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Biomedical subjects

L Beani

Publications and source records attributed to L Beani.

At least 127 records · Page 7Linked to original sources
PubMed1979

Inhibition of acetylcholine outflow from guinea-pig cerebral cortex following locus coeruleus stimulation.

Experiments were performed in unanaesthetized guinea-pigs in order to obtain direct evidence that the noradrenergic projections from locus coeruleus (L.C.) to cerebral cortex inhibit the acetylcholine (ACh) release. The animals were provided with left and right epidural cups, to collect outflowing ACh and with a stimulating electrode, positioned in the left L.C. The electrical stimulation of L.C. caused a significant reduction of ACh outflow from both parietal areas. This effect was abolished, reduced or prevented by phentolamine, phenoxybenzamine or reserpine plus alpha-mt pretreatment, hence showing to be alpha-mediated.

Acetylcholine↗
PubMed1978

Noradrenaline inhibition of acetylcholine release from guinea-pig brain.

The effect of noradrenaline (NA) on acetylcholine (ACh) release from guinea-pig brain was investigated in superfused cerebral cortex slices and in unrestrained unanaesthetized animals provided with epidural cups. The amine reduced the ACh release from electrically stimulated tissue and its effect was antagonized by phentolamine and phenoxybenzamine, but not by propranolol and spiroperidol. The injection of NA (150 microgram) into the cerebral ventricles caused sedation, E.Co.G. synchronization and reduced ACh outflow from the parietal cortex. This inhibition was counteracted by alpha-blocking agents. A lower dose of NA (50 microgram) did not change the behaviour, but produced a late increase in ACh outflow, prevented by spiroperidol. These results fit well with the hypothesis that NA restrains, via alpha-receptors, the ACh secretion from the nerve endings and indirectly support the view that the amine reduces the firing rate of the corticopetal cholinergic neurones. The late increase in ACh outflow, observed in vivo, may be referred to secondary activation of the dopaminergic neurones, known to enhance the cortical ACh release in this animal species.

Acetylcholine↗
PubMed1971

Vagal non-adrenergic inhibition of guinea-pig stomach.

1. The effect of vagal and sympathetic stimulation on the mechanical and electrical activity (intracellular recording) of the body of the guinea-pig stomach was investigated in vitro.2. Following atropine, 1 x 10(-6)-1 x 10(-7) g/ml., vagal responses were reversed from excitatory to inhibitory.3. Sympathetic blockade, produced by alpha- and beta-receptor antagonists and adrenergic neurone-blocking agents, reduced or abolished sympathetic, but not vagal inhibition.4. Hexamethonium (5 x 10(-5) g/ml.) reduced vagal relaxation to 11-30% according to the stimulation rate. The residual response was maintained in the presence of 5-hydroxytryptamine tachyphylaxis.5. Many muscle cells were observed to be under the influence of both vagus and sympathetic nerves: the effect of sympathetic stimulation was always inhibitory in nature, but high stimulation rates were required. The effect of vagal stimulation was both excitatory and inhibitory even in the absence of atropine: low stimulation rates gave rise either to E.J.P.s (excitatory junctional potentials), often followed by spikes, or to I.J.P.s (inhibitory junctional potentials).6. In some spontaneously firing cells the interruption of electrical activity produced by vagal stimulation at 2/sec and sympathetic stimulation at 20/sec was recorded for a long enough time to check the effect of guanethedine (5 x 10(-6) g/ml.): the drug selectively blocked sympathetic inhibition.7. The significance of the inhibitory non-adrenergic transmitter, released by the intramural neurones activated by preganglionic vagal fibres, is discussed.

Action Potentials↗
PubMed1969

The effect of catecholamines and sympathetic stimulation on the release of acetylcholine from the guinea-pig colon.

1. In isolated guinea-pig terminal colon, the effect of sympathetic stimulation on contraction and acetylcholine release elicited by pelvic and transmural stimulation was investigated.2. Sympathetic stimulation reduced the nerve-mediated contractile responses more than those produced by added acetylcholine.3. Sympathetic stimulation also reduced the acetylcholine released during pelvic and transmural stimulation at low frequency. The inhibitory effect on acetylcholine released from resting colons is concealed by the simultaneous release of acetylcholine in considerable amounts from stimulated periarterial nerves which probably contain parasympathetic fibres.4. The inhibitory effect of endogenous and exogenous catecholamines prevails when cholinergic neurones fire at low rates. It was confirmed that adrenaline is more active than noradrenaline.5. The release of acetylcholine from unstimulated colons was for the most part maintained by nerve-conducted activity, because tetrodotoxin was able to reduce it to about one-tenth.6. It is suggested that the sympathetic control of gastrointestinal tone and motility is exerted through two different routes: inhibition of intramural cholinergic plexuses and direct relaxation of smooth muscle cells.7. The possible site and mechanism of action of catecholamines on intramural cholinergic structures is briefly discussed.

Acetylcholine↗