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Biomedical subjects

G Biggio

Publications and source records attributed to G Biggio.

At least 217 records · Page 12Linked to original sources
PubMed1977

Changes in gastro-intestinal serotonin content associated with fasting and satiation.

Rats fasted for 24 h were fed for 3 h, after which time food was removed. Food intake decreased serotonin levels in the stomach and duodenum by 30 and 40%, respectively. These changes persisted for about 3 h. Food intake did not change tryptophan content in the stomach, while, in the duodenum, tryptophan level rose by 100% at the end of the feeding period and remained elevated for about 9 h.

Animals↗
PubMed1977

On the mechanism of the decrease in cerebellar cyclic GMP content elicited by opiate receptor agonists.

Morphine, dextromoramide (4 mumol/kg i.p.) and vimonol R2 (17 mumol/kg i.p.) in analgesic doses (28 to 112 mumol/kg i.p.) decreased 3',5'-cyclic guanosine monophosphate (cGMP) in rat cerebellar cortex; morphine also decreased the cGMP content in deep cerebellar nuclei. Intrastriatal but not intracerebellar injections of morphine (20 mug) decreased cerebellar cGMP content. Naltrexone, an opiate receptor antagonist, but only apomorphine, a dopaminergic receptor agonist, blocked the effect of morphine on cerebellar cGMP. Pretreatment with 3-acetylpyridine (3-AP) which destroys the climbing fibers, failed to antagonize the effect of morphine on cerebellar cGMP. These results suggest that activation of opiate receptors in striatum decreases cerebellar cGMP content presumably by reducing activity in the mossy fiber excitatory input to cerebellum.

Analgesics↗
PubMed1977

Mechanisms by which diazepam, muscimol, and other drugs change the content of cGMP in cerebellar cortex.

THE CEREBELLUM CONSISTS OF TWO PARTS: the cerebellar nuclei whose connections to the various parts of the central nervous system coordinate muscle movements, and the cerebellar cortex which exerts an inhibitory influence on the cerebellar nuclei through the release of gamma-aminobutyric acid (gammaAbu) from Purkinje cells. The activity of Purkinje cells is regulated by two excitatory inputs to the cerebellar cortex-the climbing and mossy fibers-and by a neuronal network within the cortex which inhibits the activity of Purkinje cells through the release of gammaAbu from interneurons. The net activity of Purkinje cells is related to their content of guanosine 3':5'-cyclic monophosphate (cGMP) which increases or decreases according to changes in the activity of climbing and mossy fibers as well as to changes in the activation of gammaAbu receptors. When these receptors are activated, the cGMP of Purkinje cells decreases; when they are inhibited, the cGMP increases.The cGMP content of the cerebellar cortex is altered by drugs that change either the excitatory input of climbing or mossy fibers or the inhibitory input mediated by the activation of gammaAbu receptors. Mechanisms by which various drugs alter the cerebellar content of cGMP were investigated. By using various experimental designs, it was shown that diazepam and muscimol lowered the cGMP content by activating gammaAbu receptors. In contrast, morphine and haloperidol lowered the cerebellar cortex cGMP by decreasing the excitation of mossy fibers whereas harmaline increased the cGMP by increasing the excitation of the climbing fibers.

Alkaloids↗
PubMed1977

Pharmacologically induced changes in the 3':5'-cyclic guanosine monophosphate content of rat cerebellar cortex: difference between apomorphine, haloperidol and harmaline.

