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Radioisotope CSF flow studies in leptomeningeal metastases.

BACKGROUND: Leptomeningeal metastases is a frequent neuro-oncologic complication in patients with cancer. OBJECTIVE: Radionuclide CSF flow studies provide a unique method of evaluating CSF compartments in patients with leptomeningeal metastases. METHODS: Radionuclide CSF flow studies are performed by injecting (111)Indium-DTPA into either the ventricular or lumbar CSF compartment. (111)Indium-DTPA is entrained by CSF and flows through CSF compartments based on normal CSF physiology. RESULTS: Normal times to appearance of (111)Indium-DTPA following intraventricular injection in either adults or children are as follows: ventricles (median 1 minute); cisterna magna/basal cisterns (5); cervical (15); thoracic (20); and lumbar (30) spinal subarachnoid spaces; and sylvian cisterns (50). Normal times to appearance of (111)Indium-DTPA following intralumbar injection are as follows: lumbar (1); thoracic (22.5); cervical (32.5) spinal subarachnoid spaces; cisterna magna/basal cisterns (37.5); sylvian cisterns (65); ventricles (1,440); and cerebral convexities (1,440). In 30 consecutive patients, 47% of patients had documented compartmentalization of CSF by (111)Indium-DTPA CSF flow studies. 13% had base of brain obstruction of whom 50% responded with re-establishment of normal CSF flow and 33% had spinal subarachnoid space block of whom 40% following therapy had re-establishment of normal CSF flow. In 61 consecutive patients, 33% of patients had abnormal spinal CSF flow studies which better demonstrated interruption of CSF flow when compared to CT myelography and spine MR. In 40 patients, all with CSF block, 20 of whom responded to therapy with re-establishment of normal CSF flow as compared to 20 with refractory CSF block, significant differences were seen in median survival and cause of death favoring patients with normal or restored CSF flow. CONCLUSIONS: Radioisotope CSF flow studies in patients with leptomeningeal metastasis appear to have two practical uses. First, radioisotope CSF flow studies by documenting normal CSF flow predict for homogeneous distribution of intra-CSF chemotherapy. Secondly, in patients with CSF flow obstruction refractory to site of obstruction therapy, limited survival, rapid leptomeningeal disease progression and death due to progressive CNS disease is predicted.

Adult↗
PubMed1981

The role of dopaminergic and serotonergic mechanisms in the development of swimming ability of young rats.

Neonatal swimming behavior was studied after a single subcutaneous injection of L-dopa methyl ester (50 mg/kg; 200 mg/kg) apomorphine (0.1 mg/kg; 1.0 mg/kg), DL-amphetamine (0.5 mg/kg; 10 mg/kg), haloperidol (0.5 mg/kg; 1.0 mg/kg), L-tryptophan (50 mg/kg; 100 mg/kg), methysergide (1.0 mg/kg; 5.0 mg/kg) as well as intraventricular injection of 100 microgram 6-OHDA. 1-, 3-, 5- and 7-day-old rats were placed into a temperature-controlled aquarium (37 degrees C) and the pattern of motor coordination, latency time to swimming (LTS) and the number of foreleg strokes for 10 s (FS) were measured. When compared to the physiological saline-injected controls, rats that received L-dopa showed a striking increase of FS at all ages but the most striking improvement of motor coordination was found in newborn rats. On day 1 both doses of DL-amphetamine induced increases in FS and improvement of motor coordination, whereas apomorphine failed to show any effect at this age. On days 3, 5 and 7 low doses of DL-amphetamine and apomorphine increased the FS. However, high doses resulted in a decrement in swimming performance. Haloperidol impaired swimming on day 1 but produced a significant increase of FS on days 5 and 7. Neonatal injection of 6-OHDA delayed development of motor coordination, reduced FS and increased LTS. On days 3, 5 and 7 high doses of L-tryptophan elicited an increase of FS, while high doses of methysergide caused significant impairment of performance. It is suggested that the brain rapidly converts the administered L-dopa to dopamine during the first week of life and there appears to be a strong dependent relationship between the pattern of motor coordination and the amount of available dopamine in the developing brain.

Age Factors↗
PubMed1979

Biochemical and pharmacological properties of a neurotoxic protein isolated from the blood serum of heavily burned patients.

Blood serum of heavily burned patients contains neurotoxic substances which are not present in normal control sera. In the present paper, we describe the purification by gel filtration and ultracentrifugation of such a neurotoxic factor. The purified factor appeared to be a high molecular weight (2 to 3.10(6) daltons) lipoprotein. This factor was present in all the sera of patients with more than 35 per cent of the body surface burned. When injected into rabbits the lipoprotein caused a flattening of the EEG tracing, then trembling and convulsions with bursts of spikes on the EEG. The activity of this neurotoxic substance was enhanced when the permeability of the blood-brain barrier was increased by previous intraventricular injection of collagenase. The presence of such a neurotoxic factor in the blood serum of burned patients, together with the increased serum collagenase activity they exhibit may explain the neurotoxic symptoms observed in them.

