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Biomedical subjects

A Poli

Publications and source records attributed to A Poli.

At least 163 records · Page 9Linked to original sources
PubMed1986

Cholinergic, GABAergic and excitatory amino acidic neurotransmission in the goldfish vagal lobe.

Some neurotransmitter systems operating in the goldfish vagal lobe, an hypertrophied gustatory center, have been studied by means of experimental (kainic acid injection and vagal rhizotomy), neurochemical and ultrastructural methods. The use of the neurotoxin, kainic acid, revealed the existence of cholinergic and GABAergic neurons in the vagal lobe. The results of histochemical observations and biochemical assays performed after rhizotomy of sensory and motor vagal roots, suggest that the motor neurons of the vagal motor layer are cholinergic. The same experiments also indicate that the primary gustatory afferents distributing to the sensory layer of the vagal lobe are, at least in part, cholinergic. By contrast, no decrease of excitatory amino acid uptake was demonstrated following the experimental lesions. GABA is likely to play an important role in the goldfish vagal lobe, particularly in the sensory layer, where the highest level of its synthetic enzyme, glutamate decarboxylase, is recorded. The significant decrease of glutamate decarboxylase in the sensory layer after vagal rhizotomy suggests that either GABAergic primary afferents reach the vagal lobe, or that deafferentation results in a decreased GABA synthesis in intrinsic GABAergic neurons.

Acetylcholinesterase↗
PubMed1986

Colonisation of Haemophilus influenzae and Streptococcus pneumoniae in the upper respiratory tract of neonates in Papua New Guinea: primary acquisition, duration of carriage, and relationship to carriage in mothers.

In order to determine the age of acquisition and duration of carriage of the first strains of Haemophilus influenzae and Streptococcus pneumoniae in the upper respiratory tract of Papua New Guinea children, 25 babies were recruited at, or shortly after birth. Nasal secretions from mothers and children were cultured at 1- to 2-weekly intervals. H. influenzae and S. pneumoniae were acquired within the neonatal period by 60% of the infants, and all were colonised by both organisms within the first 3 months of life. Carriage periods for H. influenzae ranged from 6 to 221 days (mean, 74 days), and for S. pneumoniae from 5 to 290 days (mean, 96 days). Penicillin resistance was detected in 36% of the first acquired strains of pneumococci. Mothers, generally either did not carry H. influenzae or S. pneumoniae, or harboured types different to those first acquired by their infants. However, one-third of mothers subsequently became colonised with H. influenzae and S. pneumoniae types similar to those carried by their babies.

Carrier State↗
PubMed1986

Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging.

A study in vitro of specimens of human aortic and common carotid arteries was carried out to determine the feasibility of direct measurement (i.e., not from residual lumen) of arterial wall thickness with B mode real-time imaging. Measurements in vivo by the same technique were also obtained from common carotid arteries of 10 young normal male subjects. Aortic samples were classified as class A (relatively normal) or class B (with one or more atherosclerotic plaques). In all class A and 85% of class B arterial samples a characteristic B mode image composed of two parallel echogenic lines separated by a hypoechoic space was found. The distance between the two lines (B mode image of intimal + medial thickness) was measured and correlated with the thickness of different combinations of tunicae evaluated by gross and microscopic examination. On the basis of these findings and the results of dissection experiments on the intima and adventitia we concluded that results of B mode imaging of intimal + medial thickness did not differ significantly from the intimal + medial thickness measured on pathologic examination. With respect to the accuracy of measurements obtained by B mode imaging as compared with pathologic findings, we found an error of less than 20% for measurements in 77% of normal and pathologic aortic walls. In addition, no significant difference was found between B mode-determined intimal + medial thickness in the common carotid arteries evaluated in vitro and that determined by this method in vivo in young subjects, indicating that B mode imaging represents a useful approach for the measurement of intimal + medial thickness of human arteries in vivo.

Adult↗
PubMed1986

Indenolol kinetics versus pharmacodynamics in hypertension.

A kinetic model has been employed to compare the duration of the antihypertensive activity of indenolol to its plasma half-life both after single administration and at steady-state. After a 14 day run-in period with placebo, 60 or 120 mg indenolol were given to hypertensive patients I or II grade, according to W.H.O. guidelines, once a day for 14 days. Blood samples were drawn and blood pressure recorded at intervals after the first dose, during treatment and after the last dose of the compound. Both plasma concentration and mean arterial pressure difference curves were fitted by a first order input-output model, where plasma half-life was 4 h, while pharmacological half-life was 24 h for both dose-levels tested. Therefore, with once-a-day dose regimen an accumulation of the antihypertensive effect of indenolol was demonstrated, with 99% steady-state of blood pressure reached after 7 days, while the drug did not accumulate in the central compartment.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of d,1-propranolol and haloperidol on aggressive behavior induced in mice by isolation and isolation plus amphetamine treatment.

