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At least 19 recordsLinked to original sources
PubMed1977

Histochemical evidence of altered development of cholinergic fibers in the rat dentate gyrus following lesions. II. Effects of partial entorhinal and simultaneous multiple lesions.

It has been concluded previously that the septohippocampal fibers which project to the rat dentate gyrus extend or branch in the denervated area of the molecular layer following a complete ipsilateral entorhinal lesion. The septohippocampal fibers thus appear to replace some of the perforant fibers which degenerate as a result of the lesion. The reactive fibers eventually become localized to a much smaller and more superficial area after lesions of immature rats than after lesions made in adulthood. To determine whether this difference in the response results from a selective reaction to loss of the lateral perforant path in the immature rat, various portions of the entorhinal cortex were removed at the age of 11 days, and the cholinergic septohippocampal fibers were visualized by acetylcholinesterase histochemistry. An alternative possibility, that the difference between immature and adult rats is attributable to an interaction with other reactive afferents, was tested by removing other sources of input (the contralateral entorhinal cortex, contralateral hippocampal formation or both) along with the ipsilateral entorhinal cortex at the age of 11 days and then demonstrating the septohippocampal fibers histochemically. Lesions of the lateral part of the ipsilateral entorhinal cortex (source of the lateral perforant path) at 11 days of age evoked a septohippocampal reaction along the outer edge of the molecular layer, where the lateral perforant path fibers normally terminate. This result matched that produced by a complete entorhinal lesion. Lesions of the medial entorhinal cortex evoked no obvious reaction. In contrast, the septohippocampal fibers in adult rats proliferated in the denervated area of the molecular layer after lesions of either part of the entorhinal cortex. Combining lesions of other sources of innervation to the dentate gyrus with an ipsilateral entorhinal lesion at 11 days of age did not alter the response of septohippocampal fibers, as determined histochemically. Neither did the septohippocampal fibers react to removal of commissural afferents alone. The response at any age was unaffected by prior or subsequent removal of the contralateral entorhinal cortex. These results indicate that in immature rats the septohippocampal fibers respond only to loss of the lateral perforant path, but these same fibers can later react to loss of any part of the perforant path. They are regarded as support for the hypothesis that the reactive septohippocampal fibers preferentially interact with dendritic growth cones. Our results do not support explanations based on a hypothetical attraction between septohippocampal and crossed perforant path fibers (which react in the same area) or on competition with commissural fibers (which reinnervate an adjacent area). We suggest further that proximity to the degenerating elements does not in itself determine the pattern of reinnervation after lesions of the central nervous system.

Acetylcholinesterase↗
PubMed1977

Histochemical evidence of altered development of cholinergic fibers in the rat dentate gyrus following lesions. I. Time course after complete unilateral entorhinal lesion at various ages.

The entorhinal cortex of rats was removed at various times during development, and the reaction of the cholinergic septohippocampal input to the dentate gyrus was examined by use of acetylcholinesterase histochemistry. When the ipsilateral entorhinal cortex is completely removed, the outer 70-75% of the molecular layer of the dentate gyrus is almost completely denervated. After such a lesion at 5 to 33 days of age, the acetylcholinesterase staining initially intensified throughout the denervated area, indicating that the septohippocampal fibers branched or elongated. This reaction could be detected within one day after a lesion at 11 days of age and within three or five days after lesions at earlier or later times. Whereas the initial response of the septohippocampal fibers was independent of the age at which the lesion was made, their final localization depended on the developmental state of the animal. After lesions at the age of 5 or 11 days, the reactive septohippocampal fibers became restricted to the outer one-sixth to one-third of the molecular layer within two days after appearance of their initial reaction. A similar concentration of reactive fibers was demonstrable after lesions at 16, 18 or 21 days of age, but some reaction persisted in the middle third of the molecular layer. Finally, after lesions at 26 or 33 days of age the proliferating cholinergic fibers ultimately were uniformly distributed throughout the outer 60% of the molecular layer. These results suggest that septohippocampal fibers initially extend or sprout throughout the denervated area to replace the lost perforant path fibers. However, the reactive fiber population becomes restricted to the outer edge of the molecular layer if the entorhinal lesion is made before the period of cholinergic synaptogenesis and concentrates in this same zone if it is made while cholinergic synapses are forming. We suggest that either the proliferative reaction continues in the outer part of the molecular layer and subsides in other parts of the denervated area or septohippocampal fibers move outward through the molecular layer to assume a more superficial location. After entorhinal lesions at 16 days of age or later the pale-staining zone (containing fibers that originate in hippocampus regio inferior) immediately deep to the denervated area widened. If the lesion was made earlier, this zone never developed at most septotemporal levels of the dentate gyrus. These results are probably related to the extension of regio inferior fibers into the denervated area.

