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Biomedical subjects

D L Felten

Publications and source records attributed to D L Felten.

At least 109 records · Page 6Linked to original sources
PubMed1984

Sympathetic innervation of lymph nodes in mice.

Noradrenergic innervation of popliteal and mesenteric lymph nodes in mice was examined with fluorescence histochemistry. Dense varicose plexuses entered the nodes with the vasculature in the hilar region and continued with the vasculature into the medullary region. Fine, delicate varicosities and small vascular plexuses continued into the cortical and paracortical regions surrounding the germinal centers; some varicosities ended among lymphocytes. A subcapsular plexus contributed fibers into the cortical and paracortical regions. Chemical measurements revealed the presence of norepinephrine in lymph nodes that was depletable with 6-hydroxydopamine. Depletion of norepinephrine from lymph nodes with this agent resulted in a diminished primary immune response in draining lymph nodes following subcutaneous injection of an antigen in two mouse strains, but had no effect in two other strains. These findings suggest that noradrenergic fibers innervate both the vasculature and parenchymal regions of lymph nodes, and may participate in the modulation of immune responses in these organs.

Adrenergic Fibers↗
PubMed1984

Catecholamine innervation of cervical dendrite bundles: possible phrenic nucleus innervation.

The catecholaminergic innervation of three recently described dendrite bundles (midline, central and lateral) in the cervical spinal cord of the adult Long-Evans hooded rat [41] was examined using Golgi impregnation, fluorescence histochemistry for catecholamines, and cholinesterase histochemistry. The midline and lateral bundles were similar in appearance to those described by the Scheibel and Scheibel [50,51], while the central bundle, present in the region of the phrenic nucleus, has not been described previously. Analysis of Golgi-Cox impregnated horizontal sections demonstrated the presence of fine varicose fibers within all three bundles. These profiles entered the bundles at right angles, either singly or within small transverse dendritic subunits, then turned in a rostral or caudal direction, and coursed adjacent to dendrites of motoneurons in the bundles. Catecholamine histofluorescence in horizontal sections revealed abundant varicosities within all three bundles, similar in size and appearance to the varicose fibers seen in Golgi-Cox impregnated sections. Catecholamine fibers entered the dendrite bundles at right angles then turned rostrally or caudally and coursed horizontally within the bundles. Varicose fluorescent profiles formed pericellular rings around the motoneurons and linear profiles adjacent to the dendrites, sometimes outlining the entire proximal portion of primary dendrites. Catecholamine fibers entered the dendrite bundles at right angles then turned rostrally or caudally to course adjacent to the dendrites within the bundles. Cholinesterase histochemistry in alternate sections revealed staining of motoneurons and their dendrites, and confirmed the location of the catecholamine varicosities within the motoneuron dendrite bundles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

MPTP alters central catecholamine neurons in addition to the nigrostriatal system.

The present studies were undertaken to determine if MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) treatment in mice alters catecholamine or serotonin systems of the brain in addition to reported effects on the dopaminergic nigrostriatal system. Male Swiss-Webster mice were injected with 30 mg/kg MPTP daily for three days. Treated and control animals were sacrificed 10 and 24 days after the last injection, and brains were prepared for serotonin immunocytochemistry and catecholamine histofluorescence. MPTP treatment resulted in a reduced number of neurons and a reduced intensity of the fluorescence in the remaining cell bodies of substantia nigra pars compacta. A reduced presence of catecholamine varicosities in the medullary raphe nuclei and the ventromedial reticular formation of the medulla was observed. Immunocytochemical studies revealed no alteration in the number of serotonin positive cell bodies in the dorsal and median raphe nuclei. We suggest that MPTP treatment selectively alters some non-nigrostriatal catecholamine systems of the brain stem in addition to its toxic effects on the dopaminergic nigrostriatal system, while leaving other non-nigrostriatal catecholamine systems intact.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1983

Noradrenergic innervation of the penis in control and streptozotocin-diabetic rats: evidence of autonomic neuropathy.

