Degeneration and regeneration of adrenergic nerves in mesenteric blood vessels, iris and atrium of the rat after 6-hydroxydopamine injection

1975 ◽  
Vol 4 (2) ◽  
pp. 157-176 ◽  
Author(s):  
H. P. Lorez ◽  
H. Kuhn ◽  
G. Bartholini
Keyword(s):  
Blood Vessels ◽  
Adrenergic Nerves ◽  
6 Hydroxydopamine

scholarly journals Nerve Fibers Containing Neuropeptide Y in the Cerebrovascular Bed: Immunocytochemistry, Radioimmunoassay, and Vasomotor Effects

1987 ◽  
Vol 7 (1) ◽  
pp. 45-57 ◽  
Author(s):  
L. Edvinsson ◽  
J. R. Copeland ◽  
P. C. Emson ◽  
J. McCulloch ◽  
R. Uddman
Keyword(s):  
Neuropeptide Y ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Calcium Entry Blocker ◽  
Cervical Ganglion ◽  
Prostaglandin F ◽  
6 Hydroxydopamine

Perivascular nerve fibers containing neuropeptide Y (NPY)-like immunoreactivity were identified around cerebral blood vessels of human, cat, guinea pig, rat, and mouse. The major cerebral arteries were invested by dense plexuses; veins, small arteries, and arterioles were accompanied by few fibers. Removal of the superior cervical ganglion resulted in a reduction of NPY-like material in pial vessels and dura mater. Pretreatment with 6-hydroxydopamine or reserpine reduced the number of visible NPY fibers and the concentration of NPY in rat cerebral vessels. Sequential immuno-staining with antibodies toward dopamine-β-hydroxylase (DBH) (an enzyme involved in the synthesis of noradrenaline) and NPY revealed an identical localization of DBH and NPY in nerve cell bodies in the superior cervical ganglion and in perivascular fibers of pial blood vessels, suggesting their coexistence. Administration of NPY in vitro resulted in concentration-dependent contractions that were not modified by a sympathectomy. The contractions induced by noradrenaline, 5-hydroxytryptamine, and prostaglandin F2α and the dilator responses to calcitonin gene-related peptide were not modified by NPY in rat cerebral arteries. However, the constrictor response to NPY was reduced by 70% in the presence of the calcium entry blocker nifedipine, and abolished following incubation in a calcium-free buffer. These data suggest an interaction of NPY at a postsynaptic site, which for induction of contraction may open calcium channels in the sarcolemma of cerebral arteries.

scholarly journals Galanin is localized in sympathetic neurons of the dog liver

1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Sympathetic Neurons ◽  
Sympathetic Nerves ◽  
Liver Parenchyma ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminals ◽  
6 Hydroxydopamine ◽  
Hepatic Nerves ◽  
Dog Liver

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.

A role of the central catecholamine neuron in cerebral circulation

1986 ◽  
Vol 65 (3) ◽  
pp. 370-375 ◽  
Author(s):  
Hideyoshi Yokote ◽  
Toru Itakura ◽  
Kunio Nakai ◽  
Ichiro Kamei ◽  
Harumichi Imai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Vessels ◽  
Cerebral Circulation ◽  
Intracerebral Injection ◽  
Neuron System ◽  
Content Type ◽  
6 Hydroxydopamine ◽  
Catecholamine Neuron

✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.

The Croonian Lecture, 1964 The release and fate of the transmitter liberated by adrenergic nerves

1965 ◽  
Vol 162 (986) ◽  
pp. 1-19 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Blood Vessels ◽  
Vascular System ◽  
Sympathetic Innervation ◽  
Muscle Cells ◽  
Blood Stream ◽  
The Body ◽  
Adrenergic Nerves ◽  
Local Motion ◽  
Specific Enzyme

