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A Arce

Publications and source records attributed to A Arce.

At least 73 records · Page 4Linked to original sources
PubMed1977

The biosynthesis of brain gangliosides. Separation of membranes with different ratios of ganglioside sialylating activity to gangliosides.

Brain subcellular fractions were analysed for ganglioside-sialylating activity by measuring the incorporation of N-[3H]acetylneuraminic acid from CMP-N-[3H]acetylneuraminic acid into endogenous ganglioside acceptors (endogenous incorporation) and into exogenous lactosyceramide (haematoside synthetase activity). The ratios of endogenous incorporation to gangliosides and of haematoside synthetase to gangliosides for the synaptosomal and mitochondrial fractions from a washed crude mitochondrial fraction were lower than those obtained for other membrane fractions. The differences appear to reflect intrinsic characteristics of each membrane fraction. The results of labelling in vitro and the time course of labelling of gangliosides of the different subcellular fractions in vivo after injection of N-[3H]acetylmannosamine are consistent with the possibility of a subcellular site for synthesis of gangliosides different from that of ganglioside deposition.

Animals↗
PubMed1976

Incorporation of sialyl groups into a brain unidentified compound with lipophilic properties.

Lactosylceramide (I), galactosylceramide (II) and lipids extracted from rat brain with methanol (III) were assayed as AcNeu acceptors from CMP-[3H] AcNeu. Rat brain microsomes in 3.2% Triton CF54 or the 100 000 g supernatant of these microsomes were used as enzyme source. For quantification of reaction products two methods were used: a) precipitation with a TCA-PTA reagent followed by extraction of the precipitate with C:M (2:1) ; b) extraction with C:M (2:1) and partition by Folch's method without salt; radioactivity was measured in the washed lower phase. No incorporation into II was detected. Using method a), incorporation into I and III was obtained. It was also found that 35% of the activity toward I and 65% of that toward III was solubilized. Using method b) of quantification, radioactivity was found in the lower phase when III was the acceptor. The product of sialylation of III was soluble in ether. Run in a column of Sephadex LH20 was eluted with chloroform in the same fraction in which a proteolipid fraction was eluted. The possibilities that the compound is either a proteolipid protein or a glycopeptide containing sialic acid are discussed.

Animals↗
PubMed1974

Rat brain microsomal gangliosides. Accessibility to a neuraminidase preparation and the possible existence of different pools in relation to their biosynthesis.

1. Treatment of rat brain microsomal membranes with a neuraminidase preparation from Clostridium perfringens resulted in an almost complete conversion of polysialogangliosides into monosialogangliosides. 2. Neuraminidase treatment of the membranes did not increase the incorporation of N-[(3)H]acetylneuraminic acid from CMP-N-[(3)H]acetylneuraminic acid into the gangliosidic fraction, indicating that a monosialoganglioside is an acceptor of N-acetylneuraminic acid in these membranes only if, in addition to having the right chemical structure, it is in a proper position, probably in relation to the endogenous sialyltransferases. 3. These experiments also indicated that no independent turnover of the neuraminidase-labile N-acetylneuraminyl groups of gangliosides occurred in vitro. 4. N-[(3)H]Acetylneuraminic acid from endogenous polysialogangliosides labelled in vitro was released by neuraminidase at a slower rate than N-acetylneuraminic acid from unlabelled gangliosides of the same membranes. From this it was concluded that recently synthesized polysialogangliosides (completed in vitro) are in the membranes in a position less accessible to neuraminidase than are those synthesized earlier which were present in the membranes at the start of the labelling experiment.

Animals↗
PubMed1971

The biosynthesis of gangliosides. The incorporation of galactose, N-acetylgalactosamine and N-acetylneuraminic acid into endogenous acceptors of subcellular particles from rat brain in vitro.

