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A Bayon

Publications and source records attributed to A Bayon.

At least 19 recordsLinked to original sources
PubMed1991

Evidence for enkephalin- and endorphin-immunoreactive cells in the anterior pituitary of the axolotl Ambystoma mexicanum.

An immunohistochemical study of opioid peptides in the hypophysis of the axolotl, Ambystoma mexicanum, was carried out with antisera against leu-enkephalin, beta-endorphin, met-enkephalin, and dynorphin A (1-8). We found leu-enkephalin immunoreactivity in some fibers of the neural lobe and the median eminence. In contrast to previous reports on mammals and other vertebrates, we found leu-enkephalin immunoreactivity in many cells scattered throughout the anterior lobe. As in other vertebrates, the beta-endorphin immunoreactivity was present in all the cells of the intermediate lobe and in a few cells of the anterior lobe. Met-enkephalin and dynorphin A (1-8) immunoreactivities were only present in the neural lobe and the median eminence. The presence of leu-enkephalin and beta-endorphin in the anterior lobe suggests that these peptides could be acting as hormones released from the hypophysis of the unmetamorphosed amphibian.

Ambystoma mexicanum↗
PubMed1989

Synthetic peptides corresponding to the sequence of noxiustoxin indicate that the active site of this K+ channel blocker is located on its amino-terminal portion.

A nonapeptide Thr-Ile-Ile-Asn-Val-Lys-Cys-Thr-Ser (NTX1-9) and a decapeptide Met-Asn-Gly-Lys-Cys-Lys-Cys-Tyr-Asn-Asn (NTX30-39) corresponding to the N-terminal and C-terminal sequences respectively of Noxiustoxin (NTX) were synthesized by the solid phase method of Merrifield (1963). The first synthetic peptide (NTX1-9) was shown to be toxic to mice independently of the route of administration: intraperitoneally, subcutaneously or intraventricularly (100-200 micrograms/20 g mouse weight). The second (NTX30-39) was not toxic even at higher dose (400 micrograms/20 g mouse). When the effects of the peptide NTX1-9 and of the authentic toxin (Noxiustoxin) were studied on the liberation of [3H] 4-aminobutyric acid (3H-GABA) from mouse synaptosomes, both gave essentially the same results, except that peptide NTX1-9 was needed at higher concentration. Synthetic peptide NTX30-39 had no effect in the same preparation at even higher doses. The GABA release produced by toxic peptide NTX1-9 was not affected by tetrodotoxin but was completely abolished by the presence of the K+ ionophore valinomycin, mimicking the effect of native NTX in the same system (Sitges et al., 1986). These results indicate that the toxic active site of Noxiustoxin is possibly located in or near the N-terminal amino acid portion of the molecule.

Amino Acid Sequence↗
PubMed1985

Characterization of the prodynorphin and proenkephalin neuropeptide systems in rat hippocampus.

Opioid peptides derived from prodynorphin were localized immunocytochemically to dentate granule cells and mossy fibers of the rat hippocampus with antisera against dynorphin A(1-17) and dynorphin B. Extracts of microdissected hippocampal regions were resolved by reverse phase and molecular exclusion chromatography to identify the molecular forms of the dynorphin A immunoreactivity and to quantify regional contents. Results demonstrated that the relative concentration of dynorphin A within each dissected region of hippocampus agreed well with the distribution of dynorphin A detected by immunocytochemical methods. Immunostaining of proenkephalin-derived opioid peptides, [Leu5]enkephalin and bovine adrenal medullary peptide-22P, was concentrated in cell bodies of the entorhinal cortex, nerve fibers in the perforant pathway, and terminals in the outer molecular layer of the dentate gyrus. Light immunostaining of granule cells and mossy fibers with these antisera was also found. The relative concentration of [Leu5]enkephalin immunoreactivity in each microdissected region of the hippocampus also agreed well with the distribution of [Leu5]enkephalin immunostaining. Chromatography of hippocampal regional extracts demonstrated that the immunoreactivity measured was due to the presence of authentic [Leu5]enkephalin. The probable neurotransmitter function of both [Leu5]enkephalin and dynorphin A was shown by their calcium-dependent release after in vitro depolarization of hippocampal tissue. The reported presence of beta-endorphin in hippocampus was not verified. Comparison of the hippocampal distribution and content of prodynorphin and proenkephalin-derived opioids suggests that separate populations of neurons containing these two peptide families form distinct neurotransmitter systems of roughly equal concentration.

Animals↗
PubMed1984

Reversal of rapid eye movement sleep without atonia by chloramphenicol.

Bilateral pontine tegmental lesions produce in cats the phenomenon known as rapid eye movement (REM) sleep without atonia. During episodes of REM sleep without atonia cats are capable of exhibiting such complex behaviors as head-raising, body-righting, standing, and in some cases, walking and attacking. Since release of such behaviors implies disinhibition of specific motor systems, the purpose of this study was to determine whether the administration of chloramphenicol (CAP), which is known to attenuate the firing frequencies of cells that become activated during REM and motor activity, could reverse this phenomenon. Cats with dorsolateral tegmental pontine (DLTP) lesions producing REM without atonia were thoroughly studied in terms of the muscular and behavioral activity they displayed during REM before and after systemic CAP administration. Thiamphenicol (TAP), a CAP analogue that does not reduce neuronal firing frequency during REM sleep, was used as a control drug. The results of these experiments showed that CAP but not TAP induced a return of the atonia during REM sleep. It is suggested that the return of atonia induced by CAP in DLPT lesioned cats is caused by attenuation in the activity of medial reticular neurons which have somatotopical representation. Such cells, which have high levels of activity during REM sleep and motor activation is wakefulness, are normally overwhelmed by the inhibitory mechanism of the atonia of REM. The return of atonia and consequent reduction in complex behavior following CAP administration may be due to withdrawal of the excitatory influence of these neurons.