We measured the aggressive behavior of isolated mice treated or not with d,1-amphetamine (6.0 mg/kg, ip) and injected with different doses of d,1-propranolol (10.0, 20.0 or 30.0 mg/kg, ip) or haloperidol (0.5 or 1.0 mg/kg). d,1-Amphetamine (6.0 mg/kg, ip) decreased the aggressiveness of the isolated mice and induced stereotyped behavior. Haloperidol antagonized amphetamine-induced stereotypy, increased the latency to the 1st attack and decreased duration of fighting and frequency of attacks in mice treated or not with amphetamine. d,1-Propranolol did not change stereotypy but decreased aggressiveness in a dose-dependent way, being more effective against aggression induced by isolation per se. These results are discussed in terms of the interference of the drugs with the activity of either catecholaminergic neurons or midbrain reticular formation. The latter effect seems to be the most likely explanation for the observed anti-aggressive effects of haloperidol and d-1, propranolol.

Aggression↗
PubMed1986

Increase of serum lipid-associated sialic acid concentration in dogs with neoplasms.

Serum concentrations of lipid-associated sialic acid (LASA) were determined in sera obtained from 26 apparently healthy dogs (group 1), 56 dogs with nonneoplastic disorders (group 2), and 100 dogs with neoplasms (benign [group 3], malignant [group 4]), using a simple, reliable, rapid spectrophotometric procedure. The LASA concentrations were significantly increased (P less than 0.01) in group 4 dogs (malignant neoplasms) when compared with those in dogs from groups 1, 2, and 3. The sensitivity of the test was between 71.5% and 100%, and specificity was 92.3% for group 1, 67.8% for group 2, and 80.6% for group 3. A preliminary study concerning variations of serum LASA values as a marker after surgical treatment of tumor showed a good correlation between effectiveness of therapy and serum LASA concentrations.

Adenocarcinoma↗
PubMed1985

[3H] kainic acid binding sites in the synaptosomal-mitochondrial (P2) fraction from goldfish brain.

Binding of [3H]kainic acid to the synaptosomal-mitochondrial fraction (P2) of the goldfish brain was studied. Specific binding to this fraction represents about half of the total binding capability of the homogenate particulate material and is enriched in synaptic membranes; it is greater by about two orders of magnitude than those given for rat brain and pigeon optic tectum membranes. Association of the ligand-site complex has a time constant lower than 1 min and the same is true for the main component of the dissociation process. The binding equilibrium is apparently not affected by substances contained in the fraction material. The analysis of the dose-response data showed a main receptor population (B max = 139 pmol/mg protein) which displayed positive cooperativity (nH = 1.29). The same behaviour was shown by washed membranes from the same fraction but, in this case, the affinity for the ligand was lower (apparent affinity constants: K'D = 0.28 nM for the intact fraction and K'D = 0.38 nM for membranes). A smaller population of sites with higher affinity was also detected both in the intact fraction and in membranes. Among the substances tested as displacers of kainic acid from the synaptosomal sites, the most effective were quisqualate and L-glutamate. Folic acid and its dihydro and tetrahydro derivatives were half as potent as glutamate whereas methyltetrahydrofolic acid and folinic acid had a very weak action. The difference between these sites and those detected on rat brain membrane preparations is discussed.

Animals↗
PubMed1985

Neurotransmitter-related markers in the normal and experimentally lesioned telencephalon of the goldfish.

The telencephalon of teleost fish shows high affinity uptake for D-[3H]aspartate, intermediate levels of GABAergic markers and low levels of cholinergic enzymes. Experimental results (resection of the olfactory tracts or unilateral kainic acid administration in the telencephalon) suggest that: the projection from the olfactory bulbs to telencephalic targets is mediated by aspartate and/or glutamate; and a population of GABAergic neurons is present in a telencephalic area which is considered homologous to part of the striatal complex of land vertebrates. From the present results, it appears that the neurochemical approach can be used, in conjunction with neuroanatomical methods, to study evolutionary problems of telencephalic function.

Acetylcholinesterase↗
PubMed1985

Effects of d,l-propranolol on open field behavior of rats.

Rats were administered with different doses of d,l-propranolol or d,l-propranolol plus amphetamine before open-field observations. Results show that d,l-propranolol decreased locomotion and rearing frequencies and increased immobility duration in rats. An antagonism between the effects of amphetamine and d,l-propranolol on general activity of rats was also observed. Results are discussed in the light of a possible interference of the drugs with the activity of either noradrenergic neurons or mid-brain reticular formation.

Amphetamine↗
PubMed1985

Kainic acid differentially affects the synaptosomal release of endogenous and exogenous amino acidic neurotransmitters.

