that do not induce overt behavioral side effects. Glutamate microinjections into the NTS, but not immediately surrounding the NTS, also inhibit the tail-flick reflex, demonstrating that activation of NTS cell bodies, and not fibers of passage, mediates antinociception from this region. In contrast, morphine microinjections into the NTS have no effect on the tail-flick reflex in anesthetized rats. These findings provide further evidence that the NTS is involved in the modulation of nociception.

Analgesia↗
PubMed1988

Sequence of the small double-stranded RNA genomic segment of infectious bursal disease virus and its deduced 90-kDa product.

The smaller dsRNA segment of the genome of infectious bursal disease virus (IBDV) encodes a single polypeptide of approximately 90 kDa (VP1). The consensus nucleotide sequence, derived from independent and overlapping cDNA clones, contains a single open reading frame which begins with an exact Kozak sequence and could encode a polypeptide of 878 amino acid residues. It has been suggested that VP1 could be the viral RNA-dependent RNA polymerase. A comparison of the predicted amino acid sequence of this protein with those of other DNA-dependent and ssRNA-dependent RNA polymerases has failed to reveal any homology between VP1 and the conserved regions in these enzymes. It is possible that the polypeptide encoded by the IBDV virus may represent a new class of polymerases which are involved in the replication of double-stranded RNA genomes.

Amino Acid Sequence↗
PubMed1987

GABAergic modulation of the analgesic effects of morphine microinjected in the ventral periaqueductal gray matter of the rat.

The possibility that GABAergic neurons in the ventral periaqueductal gray matter modulate the analgesic effects of morphine microinjected into this brain area was investigated in the rat. Microinjection of 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin 3-ol (THIP) (0.4 microgram in 0.2 microliter), a GABA agonist, in the ventral periaqueductal gray matter significantly reversed the increase of tail-flick latency induced by a prior injection of morphine sulfate (4 micrograms in 0.2 microliter) at the same site. Conversely, microinjection in the same region of picrotoxin (10 ng in 0.2 microliter), a GABA antagonist, significantly potentiated the analgesic effect of the same dose of morphine. These results suggest the existence of GABAergic neurons that tonically inhibit periaqueductal gray output neurons involved in centrifugal pain inhibition. The analgesic effects of opiates may, at least in part, result from disinhibition of these GABAergic neurons.

Animals↗
PubMed1987

Site specificity in the development of tolerance to stimulation-produced analgesia from the periaqueductal gray matter of the rat.

Pentobarbital-anesthetized rats were subjected to 21 min of continuous electrical stimulation of the caudal periaqueductal gray matter (PAG) at the current threshold for analgesia. Stimulation at ventral PAG sites supported analgesia for only 1 or 2 min in most animals. Stimulation at more dorsal PAG sites supported analgesia for the entire 21 min of stimulation. This demonstration of acute tolerance with continuous ventral, but not more dorsal, PAG stimulation corresponds well with previous evidence suggesting opioid mediation of analgesia from this brain region.

Analgesia↗
PubMed1987

Diazepam dissociates the analgesic and aversive effects of periaqueductal gray stimulation in the rat.

Electrical stimulation of the periaqueductal gray matter (PAG) of the rat can produce both analgesia and aversive reactions. To determine if these two effects can be dissociated, diazepam, a benzodiazepine, was administered to rats chronically implanted with electrodes in the PAG. The threshold for stimulation-produced analgesia or aversion, whichever was lowest, was determined before and after drug administration. Diazepam (1 mg/kg) attenuated stimulation-produced aversive reactions at 12 of 20 stimulation sites, allowing analgesia to be measured at the same threshold. Diazepam did not alter baseline pain sensitivity or thresholds for stimulation-produced analgesia. These results indicate that aversive reactions and analgesia from PAG stimulation can be pharmacologically dissociated.

Analgesia↗
PubMed1987

Characterization of the analgesic effects of the benzodiazepine antagonist, Ro 15-1788.

Three experiments were carried out in rats to evaluate the analgesic effects of the benzodiazepine antagonist, Ro 15-1788. Expt. 1 demonstrated a diazepam reversible analgesic effect of Ro 15-1788 using the tail-flick test. Expt. 2 analyzed the effects of Ro 15-1788 in the hot-plate test at various doses. Low doses of Ro 15-1788 proved analgesia 20 min after drug injection, whereas high doses had no analgesic effect on the 20 min test, but were effective on the 50 min test. Expt. 3 demonstrated that the opiate antagonist, naloxone, had no effect on analgesia produced by Ro 15-1788 in the hot-plate test. The analgesic effects of Ro 15-1788 may be attributable to its reported anxiogenic properties.

Analgesics↗
PubMed1987

Barbiturate-induced inhibition of a spinal nociceptive reflex: role of GABA mechanisms and descending modulation.