Animals↗
PubMed1983

The cytology of dopaminergic and nondopaminergic neurons in the substantia nigra and ventral tegmental area of the rat: a light- and electron-microscopic study.

The results of this study support the conclusion that dopaminergic cells can be distinguished from non-dopaminergic cells, at both the light- and electron-microscopic level, by cytological features, and particularly by the pattern of Nissl substance. In both the substantia nigra and the ventral tegmental area, two main categories of cell type can be identified in Nissl preparations: (1) dark-staining, basophilic cells with large masses of Nissl substance and (2) light-staining cells with more translucent cytoplasm. The following findings provide evidence that the basophilic cells of both substantia nigra and ventral tegmental area are the dopaminergic cells. (1) There is a good correlation between the topographic distribution of basophilic cells and that of dopaminergic cells mapped by both histofluorescence and immunohistochemical methods. (2) After unilateral destruction of the dopaminergic neurons by intracerebral injection of 6-hydroxydopamine in the dopaminergic pathway, the basophilic cells in the substantia nigra and ventral tegmental area disappeared on the lesion side, while the lighter-staining cells appeared unaffected. (3) In normal rats, and in rats with unilateral 6-hydroxydopamine lesions, intraventricular injection of [3H]norepinephrine was used for specific labeling of dopaminergic neurons. In autoradiograms of semithin sections, such labeling was observed only in dark-staining and not in light-staining cells, and in cases of unilateral 6-hydroxydopamine lesion was totally absent on the lesion side. Electron-microscopy showed much of the cytoplasm of the basophilic dopaminergic cells to be densely filled with free ribosomes associated with large, well organized complexes of rough endoplasmic reticulum. The cytoplasm of the light, non-dopaminergic cells contains only sparse free ribosomes and small, widely spaced aggregates of rough endoplasmic reticulum. Both cell types occur in a similar variety of size and shape.

Animals↗
PubMed1983

Involvement of hypothalamic luteinizing hormone-releasing hormone in the regulation of the estrous follicle-stimulating hormone surge in the female golden hamster.

Hypothalami collected from female hamsters during proestrus and estrus were assessed for LHRH content by bioassay and RIA. During estrus, as serum FSH levels rose, a depletion of hypothalamic LHRH was observed. The pattern of hypothalamic LHRH accumulation and depletion during proestrus and estrus as well as changes in serum and pituitary FSH concentrations were altered as a result of phenobarbital administration at 1200 h on proestrus. The effects of phenobarbital upon hypothalamic LHRH content as well as serum and pituitary FSH concentrations were overridden by the injection of purified FSH into the third ventricle of the hypothalamus at 1500 h during proestrus. The results of the present study suggest that the estrous FSH surge in hamsters is mediated, at least in part, by a concurrent discharge of hypothalamic LHRH. Further, intraventricular injection of FSH elicits a selective increase in serum FSH during estrus by influencing this LHRH-dependent system.

Animals↗
PubMed1976

The effects of neurally active amino acids on prolactin secretion.

Several neurally active amino acids were injected into the third ventricle of anesthetized male rats. Two or eight mumole of GABA produced significant increases in the plasma concentrations of prolactin (PRL), indicating increased PRL release from the pituitary. Two mumole of glycine was also effective in elevating PRL levels. The intraventricular injection of the lowest dose of GABA (1.0 mumole), glutamate (0.4 or 2.3 mumole), lysine (0.2 or 2.0 mumole), or 0.9% NaCl did not alter PRL levels significantly. Plasma PRL concentrations did not increase following the injection of GABA or glycine directly into the anterior pituitary gland. The results suggest that GABA and glycine may play a role in the neural regulation of PRL secretion.

Amino Acids↗
PubMed1996

Effects of intraventricular transplantation of NGF-secreting cells on cholinergic basal forebrain neurons after partial immunolesion.

The aim of the present study was to examine the effects of nerve growth factor on brain cholinergic function after a partial immunolesion to the rat cholinergic basal forebrain neurons (CBFNs) by 192 IgG-saporin. Two weeks after intraventricular injections of 1.3 micrograms of 192 IgG-saporin, about 50% of CBFNs were lost which was associated with 40-60% reductions of choline acetyltransferase (ChAT) and high-affinity choline uptake (HACU) activities throughout the basal forebrain cholinergic system. Two groups of lesioned animals received intraventricular transplantations of mouse 3T3 fibroblasts retrovirally transfected with either the rat NGF gene (3T3NGF+) or the retrovirus alone (3T3NGF-) and were sacrificed eight weeks later. In vivo production of NGF by 3T3NGF+ cells was confirmed by NGF immunohistochemistry on the grafts and NGF immunoassay on cerebrospinal fluid (CSF) samples. Both ChAT and HACU activities returned to normal control levels in the basal forebrain and cortex after 3T3NGF+ transplants, whereas no recovery was observed in 3T3NGF- transplanted animals. There was a 25% increase in the size of remaining CBFNs and an increased staining intensity for NGF immunoreactivity in these cells after NGF treatments. Acetylcholinesterase (AChE) histochemistry revealed that the optical density of AChE-positive fibers in the cerebral cortex and hippocampus were reduced by about 60% in immunolesioned rats which were completely restored by 3T3NGF+ grafts. In addition, decreases in growth-associated protein (GAP)-43 immunoreactivity after immunolesion and increases in synaptophysin immunoreactivity after 3T3NGF+ grafts were observed in the hippocampus. Our results further confirm the notion that transfected NGF-secreting cells are useful in long-term in vivo NGF treatment and NGF can upregulate CBFN function. They also highly suggest that NGF induces terminal sprouting from remaining CBFNs.