Presynaptic actions of kainic acid have been tested on uptake and release mechanisms in synaptosome-enriched preparations from rat hippocampus and goldfish brain. Kainic acid increased in a Ca2+-dependent way the basal release of endogenous glutamate and aspartate from both synaptosomal preparations, with the maximum effect (40-80%) being reached at the highest concentration tested (1 mM). In addition, kainic acid potentiated, in an additive or synergic way, the release of excitatory amino acids stimulated by high K+ concentrations. Kainic acid at 1 mM showed a completely opposite effect on the release of exogenously accumulated D-[3H]aspartate. The drug, in fact, caused a marked inhibition of both the basal and the high K+-stimulated release. Kainic acid at 0.1 mM had no clear-cut effect, whereas at 0.01 mM it caused a small stimulation of the basal release. The present results suggest that kainic acid differentially affects two neurotransmitter pools that are not readily miscible in the synaptic terminals. The release from an endogenous, possibly vesiculate, pool of excitatory amino acids is stimulated, whereas the release from an exogenously accumulated, possibly cytoplasmic and carrier-mediated, pool is inhibited or slightly stimulated, depending on the external concentration of kainic acid. Kainic acid, in addition, strongly inhibits the high-affinity uptake of L-glutamate and D-aspartate in synaptic terminals. All these effects appear specific for excitatory amino acids, making it likely that they are mediated through specific recognition sites present on the membranes of glutamatergic and aspartatergic terminals. The relevance of the present findings to the mechanism of excitotoxicity of kainic acid is discussed.

Animals↗
PubMed1984

Apolipoprotein C-II deficiency. The role of apolipoprotein C-II in the hydrolysis of triacylglycerol-rich lipoproteins.

Kinetic studies were performed incubating lipoprotein lipase and hepatic triacylglycerol lipase from human postheparin plasma with triacylglycerol-rich lipoproteins from two patients with apolipoprotein C-II deficiency. These lipoproteins differed in their lipid and apolipoprotein composition from normal very-low-density lipoproteins and chylomicrons. The addition of isolated apolipoprotein C-II and normal or apolipoprotein C-II-deficient high-density lipoproteins caused an increase of Vmax and a decrease of the Km for lipoprotein lipase-induced hydrolysis. Hepatic triacylglycerol lipase activity was not influenced by the presence of apolipoprotein C-II in the incubation medium, but was inhibited by increasing amounts of high-density lipoproteins. Binding studies were performed in order to analyze the interactions between lipolytic enzymes, apolipoprotein C-II, and triacylglycerol-rich lipoproteins. Apolipoprotein C-II was, as expected, rapidly taken up by apolipoprotein C-II-deficient very-low-density lipoproteins and chylomicrons when they were incubated with normal high-density lipoproteins or with the purified apolipoprotein. This uptake was inhibited by the addition of increasing amounts of lipoprotein lipase in conditions in which no lipolysis could occur. Binding of lipoprotein lipase to apolipoprotein C-II-deficient very-low-density lipoproteins or chylomicrons was not affected by the addition of apolipoprotein C-II when an excess of triacylglycerol-rich lipoprotein was present. The stability of lipoprotein lipase was also studied. Apolipoprotein C-II and high-density lipoproteins were unable to prolong the half-life of the enzyme activity, while triacylglycerol-rich particles effectively stabilized lipoprotein lipase. We conclude that binding of lipoprotein lipase to the substrate surface is not affected by apolipoprotein C-II. It is more likely that the peptide catalyzes the conversion of lipoprotein lipase from a less to a more active form.

Adult↗
PubMed1984

Evidence for a neurotransmitter role of aspartate and/or glutamate in the projection from the torus longitudinalis to the optic tectum of the goldfish.

Different experimental approaches have been used to demonstrate that aspartate and/or glutamate is a transmitter(s) in the projection from the torus longitudinalis to the marginal layer of the optic tectum in the goldfish. Slices of the optic tectum incubated in vitro in the presence of D-[3H]aspartate and processed for light microscopic autoradiography, demonstrated a preferential accumulation of the labeled compound in the marginal layer. Under the same experimental conditions several neurons in the central part of the torus longitudinalis selectively accumulated D-[3H]aspartate. Synaptosome-enriched preparations from the optic tectum showed high-affinity uptake for D-[3H]aspartate and the rate of the uptake was significantly decreased after disconnection from the ipsilateral torus longitudinalis. The same subcellular preparations showed Ca2+-dependent release of previously accumulated D-[3H]aspartate under high potassium stimulation. This release was significantly reduced in preparations from optic tecta 5 days after cutting their connection with the ipsilateral torus longitudinalis. Finally, D-[3H]aspartate injected in the optic tectum retrogradely labeled the fiber systems connecting the marginal layer with the ipsilateral torus longitudinalis as well as neuronal cell bodies in the torus longitudinalis itself. From autoradiographic experiments it was, in addition, noticed that several tectal neurons selectively accumulated D-[3H]aspartate in the cell bodies as well as in main dendritic trunks. This observation suggests tht aspartate and/or glutamate may be a transmitter(s) in some intrinsic circuits and extrinsic projections of the optic tectum.

Animals↗