PubMed Health⌕ Search

Biomedical subjects

M A Carrasco

Publications and source records attributed to M A Carrasco.

11 recordsLinked to original sources
PubMed1991

Inositol 1,4,5-triphosphate phosphatase activity in membranes isolated from amphibian skeletal muscle [corrected].

The hydrolysis of [3H]inositol 1,4,5-trisphosphate by a soluble fraction and by isolated transverse tubule and sarcoplasmic reticulum membranes from frog skeletal muscle was studied. Transverse tubule membranes displayed rates of hydrolysis several-fold higher than those of sacroplasmic reticulum and soluble fraction; Km and Vmax were 25.2 microM and 44.1 nmol/mg/min, respectively. Transverse tubule membranes sequentially hydrolyzed inositol trisphosphate to inositol bisphosphate, inositol 1-phosphate and inositol, indicating that these membranes have inositol bis- and monophosphatases in addition to inositol trisphosphatase.

Animals↗
PubMed1988

Calcium modulation of phosphoinositide kinases in transverse tubule vesicles from frog skeletal muscle.

Highly purified transverse tubule membranes isolated from frog skeletal muscle phosphorylate phosphatidylinositol to phosphatidylinositol 4-phosphate and phosphatidylinositol (4,5)-bisphosphate. The two phosphorylation reactions have different calcium requirements. Phosphorylation of phosphatidylinositol to phosphatidylinositol 4-phosphate, which takes place in both isolated transverse tubules and sarcoplasmic reticulum membrane, is independent of calcium in a range of concentrations from 10(-9) to 10(-6) M, and is progressively inhibited to 10% of the maximal values by increasing calcium to 10(-4) M or higher (K0.5 = 5 X 10(-6) M). In contrast, phosphorylation of phosphatidylinositol 4-phosphate to phosphatidylinositol (4,5)-bisphosphate, a reaction exclusively present in transverse tubule membranes, is maximal at calcium concentrations higher than 2 X 10(-6) M and decreases to 30% of maximal values at calcium concentrations of 2 X 10(-7) M or lower (K0.5 = 10(-6) M). Unlike frog membranes, transverse tubules from rabbit muscle need exogenous phosphatidylinositol 4-phosphate in order to produce the bisphosphate derivative in the same range of calcium concentrations. Inositol (1,4,5)-trisphosphate has been proposed recently as a chemical messenger in excitation-contraction coupling in skeletal muscle. Calcium regulation of the synthesis of phosphatidylinositol (4,5)-bisphosphate, the membrane-bound precursor of inositol (1,4,5)-trisphosphate, might have physiological implications regarding modulation of excitation-contraction coupling by intracellular calcium levels.

1-Phosphatidylinositol 4-Kinase↗
PubMed1987

Inositol 1,4,5-trisphosphate-induced Ca2+ release from the sarcoplasmic reticulum and contraction in crustacean muscle.

Intracellular applications of a fixed amount (0.2 to 8 nmol) of inositol 1,4,5-trisphosphate (InsP3) over a brief period (2 s) into barnacle muscle fibers induced vigorous contractures. Peak tension attained during the first application depended on [InsP3]: the maximum tension evoked by the injection of 8 nmol was 1.6 kg/cm2. Peak tension during a second application of a high dose of InsP3 (greater than 10 microM) was always smaller than that during the first application. Extracellular Ca2+ could be omitted with no measurable effects on either the amplitude or time course of the contractures evoked by InsP3. Aequorin was used to measure InsP3-evoked Ca2+ release from intracellular stores in minced muscle fibers from lobster and in skinned muscle fibers from barnacle. Provided the sarcoplasmic reticulum was preloaded with Ca2+, application of InsP3 induced a transient Ca2+ release that was [InsP3] dependent. During each transient, [Ca2+] rose rapidly to a peak value (t1/2 less than 5 s) and then slowly returned (t1/2 less than 100 s) to a basal level. Maximum Ca2+ release was obtained at [InsP3] less than 100 microM and amounted to 4 nmol Ca2+/g of muscle, enough to increase [Ca2+]i from 0.1 to 8 microM had the Ca2+ release occurred in the intact fiber. Successive applications of a fixed amount of InsP3 elicited successive transient increases in Ca2+. The effects of [Ca2+] on the incorporation of [3H]inositol into the pools of phosphatidylinositol, phosphatidylinositol 4-phosphate, and phosphatidylinositol 4,5-bisphosphate pools were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Phosphorylation of phosphatidylinositol by transverse tubule vesicles and its possible role in excitation-contraction coupling.