Acetylcholinesterase↗
PubMed1979

Innervation of the canine inferior vena cava. Distribution of adrenergic and cholinergic excitatory fibers among the embryologically distinct segments.

The innervation of three embryologically distinct segments of the canine inferior vena cava was investigated. These segments were termed A (supradiaphragm), B-C (intrahepatic and that between liver and renal veins), and D (infrarenal). Strips were cut from these segments, and their isometric tensions were recorded. Transmural electrical stimulation induced contractile responses in circular strips from segment B-C (66.5% of the maximum norepinephrine-induced response) and in those from D (14.4%), but not in A. These responses almost completely disappeared in the presence of phenoxybenzamine. In segment B-C, however, the remaining small contraction was markedly enhanced by neostigmine and abolished by atropine. The same phenomenon was also observed in the contraction remaining after reserpinization. Longitudinal strips from segment C responded similarly. Concentration-response curves of circular strips for acetylcholine were shifted by neostigmine markedly to the left only in segment B-C, while no significant shift occurred in A and D. It was concluded that the adrenergic innervation is remarkably dense in B-C, sparse in D, and probably lacking in A. In addition, a cholinergic excitatory innervation is present in segment B-C.

Acetylcholine↗
PubMed1978

Intrahepatic distribution of nerves in the rat.

The intrahepatic distribution of nerves in the rat was studied using neurohistochemical and electron microscopic methods. Innervation was restricted primarily to vessels in the portal space and hilus. Both adrenergic and cholinergic fibers were observed in the adventitia of hepatic arteries, and to a lesser extent adjacent to portal veins. Some of the cholinergic fibers, however, were not contiguous with the vasculature. Near the hilus many of these fibers were associated with ganglia while peripherally some coursed into the immediately adjacent parenchyma where end bulbs abutted on hepatocytes. Ultrastructurally, scattered small nerves, devoid of neurolemma, were found contiguous with the portal lamina of hepatocytes. Nerve fibers deeper within the lobule were not seen but numerous gap junctions were observed between contiguous hepatocytes. Central and sublobular hepatic veins lacked innervation but adrenergic nerves were demonstrated in the walls of larger hepatic veins. Innervation of the biliary system was sparse. While nerves were interposed between vessels and bile ducts, such nerves tended to be associated more closely with the vasculature.

Acetylcholinesterase↗
PubMed1976

Fluorescence histochemical study of the pancreas in the cat.