Harmaline increases cerebellar 3':5'-cyclic guanosine monophosphate (cGMP) content in a dose-related manner; this increase is prevented by a pretreatment with 3-acetylpyridine (3-AP) (0.66 mmol/kg) which destroys climbing fibers and inhibits harmaline-induced tremor. The cerebellar cGMP content increases after isoniazid; this response remains unchanged in rats pretreated with 3-AP. Since isoniazid decreases cerebellar gamma-aminobuturic acid (GABA) levels, the increase in cGMP content might reflect a reduction in the availability of GABA at the level of postsynaptic receptors. Apomorphine (a dopamine receptor agonist) and haloperidol (a dopamine receptor blocker) increase or decrease the cGMP content of cerebellar cortex, respectively. Neither drug changes the guanylate cyclase activity of cerebellar homogenates; moreover their action on cerebellar cGMP content persists after 3-AP. Chloropromazine, like haloperidol, decreases the cerebellar cGMP content. The increase in cerebellar cGMP content elicited by apomorphine can be differentiated from that elicited by harmaline or isoniazid; presumably apomorphine indirectly activates mossy fibers. The decrease in cerebellar cGMP content elicited by haloperidol can be differentiated from that elicited by diazepam; perhaps haloperidol reduces the mossy fiber input to the cerebellum. We suggest that the cGMP content of cerebellar cortex fluctuates in response to changes in the afferent stimulatory input to the cerebellum; it increases when the activity of either climbing or mossy fibers is increased; it decreases when either of these two stimulatory inputs is reduced.

Alkaloids↗
PubMed1977

Modulation of brain tryptophan hydroxylase activity by brain tryptophan content.

Although hydroxylation of tryptophan (TP) is considered to be the rate-limiting step in serotonin synthesis, the mechanism whereby tryptophan hydroxylase (TPH) participates in the regulation of serotonin synthesis is still in question. Since the brain TP concentration is probably near the Km for tryptophan hydroxylase, changes in brain TP content could affect the rate of its hydroxylation. However, it has not been established whether in vivo the activity of TPH and TP in several brain nuclei and other regions of rat brain after treatments known to lower brain TP levels. Chlorimipramine, loading with neutral amino acids and a TP-deficient diet decreased the TP content of some, but not all, brain regions studied. Whenever TP decrease withe TP injections. Several brain nuclei accumulate TP at different rates after a TP load. These data suggest possible mechanisms for regulation of serotonin synthesis in the face of fluctuating plasma levels of TP.

Amino Acids↗
PubMed1976

Climbing fiver activation and 3', 5'-cyclic guanosine monophosphate (cGMP) content in cortex and deep nuclei of cerebellum.

Harmaline (28 mumoles/kg u.v.), cold exposure (4C) or isoniazid (2.2 mmoles/kg s.c.) increased the cGMP content in rat cerebellar cortex several fold. Isoniazid but not harmaline or cold exposure increased cGMP in the deep cerebellar nuclei (nuclei interpositus, vestibularis and fastigius) and striatum. In rats treated with the nicotinamide antagonist 3-acetylpyridine (3-AP) (0.66 mumoles/kg i.p. 4 days before) the tremorogenic effect of harmaline and the increase of cerebellar cortex cGMP produced by this alkaloid was abated. Similarly the increase of cGMP following exposure to cold was reduced. In contrast isoniazid and glutamate (10 mumoles intraventricularly) increased cGMP to the same extent in control and 3-AP treated rats. Since 3-AP produces in rat a massive degeneration of the inferior olivary nucleus and of the climbing fibers but leaves intact all the other cerebellar elements, these experiments suggest that an increase of cGMP content in postsynaptic cerebellar elements (presumable Purkinje cells) may be an expression of an increased release of an excitatory transmitter from either the climbing fivers or the parallel fibers.

Animals↗
PubMed1975

Tryptophan-free diet: a new means for rapidly decreasing brain tryptophan content and serotonin synthesis.

Changes in the synthesis rate of brain serotonin are positively correlated with changes in the concentration of brain tryptophan, indicating that the concentration of tryptophan in the whole brain reflects that at sites of serotonin synthesis. In turn, the concentration of brain tryptophan is positively correlated with that of free serum tryptophan (tryptophan is the only amino acid bound to serum proteins) and negatively to that of other amino acids competing with tryptophan for the same transport from blood to brain. Consistently, experiments in rats have shown that treatments which increase free tryptophan in serum (in respect to competing amino acids) also increase brain tryptophan and serotonin turnover. Conversely, the ingestion of diets containing all amino acids except tryptophan cause a dramatic fall in free serum tryptophan and a parallel decline in brain tryptophan and serotonin synthesis. In man the administration of an amino acid mixture lacking trytophan produces a marked depletion in serum tryptophan concentration.

Amino Acids↗