Gangliosides bound to subcellular particles from rat brain were labelled by incubation of the particles (i) with CMP-N[(3)H]-acetylneuraminic acid and (ii) simultaneously, with CMP-N[(3)H]-acetylneuraminic acid and UDP-N-acetyl-[(14)C(1)]galactosamine or with CMP-N[(3)H]-acetylneuraminic acid and UDP-[U-(14)C]-galactose. Analysis of the labelled gangliosides showed that in (i), (a) the labelling was mostly in the neuraminidase-labile sialyl groups, (b) rigid relationships exist between the enzymes and the sialyl acceptors; the enzymes are not free to interact with all the specific substrates present in the preparation and (c) the precursor of the trisialoganglioside was the major disialoganglioside with a sialyl 2-->8 sialyl group. In (ii), (a) precursor-product relationships between the main pools of each ganglioside apparently do not exist, (b) for the labelling of Tay-Sachs ganglioside the amount formed from hematoside was at least 2.5 times that from aminoglycolipid and (c) the major monosialoganglioside was the precursor for the major disialoganglioside with a sialyl 2-->8 sialyl group.

Animals↗
PubMed1971

The biosynthesis of gangliosides. Labelling of rat brain gangliosides in vivo.

1. After injection of [6-(3)H]glucosamine into 8-day-old rats it was found that all the major brain gangliosides and their sialyl groups were labelled at essentially the same rate, except the hematoside, which was the least labelled. In 18-day-old rats it was found that the two major gangliosides with the sialyl (2-->8)-sialyl linkage, and their sialyl groups were more labelled than the hematoside, the Tay-Sachs ganglioside, the other two major gangliosides and their respective sialyl groups. 2. No difference was found in any of the cases studied between the specific radioactivities of the neuraminidase-resistant and -labile sialyl groups belonging to the same ganglioside. The same was found for the specific radioactivities of the galactosyl groups proximal and distal to the ceramide moiety of total brain gangliosides from rats injected with [U-(14)C]glucose. From this it was concluded that partial turnover of the ganglioside molecule does not occur. 3. A model for the synthesis of gangliosides is presented that accounts for results from previous experiments in vitro and the lack of precursor-product relationships observed in experiments in vivo.

Animals↗
PubMedDate not supplied

Circadian rhythms in adenohypophysial hormone levels and hypothalamic monoamine turnover in mycobacterial-adjuvant-injected rats.

The effect of Freund's adjuvant injection on 24-hour variation in circulating ACTH, prolactin, growth hormone (GH) and thyroid-stimulating hormone (TSH) levels, and of hypothalamic norepinephrine (NE) content and dopamine (DA) and serotonin (5HT) turnover was examined in adult rats. In control rats, serum ACTH and prolactin exhibited peak values at the light-dark transition while the maximum in TSH was found in the late afternoon. GH levels did not vary on a 24-hour basis. In Freund's-adjuvant-injected rats, 24-hour variations in TSH levels became blunted while 24-hour variations in prolactin and ACTH persisted. Freund's adjuvant treatment augmented serum ACTH and prolactin levels, and decreased GH and TSH levels. Hypothalamic NE content, and turnover of DA and 5HT varied on a 24-hour basis in rats receiving adjuvant's vehicle. The NE content of the anterior, medial and posterior hypothalamus peaked at 04.00 h, while that of the median eminence attained its maximum at 16.00-20.00 h. Maxima in hypothalamic DA and 5HT turnover occurred at 04.00 h regardless of the region examined. In Freund's-adjuvant-injected rats, reduced amplitude of daily variations of NE content in the median eminence and anterior and medial hypothalamus, as well as a phase advance in the 24-hour rhythm of the posterior hypothalamic NE content were seen. Mycobacterial adjuvant injection also reduced the amplitude of circadian rhythm in hypothalamic 5HT turnover, shifted the maximum in median eminence DA turnover towards light-dark transition, and decreased the amplitude of DA turnover rhythm in the anterior, medial and posterior hypothalamus. Administration of the immunosuppressant drug cyclosporine restored the augmented ACTH and prolactin levels and the depressed GH and TSH levels found in Freund's-adjuvant-injected rats. Cyclosporine was also effective to restore 24-hour rhythmicity of serum ACTH and TSH, but not of prolactin levels. Immunosuppression restored rhythmicity of NE content and of DA and 5HT turnover in anterior, medial and posterior hypothalamic regions. Cyclosporine did not modify the effect of Freund's adjuvant on median eminence but in was able to counteract the changes in the DA and 5HT turnover in the median eminence found after immunization. The results are in accord with a significant effect of immune-mediated inflammatory response at an early phase after Freund's adjuvant injection on ACTH, GH, prolactin and TSH release mechanisms, which was partially sensitive to immunosuppression induced by cyclosporine.