The noradrenergic sympathetic innervation of the penis of control and 4-month streptozotocin-diabetic rats was examined with the glyoxylic acid histofluorescence method. Noradrenergic varicosities were found in the corpora cavernosa in a dense subtunical plexus and in the perisinusoidal and trabecular regions of the erectile tissue, in the corpus spongiosum in perisinusoidal tissue, around large arteries and veins, and around small tortuous arterioles and small draining veins of the corpora cavernosa and spongiosum. Noradrenergic varicosities were diminished in number and fluorescent intensity in all regions of the penis of diabetic rats compared with controls. The subtunical plexus was absent, perisinusoidal and trabecular varicosities were sparse, and only occasional intermittent, discontinuous, dull fluorescent fibers or plexuses were found around the vessels. Quantitation with high-performance liquid chromatography revealed a significant reduction of norepinephrine in the penis of diabetic rats compared with controls. The present study suggests that long-term streptozotocin diabetes in the rat is accompanied by sympathetic autonomic neuropathy of the penis that seems to parallel changes in the noradrenergic content of penile corpora of men with diabetes and erectile impotence. The streptozotocin-diabetic rat merits further study to explore the relationship between noradrenergic innervation of the penis and erectile tissue.

Animals↗
PubMed1983

Specific binding of the muscarinic antagonist [3H]quinuclidinyl benzilate is not associated with preganglionic motor neurons in the dorsal motor nucleus of the vagus.

The present study evaluates the binding of [3H]quinuclidinyl benzilate, [3H]QNB, as a measure of cholinergic muscarinic binding in six areas of the rat medulla oblongata associated with the cranial nerves. In an experimental group, the right vagus nerve was severed in the neck in order to determine whether the specific muscarinic binding sites might be located on cells that contribute efferent fibers to the vagus nerve. The level of activity of choline acetyltransferase (ChAT) also was determined in the same six areas. Additional experiments utilizing the retrograde transport of toxic ricin, a 60,000 dalton agglutinin that acts as a potent ribosomal toxin, was carried out to further evaluate localization of specific muscarinic binding in the DMN after destruction of the preganglionic efferent cells. These results support the conclusion that specific binding of the muscarinic antagonist [3H]QNB observed in the DMN of the vagus of the rat is not associated with the large cells that contribute efferent fibers into the vagus nerve. We suggest that the specific cholinergic muscarinic binding is located on interneuronal cell surfaces, on afferent terminals of local circuit neurons, or on afferent terminals of long projection axons which arise from neurons in the brainstem, hypothalamus, or forebrain.

Acetylcholinesterase↗
PubMed1983

Degenerative neuropathy in insulin-treated diabetic rats.

Peripheral neuropathic alterations associated with diabetes and its treatment with insulin were studied in alloxan-induced diabetic rats. Treatment regimens included daily injections of Protamine Zinc Insulin (PZ), daily injections of Ultralente Insulin and subcutaneously implanted osmotic minipump delivered insulin. Non-diabetic and untreated diabetic groups served as controls. Two separate but similar studies were run, one lasting 4 weeks and the other 8 weeks. Conduction velocities performed on both sensory and motor nerves revealed no statistically significant differences among groups. Anatomical analysis of teased fibers from tibial nerves showed a significant number of fibers with ovoids, consistent with Wallerian-type axonal degeneration, only in the treated diabetic groups. Degeneration was especially severe in the PZI-treated group. Metabolic studies were performed using incorporation of radioactive isotopes ([3H]fucose, [14C]leucine) into myelin proteins of sciatic nerves. The ratio of [3H]fucose/[14C]leucine for the PZI-treated group was significantly decreased when compared to the control groups in both the 4 and 8 week study whereas the minipump-treated group showed no statistically significant difference from the control group in either study. Similar decreases in this ratio have been seen in conditions of peripheral nerve degeneration. It is concluded that daily injections of PZI insulin result in significant nerve degeneration in the alloxan diabetic rat, while continuous levels of insulin delivered by osmotic minipumps result in less degeneration.

Animals↗
PubMed1983

Neuropathic changes associated with insulin treatment of diabetic rats: electron microscopic and morphometric analysis.