The exocrine and endocrine pancreas was investigated according to the fluorescence histochemical method of Flack and Hillarp. 1) Green fluorescent adrenergic fibers were regularly seen associated with arteries and arterioles in the exocrine pancreas. 2) Cholinergic fibers as shown by cholinesterase activity, were also found in the parenchyma of pancreas. 3) Yellow fluorescent cells scattered in the exocrine parenchyma and localized to a population of pancreatic islet cells with a characteristic distribution at the islet periphery was found. 4) By the fluorescence microscopic observation, inter-or intralobular pancreatic ducts, involving the zymogen granules, can also be seen after treatment with HCL vapor. 5) Yellow fluorescent cells, beta-cells containing insulin, remained at the Islet periphery. At present, the above mentioned yellow fluorescent cells are identified as containing HPP (Human pancreatic polypeptide) according to the immunofluorescence technique. With the use of the Falck and Hillarp histochemical technique ethionine induced pancreatitis in cats has been investigated. 1) After seven days of ethionine (5 mg/kg BW oral ad.) treatment, pancreas showed histochemical changes such as hemorrhage, fat necrosis, destruction of acinar cells and degranulation of zymogen from the parenchyma of pancreas. 2) Oral administration of ethionine for ten days induced severe degranulation, rupture of vessels, especially of veins and venules and later influenced arteries or arterioles. 3) Necrosis and fibrosis began to appear in the spaces between the cellular debris and marked pancreatic atrophy could be found. 4) The destruction of Islets of Langerhans can be found in the ethionine induced pancreatic parenchyma. On the other hand, an increased number of Islets of Langerhans was also observed in the site of lobule. 5) The presented findings may also suggest that the duration of administration of ethionine is more important factor than graded doses of ethionine in the production of ethionine is more important factor than graded doses of ethionine in the production of ethionine induced pancreatitis in cats.

Adrenergic Fibers↗
PubMed1978

Development of innervation to the atrial myocardium of the rabbit.

The development of innervation to the atrial myocardium of rabbits from 20th day of gestation to 35 days postnatal was studied ultrastructurally by electron microscopy and by demonstration of catecholamines by histofluorescence. Special attention was directed to the first morphologic appearance of nerve fibers and terminals and the closeness of juxtaposition of terminals with myocardial cells. Adrenergic and cholinergic terminals were identified on the basis of their differential ability to take-up and store the "false adrenergic neurotransmitter" 5-hydroxydopamine. Adrenergic terminals were first encountered at 20 days of gestation whereas cholinergic terminals could not be positively identified until the 24th day of gestation. Throughout development adrenergic terminals were more numerous than cholinergic, about 71% of the terminals encountered being adrenergic. Many terminals approach closely (20-30 nm) to the sarcolemma of the muscle cells of the atrium. In many instances adrenergic and cholinergic fibers travel together in the same nerve bundle and are closely apposed without intervening Schwann-cell cytoplasm. Such a relationship could allow peripheral interaction between these fibers in the myocardium.

Animals↗
PubMed1977

[Mechanism of action of catecholamines on the electrically-stimulated, isolated guinea-pig gallbladder].

Effects of catecholamines on the contraction of isolated guinea-pig gallbladder induced by transmural stimulation (TM) were investigated. Tetrodotoxin and atropine prevented the TM-induced contraction. Atropine, but not tetrodotoxin, blocked the acetylcholine-induced contraction. Furthermore, the TM-induced contraction was sharply reduced during a cold storage for 1 to 4 days and then abolished 4 to 7 days later. Norepinephrine (5 X 10(-6) M) and epinephrine (4.5 X 10(-6) M) did not affect acetylcholine-induced contraction, but reduced the contractile response to TM by about 40% and 60%, respectively. Phentolamine, but not propranolol, abolished the inhibitory effects of norepinephrine and epinephrine on the contraction induced by TM. Isoproterenol and phenylephrine did not significantly modify the TM-induced contraction. These observations suggest that TM-induced contraction is produced by the release of acetylcholine from the ending of postganglionic cholinergic fibers. The possibility that norepinephrine and epinephrine act on the inhibitory alpha-adrenoreceptors in the ending of cholinergic neuron is discussed.

Acetylcholine↗
PubMed1978

[Neural regulation of glucose, sodium and potassium transport in the kidneys].

When the speed of filtration and plasma circulation are constant, the absolute sodium reabsorption is increased in kidney on the side of stimulation of nervous fibers. The stimulating effect of adrenergic nerves on the tubular transport of sodium and potassium is inhibited with guanethidin. The maximum transport of glucose is increased by the activity of cholinergic fibers of vagus nerves.

Animals↗
PubMed1978

Electrophysiological analysis reinnervation of transplants in the anterior chamber of the eye by the autonomic ground plexus of the iris.

