The role of monoamine oxidase in the response of the isolated central artery of the rabbit ear to tyramine. (33/39)

1. Monoamine oxidase activity was demonstrated histochemically throughout the media of the rabbit ear artery but not in the adventitia at its border with the media where the sympathetic nerve terminals are concentrated. Neither intensity nor distribution of enzyme activity was perceptibly altered up to 60 days after sympathetic denervation.2. Iproniazid and nialamide increased the sensitivity of the artery to intraluminal tyramine much more than that to extraluminal tyramine, so that the difference between the potencies for the two routes of administration became less marked.3. The results indicate that inactivation by monoamine oxidase in the media is a factor contributing to the relatively low potency of intraluminal tyramine on the artery.  (+info)

Effect of inhibition of catecholamine synthesis on central catecholamine-containing neurones in the developing albino rat. (34/39)

1. Tyrosine hydroxylase is thought to be the rate limiting enzyme step in catecholamine biosynthesis. Inhibition of this enzyme using alpha-methyl-p-tyrosine resulted in a time dependent depletion (and repletion) of formaldehyde induced fluorescence in catecholamine-containing neurones of the central nervous system in developing and adult rats.2. Dopamine-containing neurones were depleted faster and more completely than noradrenaline-containing neurones.3. The extent of depletion caused by alpha-methyl-p-tyrosine in the initial 6-9 h period was more or less comparable in young and adult rats from the age of 1 week onwards; this suggests that catecholamine turnover increases with age and parallels the increase in catecholamine levels.4. The extent of depletion (and repletion) 18 h after administration of the inhibitor varied in animals of different age.5. Administration of a monoamine oxidase inhibitor just before administration of alpha-methyl-p-tyrosine resulted in a reduction of the extent of depletion caused by the latter drug, indicating that monoamine oxidase is important for the breakdown of catecholamines in rats of all ages.6. It is suggested that the catecholamine-containing neurones of the newborn are biochemically as well as functionally differentiated before completion of morphological differentiation.  (+info)

The release of 5-hydroxytryptamine from rabbit small intestine in vitro. (35/39)

1. A method is described by which the lumen of intestinal segments may be perfused separately and simultaneously under identical conditions of perfusion pressure and temperature, and the rate of appearance of 5-hydroxytryptamine (5-HT) into the serosal fluid measured.2. 5-HT appeared in the serosal fluid from quiescent segments of rabbit intestine at a rate of about 4.0 ng/cm intestine/hr and about 14.0 ng/cm intestine/hr from segments performing active peristaltic movements.3. For both quiescent and active segments, when the perfusion fluid contained a monoamine oxidase inhibitor, nialamide (Niamid), the rate of appearance of 5-HT was increased and if, in addition, 5-HT was present in the perfusion fluid the rate of appearance of 5-HT in the serosal fluid was even greater.4. The rate of appearance of 5-HT from the intestine of rabbits pretreated with reserpine was about 0.8 ng/cm intestine/hr and Niamid only slightly increased this rate. However, if 5-HT as well as Niamid were present the rate of appearance of 5-HT was about 6.0 ng/cm intestine/hr.5. Possible explanations for these findings are discussed.  (+info)

Neural serotonin stimulates chloride transport in the rabbit corneal epithelium. (36/39)

Evidence is presented that serotonin acts as a neurotransmitter in the cornea of the adult rabbit. Serotonin was localized to granules in a sparse population of subepithelial corneal nerves by an electron microscopic histochemical procedure. Significant endogenous levels of serotonin and its principal metabolite, 5-hydroxyindoleacetic acid, were detected in the central cornea by a fluorometric assay. Exogenous serotonin stimulated ion transport by corneal epithelium. This effect was potentiated by monoamine oxidase inhibition and was unaffected by an alpha-adrenergic receptor antagonist. Serotonin-stimulated ion transport was inhibited by the specific antagonist, methysergide, and by the replacement of Cl- with an impermeable anion. In tracer experiments, the serotonin-stimulated ion transport was shown to be caused by increased epithelial Cl- secretion. The serotonin response was partially inhibited by the beta-adrenergic antagonist, timolol. In a companion article, assay of corneal cyclic AMP showed stimulation of cyclic AMP synthesis by serotonin, inhibition by the specific antagonist, lysergic acid diethylamide, and potentiation by monoamine oxidase inhibition. We postulate that specific serotonergic receptors are present in the corneal epithelium and that activation of these receptors by serotonin released from serotonergic neurons increases the level of cyclic AMP, which stimulates active Cl- secretion by the corneal epithelium.  (+info)

Serotonin-stimulated cyclic AMP synthesis in the rabbit corneal epithelium. (37/39)