Animals↗
PubMed1981

In vivo release of enkephalin from the globus pallidus.

Push-pull cannulae were acutely positioned through previously implanted guides in the globus pallidus of unanesthetized freely moving cats and rats. During slow-flow perfusions, enkephalin release was detected in resting conditions and increased more than 3-fold when both 50 mM K+ and 1.8 mM Ca2+ were present in the perfusing medium. Local perfusion with veratrine also enhanced enkephalin release. Furthermore, in vivo, electrical stimulation of the rat caudo-putamen enhanced enkephalin release in the pallidum. This latter finding is consistent with a functional strio-pallidal enkephalin-containing pathway previously postulated by immunohistochemical or lesion experiments.

Animals↗
PubMed1980

Regional distribution of endorphin, Met5-enkephalin and Leu5-enkephalin in the pigeon brain.

The distribution of beta-endorphin and enkephalin in the pigeon forebrain by immunohistochemistry and radioimmunoassay is essentially analogous to mammals. Both endorphin- and enkephalin-reactive fibers have a similar periventricular distribution, but the enkephalin fibers are more extensive and are also found in the paleostriatum, limbic regions and brain stem, pituitary stalk and notably, penetrating the organum vasculosum hypothalami. There was poor correlation between endorphin and enkephalin regional contents by radioimmunoassay. In contrast, a highly significant correlation was observed between Met5-enkephalin and Leu5-enkephalin regional distribution. These data support the view that enkephalin neurons and endorphin neurons are independent central neuronal systems.

Animals↗
PubMed1979

Perinatal development of the endorphin- and enkephalin-containing systems in the rat brain.

Radioimmunoassay and microdissection procedures were used to study the perinatal development of the endorphin- and enkephalin-containing systems in the rat brain. In contrast to values reported on adult rat, endorphin levels are much higher than enkephalin levels on embryonic day 16. The highest endorphin values are found in the diencephalon, midline telencephalon and medulla-midbrain regions. Perinatally, enkephalin content increases at a faster rate than endorphin in all brain regions, producing a marked drop of the endorphin/enkephalin ratios. Between postnatal days 6 and 25, both endorphin and enkephalin levels increase, approaching their adult distribution pattern. No correlation was found between regional distributions or rates of increase of endorphin and enkephalin in any of these developmental stages, suggesting that the two peptide systems develop independently from each other.

Age Factors↗
PubMed1978

In vitro release of [5-methionine]enkephalin and [5-leucine]-enkephalin from the rat globus pallidus.

Endogenous [5-methionine]enkephalin (Metenkephalin) and [5-leucine]enkephalin (Leu-enkephalin) are released from perfused slices of rat globus pallidus by increased K(+) in a Ca(2+)-dependent manner. Tissue perfused for 40 min contained only 26% of the Met-enkephalin and 44% of the Leu-enkephalin found in the freshly dissected tissue. After perfusion, the mean (+/-SEM) ratio (wt/wt) of Met-enkephalin to Leu-enkephalin was 3.4 +/- 0.2 compared with 5.8 +/- 0.2 in the fresh tissue. The degradation of trace amounts of synthetic [(3)H]enkephalins in the perfusing medium during stimulated release seems to reflect the accelerated degradation of enkephalin released from the tissue: 63% of the Met-enkephalin and 23% of the Leu-enkephalin were degraded in a medium containing bacitracin (30 mug/ml). The mean ratio (wt/wt) of the Met-enkephalin to the Leu-enkephalin recovered after release by exposure of slices to 50 mM K(+) was 2.7 +/- 0.3. When perfusates were corrected for degradation, this ratio increased to about 5.5 which is higher than that found in the perfused tissue. The differences in release, tissue loss, and catabolism of the two enkephalins may be reflecting differences in the metabolic systems operating on the pentapeptides, but this interpretation will have to be validated by in vivo release experiments. In any event these observations strongly suggest that both enkephalins can be considered candidate neurotransmitters in the rat globus pallidus.

Animals↗
PubMedDate not supplied

Dilated coronary sinus in a dog with persistent left cranial vena cava.

This paper describes the electrocardiographic, echocardiographic (two-dimensional, M-mode, contrast and Doppler) and non-selective angiocardiographic features in a 3 year old female Beagle with dilated coronary sinus due to persistent left cranial vena cava. Negative P waves in leads III and aVR and a positive P wave in lead aVL were seen. Echocardiographically, a hypoechoic circular structure was seen between the left atrium and the pericardium in the area where the coronary sinus is located. A velocity pattern with two peaks was obtained, one systolic with velocity = 0.44 +/- 0.05 m/sec and the other diastolic with velocity = 0.27 +/- 0.01 m/sec. By M-mode echocardiography, at level of the aorta and the left atrium, a linear structure was identified between the left atrium and the pericardium; this structure was characterized by phasic movements of the anterior wall during the cardiac cycle. Following a left cephalic vein injection of saline, bubbles were seen within the coronary sinus; when saline was injected into the right cephalic vein, bubbles were also seen within the coronary sinus and right atrium and ventricle. Non-selective angiocardiography confirmed a dilated coronary sinus with persistent left cranial vena cava. The right cranial vena cava was absent. The dog was clinically normal and the unusual vessel was an incidental finding.

Angiocardiography↗