Fetal rat hippocampus, cerebellum, and heart were homologously transplanted to the anterior chamber of the eye of adult female recipients. After the grafts were allowed to mature in oculo, ingrowing adrenergic and cholinergic fibers from the iris were activated by changing the illumination of the retina. Electrophysiological recordings from all three types of transplants showed changes similar to those reported for effects of adrenergic and and cholinergic inputs in situ. Pharmacological studies with the transplants indicated that these electrophysiological changes were caused by activation of local muscarinic cholinergic and beta-adrenergic synapses. These data suggest that the intraocular graft is able to induce functional adrenergic and cholinergic inputs from the ground plexus of the iris and support the hypothesis that target organ influences play an important role in synaptogenesis.

Action Potentials↗
PubMed1978

Experimental studies on the ultrastructural localization of acetylcholinesterase in the mediobasal hypothalamus of the rat.

Acetylcholinesterase (AChE) activity has been demonstrated ultrastructurally in neurons of the arcuate nucleus and associated with fibers in the arcuate nucleus neuropil and the median eminence (ME) of the rat. In addition, the effects of neonatal monosodium glutamate (MSG) treatment and Halász deafferentation on the AChE staining and localization have been studied. Neonatal MSG-treatment resulted in loss of the majority of AChE-positive neurons in the arcuate nucleus while leaving neuropil staining intact. Halász deafferentation caused a loss of arcuate neuropil activity while leaving the neuronal staining unaltered. These observations are consistent with previous biochemical results suggesting the existence of a cholinergic tuberoinfundibular system with nerve cells in the arcuate nucleus and terminals in the median eminence. In addition, the deafferentation experiments indicated that extra-hypothalamic cholinergic fibers may innervate the arcuate nucleus. Supporting evidence from other biochemical studies and the curious paucity of histochemical and biochemical AChE activity in the ME are also discussed.

Acetylcholinesterase↗
PubMed1977

Regional distribution of choline acetyltransferase and acetylcholinesterase within the amygdaloid complex and stria terminalis system.

The distribution of "marker" enzymes for cholinergic neurons has been studied in 10 subdivisions of the amygdaloid complex of the rat brain. Choline acetyltransferase activity was measured using a radiochemical method in samples dissected from fresh serial sections. Acetylcholinesterase was studied using a histochemical procedure. Both enzymes had similar patterns of distribution within the amygdaloid complex and were most concentrated in the posterior lateral and basolateral nuclei and in the nucleus of the lateral olfactory tract. These enzymes were much less concentrated in the cortical, medial, central, and basomedial nuclei. Large differences in acetylcholinesterase staining were found within the lateral posterior and the basolateral nuclei and within the pyriform cortex. Biochemical studies showed a parallel distribution of choline acetyltransferase within these nuclei. The results indicate that cholinergic neural elements in the amygdala are concentrated primarily in the basolateral complex and suggest that this region may be innervated by cholinergic fibers traveling in the ventral amygdalo-fugal pathway.

Acetylcholinesterase↗
PubMed1977

Selective induction of tyrosine hydroxylase and dopamine beta-hydroxylase by nerve growth factor: comparison between adrenal medulla and sympathetic ganglia of adult and newborn rats.

