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Biomedical subjects

W Fratta

Publications and source records attributed to W Fratta.

89 records · Page 5Linked to original sources
PubMed1976

Voraciousness induced in cats by benzodiazepines.

Different benzodiazepines, when administered to fasting cats, increased both the total amount of food eaten and also the rate at which food was ingested. Moreover, when injected to foodsatiated cats, these compounds made them resume eating voraciously. Pentobarbital also stimulated food intake, but was much less potent than the benzodiazepines tested.

Animals↗
PubMed1974

Lack of copulatory behaviour in male castrated rats after p-chlorophenylalanine.

1 The effect of p-chlorophenylalanine (PCPA) on the copulatory behaviour of normal and castrated male rats with females in oestrus was studied.2 Castration 2 months before the experiment completely prevented the increased copulatory behaviour produced by PCPA in normal rats.3 The administration of testosterone restored the copulatory behaviour in the castrated rats indicating that testosterone is essential for this behaviour.

Animals↗
PubMedDate not supplied

Existence of different forms of adrenocorticotropin in rat hypothalamus.

Adrenocorticotropin (ACTH)-like immunoreactivity and bioactivity were extracted from rat hypothalamus and fractionated by high pressure liquid chromatography. Analysis of the fractions either by radioimmunoassay or bioassay (corticosteroid production from rat adrenal cells) revealed several peaks of immunoreactivity and bioactivity. Only 20-25% of total ACTH-like immunoreactivity and bioactivity eluted with the same retention time as authentic ACTH 1-39. The results suggest that different forms of ACTH exist in rat hypothalamus.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Oxytocin concentration changes in different rat brain areas but not in plasma during aging.

The concentration of oxytocin was measured by radioimmunoassay in different brain areas, hypophysis, and plasma of male Wistar Kyoto rats during aging. Although no difference in the concentration of oxytocin in any of the above tissues among 2- and 6-month-old rats was found, in 12-month-old rats a 21% decrease was observed in both septum and hippocampus, but not in the hypothalamus, hypophysis, and plasma, when compared to values of 2- and 6-month-old rats. In 18-month-old rats, the decrease of septal and hippocampal oxytocin content was higher than that found in 12-month-old rats, but no change was found in the hypothalamus, neurohypophysis, and plasma. In 24-month-old rats, oxytocin content was similar to that found in 18-month-old rats in all tissues analyzed. The results suggest that aging induces an impairment of oxytocinergic transmission in the central nervous system but not in the neurohypophyseal system.

Aging↗
PubMedDate not supplied

Brain proteolysis of oxytocin in vitro and in vivo changes during aging in male rats.

Oxytocin proteolysis was studied in vitro with purified synaptic membranes and in vivo after injection into the hippocampus of male Wistar Kyoto rats of different ages. When oxytocin was incubated in vitro with brain synaptic membranes obtained from 2-, 6-, and 12-month-old rats, no difference in the content of C-terminal and N-terminal fragments formed by membrane-bound aminopeptidase-like and endopeptidase-like enzymes, respectively, was found after high performance liquid chromatography separation and quantification by amino acid analysis. In contrast, the content of all fragments decreased by about 20%-25% when membranes obtained from 18- and 24-month-old rats were used. When [3H-Tyr2]oxytocin was injected in vivo in the hippocampus of 2-, 6-, 12-, and 18-month-old rats, no difference in the content of free [3H]-tyrosine and other [3H]-labelled fragments was found in the hippocampal peptidic extract after high performance liquid chromatography fractionation. However, the content of all radioactive fragments was about 50% lower in the extract from 24-month-old rats. The findings suggest that oxytocin proteolysis in brain decreases during aging. Such a decrease might counterbalance the impairment of central oxytocinergic transmission caused by the age-related decrease of oxytocin content in brain.

Aging↗
PubMedDate not supplied

Effect of fipexide on passive avoidance behaviour in rats.

The effect of fipexide, administered at different intervals after the learning trial of a single step-through type passive avoidance situation was studied. The administration of fipexide immediately after the learning trial resulted in a long-lasting facilitation of passive avoidance behaviour. On the contrary, the administration of this compound 1 h prior to the retention test failed to influence passive avoidance behaviour. The results suggest that fipexide facilitates memory consolidation but does not influence retrieval processes.

Animals↗
PubMedDate not supplied

Synthesis and mu-opioid receptor affinity of a new series of nitro substituted 3,8-diazabicyclo[3.2.1]octane derivatives.