Animals↗
PubMedDate not supplied

Acute and chronic effects of superior cervical ganglionectomy on in vitro mitogenic responses of lymphocytes from submaxillary lymph nodes of pituitary-grafted rats.

Male rats were grafted an anterior pituitary within breast muscles or received a sham operation on day 5 of life. At the 60th day of life, the sympathetic denervation of rat submaxillary lymph nodes was achieved by a bilateral sympathetic superior cervical ganglionectomy (SCGx; at 15.00 h). Rats were killed either 18 h later (acute SCGx) or after 12 days (chronic SCGx) to measure lipopolysaccharide (LPS)- and concanavalin A (ConA)-induced cell proliferation in submaxillary lymph nodes, submaxillary lymph node cellularity and serum prolactin levels. In control rats, acute SCGx significantly augmented LPS or ConA activity on lymph cells while chronic SCGx had no effect. In pituitary-grafted rats, acute SCGx depressed the mitogenic effect of LPS or ConA whereas chronic SCGx augmented it. A global inhibitory effect of surgical stress on submaxillary lymph node cellularity was found in rats subjected to SCGx or its sham operation 18 h earlier. Serum prolactin levels increased significantly in pituitary-grafted rats, particularly in those subjected to chronic SCGx. In pituitary-grafted rats, a significant effect of acute SCGx was apparent, with serum prolactin levels augmenting about twice in sham-SCGx rats, and to a significantly less extent in acute SCGx rats. The results provide further evidence of the immunomodulatory role of local sympathetic nerves in submaxillary lymph nodes.

Animals↗
PubMedDate not supplied

Twenty-four hour rhythms of hypothalamic corticotropin-releasing hormone, thyrotropin-releasing hormone, growth hormone-releasing hormone and somatostatin in rats injected with Freund's adjuvant.

The effect of Freund's adjuvant injection on 24-hour variation of hypothalamic corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH), GH-releasing hormone (GRH) and somatostatin levels was examined in adult rats kept under light between 0800 and 2000 h daily. Groups of rats receiving Freund's complete adjuvant or its vehicle 3 days before sacrifice were killed at six different time intervals throughout a 24-hour cycle. In the median eminence, adjuvant vehicle-injected rats exhibited significant 24-hour variations for the four hormones examined, with maxima at noon. These 24-hour rhythms were inhibited or suppressed by Freund's adjuvant injection. In the anterior hypothalamus of adjuvant vehicle-treated rats, CRH content peaked at 1600 h, while two peaks were found for TRH and GRH levels, i.e., at 2400-0400 h and 1600 h. Freund's adjuvant injection suppressed 24-hour rhythm of anterior hypothalamic CRH, TRH and GRH content and uncovered a peak in anterior hypothalamic somatostatin levels at 0400 h. In the medial hypothalamus of adjuvant vehicle-treated rats, significant 24-hour variations were detectable for TRH (peaks at 1600 and 2400 h) and somatostatin (peak at 2400 h) which disappeared after Freund's adjuvant injection. In the posterior hypothalamus of adjuvant vehicle-treated rats, two peaks were apparent for CRH, TRH and somatostatin levels, i.e. at 1600 h and 2400-0400 h, this hormonal profile remaining unmodified after Freund's adjuvant administration. The administration of the immunosuppressant drug cyclosporine (5 mg/kg, 5 days) impaired the depressing effect of Freund's adjuvant injection on CRH, TRH and somatostatin content in median eminence, but not that on GRH. In the anterior hypothalamus, cyclosporine generally prevented the effect of immunization on hormone levels an revealed a second maximum in TRH at 0400 h. Cyclosporine also restored 24-hour variations in TRH and somatostatin levels of medial hypothalamus of Freund's adjuvant-injected rats but was unable to modify them in the posterior hypothalamus. The results further support the existence of a significant effect of immune-mediated inflammatory response at an early phase after Freund's adjuvant injection on hypothalamic levels which was partially sensitive to immunosuppression by cyclosporine.