Tibial nerves from control, untreated alloxan diabetic, and 4-week insulin treated alloxan diabetic rats were examined with light microscopy and computerized morphometric analysis of axons. Teased fiber preparations and electron microscopy were utilized to evaluate nerve degeneration. The insulin treatment regimens included daily injections of protamine zinc insulin (PZI), daily injections of ultralente insulin, and continuously delivered insulin through osmotic minipumps. Evaluation of axon:myelin ratios, teased fiber profiles, and electron microscopic cross sections of nerves demonstrated different degrees of neuropathic changes within the treated groups. The control group and untreated diabetic group showed little or no degeneration, while all insulin-treated groups showed evidence of Wallerian degeneration. Among these insulin treated groups, the PZI-treated group showed the greatest number of degenerating profiles while the minipump group showed the least. These data suggest that insulin treatment of alloxan diabetes results in axonal degeneration which closely resembles findings in human diabetic neuropathies. The substantially diminished number of degenerating axons seen in the osmotic minipump insulin-treated rats suggests that continuous delivery of insulin may decrease the neuropathic changes seen with single injection insulin therapy. Since virtually all insulin-dependent diabetic patients receive daily administration of insulin, the possibility that peripheral neuropathies may in part result from the insulin treatment requires more extensive investigation in a variety of animal models to separate the neuropathic effects of diabetes from the neuropathic effects of insulin therapy.

Animals↗
PubMed1983

Distribution of glycine, GABA, aspartate and glutamate in the rat spinal cord.

Glycine, GABA, aspartate and glutamate are putative neurotransmitters in the mammalian spinal cord. The distribution of these amino acids was determined in the rat spinal cord. Transversely, the highest levels of glycine, aspartate and glutamate were in the intermediate and ventral gray; whereas, the highest levels of GABA were in the dorsal gray. Longitudinally, the highest levels of GABA and aspartate were in the thoracic and lumbar segments; whereas, the highest levels of glycine and glutamate were in the cervical and thoracic segments, respectively. In general, the distribution of these amino acids is similar to that reported for the cat, dog and human.

Animals↗
PubMed1982

Excretion of urinary volatile metabolites in response to alloxan induced diabetes of short duration in rats.

Alterations in urine volatile metabolites due to the induction of alloxan diabetes in the rat were examined by capillary gas chromatography and gas chromatography--mass spectrometry for the five days immediately following the onset of chronic hyperglycemia. Elevations of a number of metabolites were observed including several short chain ketones, acetophenone, 2-acetylfuran and indole. The value of urine volatile metabolic profiles as characteristic indicators of the diabetic condition is demonstrated through profiles obtained from a diabetic animal which spontaneously reverted to normal.

Animals↗
PubMed1982

Structural relationships between the endogenous volatile urinary metabolites of experimentally diabetic rats and certain neurotoxins (l).

High resolution glass capillary gas chromatography and GC/MS were utilized to examine qualitative and quantitative variations from normal of urinary volatile metabolites of long-term alloxan and streptozotocin diabetic rats. Volatile metabolites were structurally compared with known neurotoxins to examine any possible relationship between these metabolites and the development of the diabetic polyneuropathy.

Animals↗
PubMed1982

Distribution and uptake of glycine, glutamate and gamma-aminobutyric acid in the vagal nuclei and eight other regions of the rat medulla oblongata.

In order to study the central neurochemical control of the vagus nerve, the contents of glycine, GABA, glutamate and five other amino acids have been measured in ten anatomically distinct regions of the rat medulla oblongata. Additionally, the high affinity uptake of glycine, GABA, glutamate, and leucine were measured in the same ten medullary regions. The data support published evidence for glutamatergic and GABAergic transmission in the nucleus of the tractus solitarius (NTS), and glycinergic inhibition in the hypoglossal nucleus. The data also lead to the suggestion that GABA and glutamate may be taken up into glial cells which exist along fiber tracts.

Afferent Pathways↗
PubMed1982

Evidence for a neurotropic role of noradrenaline neurons in the postnatal development of rat cerebral cortex.