A new series of analogues (1c-j; 2c-i) of the previously reported analgesic 3,8-diazabicyclo[3.2.1]octanes (1a,b; 2a,b) was synthesized and tested for their affinity towards mu-opioid receptors. Modifications were introduced either at the cinnamyl or the acyl side chains. The majority of the new compounds, with the exception of 1c,j and 2c, showed Ki values better or comparable with those of the models.

Animals↗
PubMedDate not supplied

Benzocondensed derivatives as rigid analogues of the mu-opioid agonist 3(8)-cinnamyl-8(3)-propionyl-3,8-diazabicyclo[3.2.1]octanes: synthesis, modeling, and affinity.

A new series of rigid analogues (1a-g, 2a-g) of the previously reported analgesic 3-cinnamyl-8-propionyl-3,8-diazabicyclo[3.2.1]octane (I) and its reverted isomer 3-propionyl-8-cinnamyl (II) were synthesized, in which the cinnamyl substituent is incorporated in benzocondensed bicyclic systems. Binding assays for the affinity towards mu receptors indicated that, while in the reverted series 2 the beta-naphthylmethyl (2d) and the benzocycloheptenylmethyl derivative (2g) favorably compared with II, all compounds 1 displayed a mu-affinity lower than that of the parent I. Modeling studies suggest that the flexibility of the cinnamyl side chain plays an important role for activity.

Analgesics, Opioid↗
PubMedDate not supplied

Localized epileptiform activity induced by murine CRF in rats.

Murine corticotropin releasing factor (rCRF), injected intracerebroventricularly into rats at a dose of 10 micrograms produced increased motor activity, grooming, and recurrent episodes of epileptic activity localized in the hippocampal leads. Such activity persisted for approximately 5 h and was characterized by recurrent trains of biphasic spikes never associated with behavioral signs of epilepsy. The intraperitoneal administration of carbamazepine (15 and 30 mg/kg) reduced the epileptic activity for approximately 90 and 120 min, respectively, whereas that of naloxone (8 mg/kg) was ineffective. The results suggest that rCRF-induced spiking activity might be a model of temporal lobe epilepsy.

Animals↗
PubMedDate not supplied

Neonatal monosodium glutamate abolishes corticotropin-releasing factor-induced epileptogenic activity in rats.

Intracerebroventricular (i.c.v.) injection of rat corticotropin-releasing factor (rCRF) at doses of 5-20 micrograms in rats induces epileptogenic activity characterized by pacemaker-like spikes localized in the hippocampal leads. Such an effect was still present in rats neonatally treated with saline but was absent in those neonatally treated with monosodium glutamate (MSG), a treatment that caused marked changes in the concentration of several brain neurotransmitters and neuropeptides in hypothalamic nuclei where CRF is highly concentrated and is believed to induce endocrinologic and behavioral effects. The present results suggest the rCRF-induced spiking activity is mediated by activation of neuronal pathways sensitive to MSG neurotoxic effect.

Animals↗
PubMedDate not supplied

Clonidine prevents corticotropin releasing factor-induced epileptogenic activity in rats.

Studies have shown that intracerebroventricular (i.c.v.) injection (10-20 micrograms) of corticotropin releasing factor (CRF) in rats induces epileptiform activity characterized by a regular (pacemaker-like) spiking pattern located in hippocampal leads. CRF has also been shown to increase the firing rate of noradrenergic neurons in the locus ceruleus. Our experiments clarified the possible role of norepinephrine (NE) in mediating hippocampal activity of CRF. Intraperitoneal (i.p.) injection of the alpha 2-agonist clonidine at a dose of 0.5-5 micrograms/kg prevented, in a dose-related manner, the hippocampal epileptiform activity induced by CRF (20 micrograms i.c.v.). Our results suggest a possible role of NE in CRF-induced spiking activity.

Animals↗
PubMedDate not supplied

Electrocortical power spectrum changes induced by microinfusion of corticotropin-releasing factor into the locus coeruleus in rats.

Rat corticotropin-releasing factor (CRF) microinfused unilaterally or bilaterally into the locus coeruleus (LC) of awake, chronically cannulated rats produced a dose-dependent ECoG desynchronization and behavioral activation. ECoG spectra analysis revealed a significant decrease of total voltage power and of 0.25-3 and 3-6 Hz frequency bands. These effects were prevented by a pretreatment into the same site with alpha-hCRF, a selective antagonist at CRF receptors and by alprazolam, a benzodiazepine derivative. In conclusion, the present results indicate that CRF produces its behavioral and ECoG activating effects by interaction with specific receptors located on LC neurons.

Alprazolam↗