The present study investigated the effect of systemically administered pentobarbital on the tail-flick (TF) reflex in rats, the neurochemical mechanism of action and the role of descending influences. Pentobarbital produced a clear inhibition of the TF response. Systemic administration of naloxone did not significantly alter this effect, thus it appears to be independent of endogenous opioid systems. Complete spinal transection resulted in a marked potentiation of pentobarbital-induced TF inhibition, demonstrating a spinal locus of action. Moreover, this observation suggests the existence of a tonic descending excitatory influence, opposing the pentobarbital-produced depression of nociceptive transmission in the intact animal. Intrathecal administration of pentobarbital caused a much more pronounced TF inhibition in transected than in intact animals, lending further support to this hypothesis. To identify the neurochemical mechanisms involved in pentobarbital-produced antinociception, the gamma-aminobutyric acid (GABA) antagonists bicuculline and picrotoxinin were administered intrathecally in spinalized animals. Both substances caused an attenuation of the pentobarbital effect, demonstrating the involvement of GABAergic transmission. The proposed descending excitatory system may act either presynaptically and cause a decreased release of GABA into the synapse or postsynaptically via endogenous GABA antagonistic neurotransmitters, which may change the conformation of the GABA-barbiturate receptor complex.

Analgesics↗
PubMed1987

The mitochondrial genotype can influence nuclear gene expression in yeast.

Isochromosomal, respiratory-deficient yeast strains, such as a mit-, a hypersuppressive petite, and a petite lacking mitochondrial DNA, are phenotypically identical in spite of differences in their mitochondrial genomes. Subtractive hybridizations of complementary DNA's to polyadenylated RNA isolated from derepressed cultures of these strains reveal the presence of nuclear-encoded transcripts whose abundance varies not only between them and their respiratory-competent parent, but among the respiratory-deficient strains themselves. Transcripts of some nuclear-encoded mitochondrial proteins, like cytochrome c and the alpha and beta subunits of the mitochondrial adenosine triphosphatase, whose abundance is affected by glucose or heme, do not vary. In the absence of major metabolic variables, yeast cells seem to respond to the quality and quantity of mitochondrial DNA and modulate the levels of nuclear-encoded RNA's, perhaps as a means of intergenomic regulation.

Base Sequence↗
PubMed1987

Different effects of chronic nicotine treatment regimens on body weight and tolerance in the rat.

The effect of different chronic nicotine administration regimens on body weight and the development of tolerance was examined in female rats. Groups of animals were either treated with nicotine via a subcutaneous continuous release pellet or via two injections each day of either a high (5.6 mg/kg) or low (0.8 mg/kg) dose. Both the Pellet and Low injection groups showed a progressive weight loss during nicotine treatment followed by a weight gain upon cessation of treatment, but the time course and size of these weight changes were quite distinct. In contrast, the High injection group gained weight during the 17 days of nicotine treatment. Tolerance, as measured by locomotor activity following an acute injection of nicotine 1 week after cessation of chronic nicotine treatment, was evident only in the Low injection group. This study demonstrates that the regimen in which nicotine is administered is an important factor in determining the behavioral effects produced by chronic nicotine treatment.

Animals↗
PubMed1987

Chronic nicotine and withdrawal effects on body weight and food and water consumption in female rats.

Female rats were used to examine the effects of chronic nicotine administration and withdrawal on food and water consumption and body weight. Rats with chronic nicotine pellet implants consumed significantly less food and water than controls for the first five days and then gradually returned to control levels of consumption. The lowest level of body weight was reached on day 9 after which there was a slow return to control weights by day 21. When the nicotine pellets were removed from the short-term exposure group on day 14, they showed significant hyperphagia and hyperdipsia and a very rapid weight gain for the next several days, which clearly outpaced the recovery of weight in the long-term nicotine exposure group. These results show that in female rats changes in weight during chronic nicotine administration and withdrawal are accompanied by changes in rates of consumption. In addition, nicotine withdrawal can cause hyperphagia and hyperdipsia even though levels of consumption had previously returned to control levels and even though the route of nicotine administration was not oral.

Animals↗
PubMed1986

Primary structure of the (1-->3,1-->4)-beta-D-glucan 4-glucohydrolase from barley aleurone.

During germination of barley grains, the cell walls of the starchy endosperm are degraded by (1-->3,1-->4)-beta-glucanases (EC 3.2.1.73) secreted from the aleurone and scutellar tissues. The complete sequence of the aleurone (1-->3,1-->4)-beta-glucanase isoenzyme II comprises 306 amino acids and was determined by sequencing nine tryptic peptides (110 residues) and aligning them with the amino acid sequence deduced from a cDNA clone encoding the 291 NH(2)-terminal residues. Although no amino acid sequence homology with a bacterial (1-->3)(1-->4)-beta-glucanase is apparent, close to 50% homology is found with two large regions of a (1-->3)-beta-glucanase from tobacco pith tissue. The gene for barley (1-->3,1-->4)-beta-glucanase isoenzyme II shares with that for the alpha-amylase isoenzyme 1 a strongly preferred use of codons with G and C in the wobble position (94% and 90%, respectively). Both enzymes are secreted from the aleurone cells during germination. Such one-sided codon usage is not characteristic for the gene encoding the (1-->3)-beta-glucanase of tobacco pith tissue or the hor2-4 gene encoding the B(1) hordein storage protein in the endosperm.

Journal Article↗