Serotonin increases the level of cyclic AMP in incubated rabbit corneas; the concentration of agonist producing half-maximal stimulation is approximately 1.5 microM. Nialamide, an inhibitor of monoamine oxidase, potentiates the response to serotonin but not to epinephrine. Amitriptyline, an inhibitor of neuronal uptake of serotonin, does not potentiate the stimulation of cyclic AMP synthesis. Lysergic acid diethylamide, but not timolol, antagonizes the response to serotonin; the half-maximal inhibitory concentration is approximately 6 nM lysergic acid diethylamide. A comparison of the time course of the increase in cyclic AMP synthesis after addition of serotonin or epinephrine to the incubation media indicates that serotonin, but not epinephrine, must penetrate a barrier to its free diffusion. We conclude that the corneal epithelium contains specific serotonergic receptors that, upon activation, cause the synthesis of cyclic AMP, which mediates the stimulation of chloride transport (c.f. companion article, Klyce et al.). The serotonergic receptors must be at a location posterior to the beta-adrenergic receptors, which are on the anterior-surface of the apical cells.  (+info)

Phasic modulation of trunk muscle efferents during fictive spinal locomotion in cats. (38/39)

In high spinal paralysed cats electromyograms were recorded from nerves supplying lumbar back muscles (longissimus dorsi) and abdominal muscles (obliquus abdominis externus) during fictive locomotion induced by I.V. injection of nialamide and L-DOPA. Activity in nerves to hind-limb muscles was also recorded. During periods of stable 'locomotor' activity in the hind-limb nerves the efferents to the back and abdominal trunk muscles were generally also rhythmically active. Three different patterns of activity were observed. The predominant rhythmic pattern showed a synchronous activation of the efferents to the back and abdominal muscles of one side together with an activation of the hind-limb flexors of that side, alternating with activation of the efferents to the corresponding contralateral muscles. This pattern was very stable and could last for about 3 h. Such a pattern of activity would be expected during the alternate stepping characteristic of walking and trotting. The second type of rhythmic locomotor activity was characterized by a synchronous bilateral activation of the efferents to the back muscles, alternating with activation of the abdominal muscles on both sides. This pattern occurred only for short periods and appears to correspond to the activity during in-phase stepping such as occurs during a gallop. Beside these well co-ordinated patterns less well co-ordinated rhythmic activities were also observed. These included regular rhythmic activity which occurred independently in different muscle groups as well as irregular rhythmic activity with unstable phase relations between different muscle groups. The rhythmic locomotor activity in efferents to trunk and limb muscles could be modulated by afferent nerve stimulation and by hypoxia. The results reveal that the spinal cord deprived of its supraspinal and peripheral control may generate a variety of different locomotor patterns, which incorporate the trunk muscles in an apparently meaningful way.  (+info)

Plasticity in reflex pathways controlling stepping in the cat. (39/39)

Previous studies have shown that stimulation of group 'I' afferents from ankle extensor muscles can prolong the cycle period in decerebrate walking cats and that the magnitude of these effects can be altered after chronic axotomy of the lateral-gastrocnemius/soleus (LGS) nerve. The effectiveness of LGS group I afferents in prolonging the cycle period decreases after axotomy, whereas the effectiveness of the uncut medial-gastrocnemius (MG) group I afferents is increased. The objectives of this investigation were to establish the time course of these changes in effectiveness and to determine whether these changes persist after transection of the spinal cord. The effects of stimulating the LGS and/or MG group I afferents on the cycle period were examined in 22 walking decerebrate animals in which one LGS nerve had been cut for 2 to 31 days. The effectiveness of LGS group I afferents declined progressively in the postaxotomy period, beginning with significant decreases at 3 days and ending close to zero effectiveness at 31 days. Large increases in the effectiveness of MG group I afferents occurred 5 days after axotomy, but there was no progressive change from 5 to 31 days. To test whether these changes in effectiveness were localized to sites within the spinal cord, the cord was transected in some decerebrate animals and stepping induced by the administration of L-DOPA L-3-4 dihydroxyphenylalanine (L-DOPA) and Nialamide. The effects of stimulating the MG and/or the LGS group I afferents on the cycle period were reexamined. In all four animals tested, stimulating the axotomized LGS group I afferents had a reduced effectiveness during locomotor activity in both the decerebrate and spinal states, whereas the increased effectiveness of the MG group I afferents was retained after transection of the spinal cord in two of five animals. Different mechanisms may be responsible for the changes in strength of the LGS and MG group I afferent pathways that project onto the rhythm generating sites in the spinal cord. This possibility follows from our observations of a linear relationship between the time after axotomy and decreased effectiveness of LGS group I afferents but no significant relationship between time postaxotomy and increased effectiveness of MG group I afferents; no significant relationship between the decreased effectiveness of LGS group I afferents and the increased effectiveness of MG group I afferents; and, after spinalization, consistent (4/4 cases) preservation of decreased LGS effectiveness but frequent (3/5 cases) loss of increased MG effectiveness.  (+info)