The effects of neonatal administration of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA; 1-4 doses of 100 mg/kg body weight s.c.) on the postnatal development of pyramidal neurons in several cortical regions of the rat was studied using a Golgi-Cox neuronal impregnation technique. Rats were sacrificed in the adult stage (eight weeks) and the following regions were studied: anterior frontal cortex, posterior frontal cortex (including motor cortex), anterior parietal cortex (including sensory cortex), posterior parieto-occipital cortex and cingulate cortex. Significant alterations were seen in animals which received four doses of 6-OHDA. These alterations can be summarized as follows: (1) a decreased length and branching of basolateral dendrites of pyramidal cells, with loss of dendritic spines, which were found in both the internal pyrimidal layer (layer V) and the external pyramidal layer (layer III), most abundantly in the frontal cortex and cingulate cortex; (2) an increased number of pyramidal cells of layer V with premature apical dendritic termination in layer III rather than the usual termination in layers I and II. This was most abundant in the cingulate cortex; (3) occasional disorientation of pyramidal cell apical dendrites away from the normal vertical plane by 15 or more degrees, seen in frontal, parietal and cingulate cortex; (4) an increased number of pyramidal cells with rounded somatic contours, found in frontal, anterior parietal and cingulate cortex. These phenomena were occasionally seen in normal cortex, but were significantly increased in their occurrence after four doses of 6-OHDA. Such alterations were not significant in rats treated with one or three doses of 6-OHDA. The extent and severity of morphological alterations correlate with reductions in endogenous noradrenaline (NA) in cerebral cortex, which was found to average 50% of control levels after one dose of 6-OHDA, and 80% reduction after three doses, and a 97-98% reduction after four doses, suggesting that the NA denervation must be almost complete to result in readily detectable significant morphological changes in the development of cortical pyramidal cells. No consistent changes in endogenous dopamine (DA) levels were observed, except for an increase in the cingulate cortex. The anatomical alterations in pyramidal cells described in the present study suggest that NA neurons which project into the cerebral cortex have a neurotrophic role in the postnatal development of cortex.

Aging↗
PubMed1982

Ultrastructural axonal pathology in experimentally diabetic and aging control rats.

Electron microscopic examination of tibial nerves from streptozotocin-diabetic, alloxan-diabetic and age-matched control rats was undertaken at two weeks and two, four, eight, and twelve months following the induction of diabetes. Many myelinated axons of both diabetic and control rats contained glycogen-like granules, axon-Schwann cell networks and fingerlike intrusions of myelin. These axonal changes were observed more frequently with advancing age and duration of diabetes, suggesting that they are related to aging or repeated injury. A larger proportion of diabetic axons than control axons were affected at early time periods, but by eight and twelve months the control axons were as frequently (or more frequently) involved as diabetic axons. Thus, experimental diabetes may confer upon peripheral myelinated axons an increased susceptability to aging or repeated injury. Specific morphologic abnormalities in peripheral myelinated axons associated uniquely with streptozotocin or alloxan diabetes in the rat were not noted.

Aging↗
PubMed1982

Effects of streptozotocin diabetes on the noradrenergic innervation of the rat heart: a longitudinal histofluorescence and neurochemical study.

The effects of the age of induction and total duration of streptozotocin diabetes on the sympathetic noradrenergic innervation of the rat heart was examined with glyoxylic acid induced histofluorescence to demonstrate the distribution of noradrenergic fibers within the heart, and with high performance liquid chromatography with electrochemical detection to measure tissue levels of the neurotransmitter norepinephrine. Diabetes was induced in male Sprague-Dawley rats at 1, 2, and 4 months of age. Within each of these groups, diabetic rats survived for periods of 1, 2, and 4 months. Additional groups of diabetic rats survived to a chronological age of 8 months. Norepinephrine levels in the hearts of diabetic rats were increased over those of control rats in all groups at 1 month duration of diabetes. Ventricles were generally affected to a greater extent than atria. At 2 months duration of diabetes, ventricular levels remained elevated while atrial norepinephrine levels were at or below control levels. At 4 months duration of diabetes, and in all groups at 8 months of age, the norepinephrine levels were at or below control levels, except in the ventricles of rats induced at 4 months of age, which remained elevated. Histofluorescence studies demonstrated the presence of axon bundles and varicose noradrenergic profiles in the diabetic rat hearts, distributed in a pattern similar to that seen in controls. However, at 1 month duration of diabetes in all groups, the density of noradrenergic varicosities in diabetic rat hearts appeared increased with abundant branched profiles. These results are surprising, since studies on genetic models of diabetes have suggested decreased norepinephrine levels in the heart. The present study suggests that during the early phases of streptozotocin induced diabetes, noradrenergic nerves are still intact and may be susceptible to pharmacologic manipulation. The later fall of norepinephrine levels back to or below control levels may indicate actual neuronal damage, suggesting that early intervention may be necessary to protect these nerves from degeneration. This issue is potentially important in view of the reported toxic effects of high NE levels on the heart, and the high incidence of death from myocardial infarct in diabetic humans with autonomic neuropathy.

Animals↗