Phosphorylation of phosphatidylinositol to phosphatidylinositol 4-monophosphate and to phosphatidylinositol 4,5-bisphosphate was demonstrated in transverse-tubule membranes isolated from frog skeletal muscle using [gamma-32P]ATP as substrate. At millimolar concentrations of Mg2+ both phosphorylation reactions were completed within 15 s at 25 degrees C. Isolated sarcoplasmic reticulum vesicles phosphorylated phosphatidylinositol to phosphatidylinositol 4-phosphate with a lower specific activity than the transverse tubules, and lacked the ability to produce phosphatidylinositol 4,5-bisphosphate. These findings show, for the first time, that isolated transverse-tubule membranes carry out one of the steps required to sustain a role for inositol trisphosphate as the physiological messenger in excitation-contraction coupling in skeletal muscle. The finding that 0.5 mM tetracaine apparently inhibits the phosphorylation of phosphatidylinositol 4-phosphate to phosphatidylinositol 4,5-bisphosphate also supports a role for these intermediates in excitation-contraction coupling.

Animals↗
PubMed1985

Response of the rat brain beta-endorphin system to novelty: importance of the fornix connection.

In control rats, a step-down inhibitory avoidance training trial using a 0.8 mA footshock, or simple exposure to the training apparatus without footshock, was followed by a decrease of beta-endorphin-like immunoreactivity measured in the hypothalamus and ventral thalamus. The effect of inhibitory avoidance training was also measured in rats submitted to a brain sham operation, to bilateral transection of the dorsal fornix, to anterior or to posterior hypothalamic deafferentation, to adrenal medullectomy, to an adrenal sham operation, to 16 daily ip injections of 0.2 mg/kg dexamethasone, or to 16 daily ip injections of 1 ml/kg saline. The diencephalic beta-endorphin-like immunoreactivity response to training was abolished by fornix transection and was unaffected by all other treatments. This suggests that the response is not mediated by anterior or posterior neural afferents to the hypothalamus, or by a hypersecretion of epinephrine by the adrenal medullae, or of ACTH by the pituitary gland. The response, instead, appears to require the integrity of the pathway that sends projections from the septo-hippocampal system to the hypothalamus. Previous evidence had suggested that the diencephalic beta-endorphin-like immunoreactivity response to training is a result of novelty, and the septo-hippocampal system has been postulated to play a role in the registration of novelty.

Adrenal Medulla↗
PubMed1985

The course of the decrease of hypothalamic beta-endorphin induced by training, and the development of the effect of beta-endorphin on the retrieval of inhibitory avoidance in rats.

Step-down inhibitory avoidance training or the simple exposure of rats to the training apparatus is followed by a decrease of hypothalamic beta-endorphin immunoreactivity at 0.1, 1.0 or 2.0 h after training. Immunoreactivity returns to normal at 6.0 h. The ip administration of 1.0 microgram/kg of human beta-endorphin 6 min prior to training produces an inhibition of the retrieval of the step-down task at 6.0 h, but not at 0, 1.0 or 2.0 h after training. This effect is reversed by a second injection of the substance immediately before testing. The possible physiological significance of this parallel development of the effect of beta-endorphin on retrieval and the depletion of the substance caused by training is discussed. The data indicate that retrieval is insensitive to the peptide when its hypothalamic stores are depleted.

Animals↗
PubMed1979

Effect of naloxone, haloperidol and propranolol on cyclic 3',5'-adenosine monophosphate content of rat amygdala.

Naloxone (0.4 mg/kg, i.p.) causes an increase of cyclic adenosine monophosphate levels in the amygdala, but not in the hippocampus, caudate, or hypothalamus, of rats. The effect is antagonized by haloperidol (0.5 mg/kg, i.p.) and by propranolol (0.5 mg/kg, i.p.). This is consistent with the hypothesis of a tonic inhibitory influence of endogenous opiates on central dopaminergic and beta-noradrenergic systems. Haloperidol had an effect of its own on amygdala cyclic adenosine monophosphate levels which was blocked by propranolol. This suggests the possibility of an antagonistic interaction between dopaminergic and beta-noradrenergic innervation on this structure.

Amygdala↗