Administration of NGF to newborn and adult rats elicits a selective increase in TH and DBH both in sympathetic ganglia and adrenal medulla. This effect does not depend on intact preganglionic cholinergic fibers. The augmented enzyme activity results from enhanced enzyme synthesis since it can be abolished by cycloheximide and NGF has been shown to enhance the incorporation of [3H]leucine into DBH molecules. The responsiveness of the adrenal medulla to NGF is also supported by light and electron microscopic autoradiograms which show that intravenously injected 125I-NGF is accumulated with high selectivity in adrenal chromaffin as compared to adjacent adrenal cortical cells. In spite of the many similarities between the response of the adrenergic neurons and adrenal chromaffin cells to NGF, there are also two distinct differences. (a) In newborn rats the ratio between the TH increase effected by a single and 10 subsequent daily injections of NGF is 1:2 in the adrenal medulla and 1:7 in the superior cervical ganglia. (b) If adrenal medullae are transferred to organ culture after intravenous injection of NGF, maximal TH response is initiated 60-90 min after NGF administration. In superior cervical ganglia only a half-maximal response is initiated at that time. After a stationary phase a second increase starts after about 6 h to reach the maximum after 12 h. The biphasic time course of the initiation of TH induction by NGF in sympathetic ganglia is in agreement with the time course of 125I-NGF accumulation after intravenous injection27 reflecting the moiety of NGF reaching the cell bodies of the adrenergic neurons directly by the blood stream (initial accumulation) and by retrograde axonal transport (second phase).

Adrenal Medulla↗
PubMed1977

Regulation of the growth and development of sympathetic neurons in vivo.

The superior cervical ganglion (SCG) in the neonatal mouse and rat has been employed as a model system to study the regulation of ontogeny of presynaptic cholinergic nerves and postsynaptic adrenergic neurons. During postnatal development presynaptic choline acetyltransferase (ChAc) activity increases 30- to 40-fold, whereas postsynaptic tyrosine hydroxylase (T-OH) activity rises 6- to 8-fold. Transection of the presynaptic cholinergic nerves innervating the SCG prevents the normal development of T-OH activity and the normal accumulation of T-OH enzyme molecules in each postsynaptic neuron. The trans-synaptic regulation of T-OH development is apparently mediated by acetylcholine and postsynaptic depolarization, since pharmacologic ganglionic blockade also prevents normal maturation. Ganglion decentralization also prevents the normal maturation of adrenergic nerve terminals, and the development of end-organ innervation by SCG. Consequently, trans-synaptic factors regulate the ontogeny of adrenergic terminals as well as perikarya. Moreover, normal efferent as well as afferent connections are apparently required for sympathetic development, since removal of salivary glands and orbital contents, target organs of the SCG, in neonates also prevents T-OH development in the ganglia. The postsynaptic neuron contributes to the development of presynaptic cholinergic fibers in SCG. Selective destruction of adrenergic neurons in neonatal mice with either 6-hydroxydopamine or antiserum to nerve growth factor prevents the normal maturation of ChAc activity in presynaptic terminals of SCG. Thus, presynaptic and postsynaptic cells appear to exert reciprocal regulatory influences during ontogeny.

Age Factors↗
PubMed1979

Fluorescence microscopic and enzyme histochemical studies of the innervation of the human spleen.

The innervation of the human spleen was investigated by the fluorescence method for adrenergic nerve fibers (52 cases) and the enzyme histochemical method for cholinergic nerve fibers (27 cases). The spleens examined were removed by laparotomy chiefly for gastric cancer. Adrenergic nerve fibers were demonstrated at the medioadventitial junction and the media in the trabecular arteries, whereas they occurred at the medioadventitial junction in the central and penicillar arteries. They were not found in the trabecular and pulp veins and venules, sheathed capillaries, avascular trabeculae, white and red pulp, and capsule. Nerves containing only a few adrenergic fibers and nerves without adrenergic fibers occurred close to the trabecular arteries. It was also demonstrated that nerves close to the trabecular arteries contain cholinergic fibers. The present study first verifies histochemically that the human spleen is innervated doubly by adrenergic and cholinergic nerve fibers.

Adrenergic Fibers↗
PubMed1979

[Histochemical and ultrastructural studies of the innervation of the lymph-vessel and blood-vessel wall. II. Cholinergic innervation].

Using the Acetylcholinesterase (AChE) tecnique applied to light and electron microscopy, was observed that the lymph vascular wall shows very few and inconstant AChE-positive fibers. The cholinergic fibers run prevalently longitudinal in the perivascular connective tissue, only brief segments show a loose network. The results are discussed and compared with blood vessels innervation.

Animals↗