Animals↗
PubMedDate not supplied

Age-dependent effect of pituitary transplants on immune responses in rat submaxillary lymph nodes: modulatory effect of the autonomic nervous system.

An anterior pituitary was grafted into the breast muscles of male rats on day 5, or under the kidney capsule on day 30 or 60 of life. At the 70th day of life (rats operated at the 5th or 30th day) or at the 100th day of life (rats operated at the 60th day), rats were injected subcutaneously with Freund's complete adjuvant, being killed 2 days later. Rats pituitary-grafted at the 30th day showed a greater hyperprolactinemia than rats grafted at the 5th or 60th day. Submaxillary lymph node natural killer (NK) activity decreased in neonatally pituitary-grafted rats and increased in rats grafted at the 30th or 60th day of life, while lymph node cellularity decreased in rats grafted at the 30th or 60th day. In the case of lipopolysaccharide (LPS)-and concanavalin A (Con A)-induced cell proliferation in lymph nodes, the only significant factor detected was age of transplantation, the effect being less evident in older animals. To examine whether the autonomic denervation of submaxillary lymph nodes affected immune responses in pituitary-grafted rats, animals were subjected to a unilateral superior cervical ganglionectomy (Gx) and/or a parasympathetic decentralization (Dc; by chorda tympani section), 10 days before immunization with Freund's adjuvant. A unilateral Gx blunted the stimulation of lymph node NK activity in rats receiving a pituitary transplant at the 30th or 60th day, but not at the 5th day. Only in sympathetically denervated lymph nodes a significant effect of pituitary transplants on LPS mitogenic effect was found, with significantly less effect of LPS in rats pituitary-grafted at the 5th or 30th day of life. Regarding Con A, a unilateral Gx or unilateral Gx plus Dc uncovered a significant depressive effect of pituitary transplants with a significantly smaller Con A mitogenic effect at each studied age in ipsilaterally Gx lymph nodes, and at 30 and 60 days of age in ipsilaterally Gx plus Dc lymph nodes. Pituitary grafts augmented Con A- induced proliferation in submaxillary lymph nodes at the 5th day of life while they decreased it at the 60th day of life. Pituitary transplants augmented cellularity at the sympathetically denervated lymph nodes and decreased it at the contralateral sham-operated side. Pituitary transplants also diminished lymph node cellularity at the Dc side, the effect being significant in rats transplanted at the 30th day of life. The results are compatible with age-dependent, inhibitory as well as promoting activities of hyperprolactinemia on immune responses in submaxillary lymph nodes, depending in part on intact autonomic nerves.

Age Factors↗
PubMedDate not supplied

Age-dependent effect of pituitary transplants on immune responses in rat spleen: modulatory effect of cyclosporine.