It is customary for Croonian lecturers, after expressing their thanks to the President and Council for the honour that they have received in being asked to give this lecture, to devote some time to a justification of their subject in terms of Mrs Croone’s suggestion that the lecture should deal with the advancement of natural knowledge on local motion. The first of these tasks, Mr President, I perform humbly and with deep gratitude, but at the same time with some surprise that Council in its wisdom should have chosen one so ill-fitted for the honour you have laid upon him. The second task is easier since my lecture will deal with the nerves which control the muscles surrounding the hollow organs of the body, blood vessels and bowels, and further justification as a theme dealing with local motion the most captious critic could not desire. Three years ago my former colleague Bernard Katz gave the Croonian Lecture on ‘ Transmission of impulses from nerve to muscle’ in which he described our present knowledge of the mechanism of the chemical mediation interposed between nerve and skeletal muscle and summarized his own brilliant contributions to this, to me, fascinating subject. Today I am dealing again with transmission from nerve to muscle, but in a different system and, I am afraid, at a quite different and lower intellectual level than that of Katz. The idea of chemical transmission from nerve to effector cell came first to T. R. Elliott in 1904 as a result of his observation, in an extensive comparative study, of the close similarities between the actions of adrenaline injected intravenously and the effects of stimulating nerves belonging to the sympathetic system. These nerves we should now call in Dale’s (1933) terminology the adrenergic nerves, those transmitting their effects whether excitatory or inhibitory by the liberation at their endings of a ‘minute charge’ of the catecholamine adrenaline or one of its analogues. The cells upon which these nerves exert their action are the smooth muscle cells controlling the movements of the hollow viscera, intestines, reproductive tract and so on, and of the muscle cells of the vascular system that regulate the diameter of the blood vessels. These are processes that do not demand high precision of timing nor do they apparently require the instant turning on and off of transmitter action with which we have grown familiar in the junction between nerve and skeletal muscle. At this junction, as Katz showed, liberation and action of acetylcholine and its inactivation by the specific enzyme cholinesterase are over in a few milliseconds, and there is no reason to believe that the liberated transmitter in the untreated junction can ever diffuse more than a few microus from its site of action. It is hemmed in by barriers of specific cholinesterase, and these are reinforced by barriers of the non-specific enzyme in blood and tissue fluids. This narrow coarctation of the transmitter acetylcholine in space and time seems, however, to be confined to places where precise timing is required, such as at the neuromuscular junction and in the ganglionic and central nervous synapse. When it is liberated as the transmitter from nerves to blood vessels, or to secretory glands, it can escape some way from its site of liberation and persist long enough to be detected by skeletal muscles sensitized by denervation, as is seen in the Sherrington, Rogowitz and Vulpian-Heidenhain phenomena. I have laboured a little this question of diffusion and action at a distance of transmitter because it constitutes prima facie one of the most striking differences between the adrenergic and the cholinergic transmitters in at least the mammalian body. It was indeed because the liberated adrenergic transmitter escaped into the blood stream and could be detected by another tissue or organ, sometimes, but not necessarily, specially sensitized, that W. B. Cannon and his colleagues in the 30’s were able to add so much to our knowledge of sympathetic innervation. Nevertheless, in spite of the relative stability of the adrenergic transmitter and its ready detection in the blood stream, little had been discovered about the quantitative aspects of its liberation and metabolism some 50 years after its existence had been postulated, whereas we now have, and have had for 30 years, quite reasonably complete information about the liberation, storage and metabolism of the unstable and ephemeral acetylcholine.

Studies of the innervation of rabbit myometrium and cervix

1989 ◽  
Vol 67 (8) ◽  
pp. 837-844 ◽  
Author(s):  
R. Bulat ◽  
M. S. Kannan ◽  
R. E. Garfield
Keyword(s):  
Electron Microscopy ◽  
Smooth Muscle ◽  
Blood Vessels ◽  
Spontaneous Activity ◽  
Isometric Contraction ◽  
Glyoxylic Acid ◽  
Adrenergic Innervation ◽  
Significant Inhibition ◽  
Adrenergic Nerves ◽  
Field Stimulation

We characterized the innervation of isolated circular and longitudinal-oriented muscle strips from the nulliparous rabbit uterus and cervix by field stimulation (FS). FS with increasing frequency (2.5–50 pps) and voltage (2.5–70 V) caused graded increases in isometric contraction with no relaxation or inhibition of spontaneous activity. Tetrodotoxin(TTX, 3.1 × 10−6 M) significantly reduced the FS response by 75% in all strips at higher stimulus frequencies. Contractile responses to FS were also significantly inhibited by atropine (3.5 × 10−6 M) in circular uterus and in longitudinal cervix. Guanethidine (5 × 10−6 M) reduced the response in all strips, as did phentolamine (3.6 × 10−6 M) in longitudinal uterus and circular cervix. Propranolol (3.9 × 10−6 M) did not significantly change the response in longitudinal uterus or circular cervix. In longitudinal uterus, combined guanethidine and atropine produced significant inhibition, but not statistically different from either drug alone. Similar results were seen in circular uterus. Electron microscopy and glyoxylic acid histofluorescence indicate that both blood vessels and smooth muscle in rabbit uterus are supplied with adrenergic nerves. The results suggest the presence of TTX-sensitive adrenergic and cholinergic excitatory innervation of rabbit uterus and cervix.Key words: uterus, myometrium, cervix, adrenergic innervation.

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