Male rats were grafted an anterior pituitary within breast muscles on day 5 or under the kidney capsule on day 30 or 60 of life. On the 70th day of life (rats operated on the 5th or 30th day) or on the 100th day of life (rats operated on the 60th day), rats were injected subcutaneously with Freund's complete adjuvant, being killed 2 days later. Rats that had received a pituitary graft on the 30th day showed a greater degree of hyper-prolactinemia than rats grafted on the 5th or 60th day. Analyzed as main factors in a factorial analysis of variance (ANOVA), pituitary transplants augmented splenic natural killer (NK) activity and lipopolysaccharide (LPS)- and concanavalin A (Con A)-induced cell proliferation, and decreased splenic cell number. As indicated by significant interactions between treatment and age of transplantation in a factorial ANOVA, splenic NK activity augmented in rats grafted on the 30th day of life, while LPS and Con A splenic cell proliferation augmented in rats grafted neonatally. Spleen cellularity decreased after pituitary transplants in 30- and 60-day-old rats. In a second study, the effect of cyclosporine on spleen immune responses was tested by administering cyclosporine (5 mg/kg) or vehicle to rats grafted as in experiment 1 for 5 days before sacrifice. Cyclosporine decreased splenic NK activity and LPS- and Con A-induced cell proliferation regardless of the presence of a pituitary graft. In rats grafted on the 30th day of life, cyclosporine reversed the effect of pituitary grafts on splenic NK activity, and ectopic pituitary augmenting NK activity in vehicle-treated rats while decreasing it in cyclosporine-injected rats. Cyclosporine reversed the inhibitory effect of pituitary transplants on spleen cell number. The high circulating prolactin levels found in rats with pituitary grafts were decreased by cyclosporine administration. The results are compatible with age-dependent promoting and inhibitory effects of hyperprolactinemia on the immune responses of the spleen, which were antagonized by cyclosporine immunosuppression.

Aging↗
PubMedDate not supplied

Effect of cyclosporine on immune responses in submaxillary lymph nodes of pituitary-grafted rats.

This work was undertaken to analyze the interrelationships between prolactin and cyclosporine in affecting immune responsiveness in submaxillary lymph nodes. Male rats received an anterior pituitary graft within breast muscles on day 5, or under the kidney capsule, on day 30 or 60 of life. On day 70 (rats operated on day 5 or 30) or on day 100 (rats operated on day 60) animals were injected with Freund's complete adjuvant and cyclosporine (5 mg/kg for 5 days), and were killed 2 days after immunization. Natural killer (NK) activity in submaxillary lymph node decreased in neonatally pituitary-grafted rats and increased in rats grafted on day 30 or 60, as did lymph node cellularity. Lipopolysaccharide (LPS)- and concanavalin A (ConA)-induced proliferation diminished in lymph nodes of rats grafted on day 30 or 60, respectively. Cyclosporine treatment diminished lymph node cell number and NK activity and increased the proliferative response to ConA. Cyclosporine depressive effect on lymph node cellularity was counteracted by the presence of a pituitary graft, as were the inhibition of NK activity and the stimulatory effect on ConA-induced cell proliferation. In pituitary-grafted rats, cyclosporine decreased submaxillary lymph node LPS-induced proliferation. Cyclosporine decreased the high circulating prolactin levels found in pituitary-grafted rats. The results are compatible with age-dependent, inhibitory and promoting activities of hyperprolactinemia on immune responses in lymph nodes, affected in a complex antagonistic and synergistic way by cyclosporine immunosuppression.

Aging↗
PubMedDate not supplied

Piribedil could modify dopamine turnover in cochleas under noise stimulation.

Dopamine (DA) is one of the putative neurotransmitters of the lateral efferent olivocochlear fibers. The cochlear DA content after noise exposure was analyzed using high-performance liquid chromatography coupled with electrochemical detection. Animals were exposed for 1 h to white noise at 70, 90 or 110 dB SPL or were kept in conditions of silence. Half of the animals were pretreated with piribedil, a D2 agonist, and the other half served as controls. In control (untreated) animals, noise stimulation resulted in a progressive decrease of cochlear DA concentration. This decrease was scarcely detected when animals were pretreated with piribedil. Present findings indicate that piribedil modifies cochlear DA turnover under noise stimulation.

Acoustic Stimulation↗