3T3 Cells↗
PubMed1994

Magnesium is more efficacious than phenytoin in reducing N-methyl-D-aspartate seizures in rats.

OBJECTIVE: Although magnesium sulfate is one of the most commonly used agents for seizure prophylaxis in preeclampsia, its efficacy relative to other anticonvulsants is incompletely investigated. The underlying mechanisms of eclamptic seizures are unknown, and there is currently no universally accepted animal model for eclampsia. However, one commonly used method for studying the relative efficacy of antiepileptic drugs is through their effect on N-methyl-D-aspartate-induced seizures. Our aim was to compare the anticonvulsant effects of phenytoin and magnesium sulfate in an N-methyl-D-aspartate-induced seizure model. STUDY DESIGN: Twenty-one female rats were each stereotaxically implanted with a chronic indwelling bipolar recording electrode in the hippocampus and an injection cannula in the lateral cerebral ventricle. After 7 days animals were randomly given 90 mg/kg magnesium sulfate (n = 7), 50 mg/kg phenytoin, or saline solution (n = 7) intravenously. Fifteen minutes after the infusions animals were given 20 micrograms/microliters N-methyl-D-aspartate by direct intraventricular injection, and seizure activity was assessed for 20 minutes thereafter. All data were analyzed with the Mann-Whitney test. RESULTS: When compared with saline solution controls, total duration of seizure activity in animals treated with magnesium sulfate was significantly decreased (p < 0.05) and time to onset of seizure activity was significantly increased (p < 0.05). However, rats that received phenytoin did not show significant changes in these parameters. The post-N-methyl-D-aspartate seizure mortality rate was 50% in the saline solution controls and 29% in the phenytoin group, whereas none of the rats that received magnesium sulfate died. CONCLUSION: These results suggest that magnesium sulfate is a significantly more effective prophylactic agent than phenytoin for N-methyl-D-aspartate-induced seizures.

Animals↗
PubMed1987

Capsaicin-induced corneal lesions in mice and the effects of chemical sympathectomy.

Effects of chemical sympathectomy on corneal changes induced in mice by a s.c. injection of capsaicin were investigated. Pretreatment with a s.c. injection of 6-hydroxydopamine (6-OHDA) on the 1st and 2nd postnatal day or on the 14th and 15th postnatal day led to a marked suppression of the capsaicin-induced corneal lesions. This suppressive effect also was evident in case of administration after capsaicin treatment. Intraventricular injection of 6-OHDA had a slight, transient effect. DSP4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], another potent substance used for sympathetic denervation, had a suppressive effect similar to that of 6-OHDA. The concentration of capsaicin in tissues of the head was unaltered with 6-OHDA. The content of substance P (SP) in the ocular anterior segments was decreased, dose-dependently, with capsaicin administration. Neonatal administration of 6-OHDA decreased the rate of capsaicin-induced reduction of SP. However, this effect of 6-OHDA was too slight to explain the suppression of the corneal lesions, as the intensity score of lesions with a large dose of capsaicin after 6-OHDA was lower than that with a small dose of capsaicin without 6-OHDA, whereas SP content in the former was still much lower than that in the latter. On the other hand, the content of norepinephrine in the ocular tissues was decreased in the presence of 6-OHDA but not capsaicin. These results suggest that the corneal changes induced by capsaicin are largely inhibited by a decreased activity in the peripheral sympathetic system.

Animals↗
PubMed1982

Microinjection of arginine8-vasopressin antiserum into the dorsal hippocampus attenuates passive avoidance behavior in rats.

Antiserum to arginine8-vasopressin was microinjected bilaterally into the dentate gyrus of the dorsal hippocampus and the effect of passive avoidance behavior was studied. After the single learning trial of a passive avoidance response, immediate bilateral injection of 1 microliter antiserum (diluted to 1/50) attenuated passive avoidance responding 24 hr later. In immunocytochemical control studies with injection of undiluted antiserum into the dentate gyrus a spreading was observed towards the ventral hippocampus and the dorsal septum. Additionally, administration into the lateral ventricle of 2 microliters of 1/50 dilution of the antiserum did not affect the behavior. For an attenuation of passive avoidance behavior via intraventricular injection, 2 microliters of a 1/10 dilution of anti-AVP was required. These data suggest that endogenous vasopressin in the septo-hippocampal system might be involved in memory processes.

Animals↗
PubMed1981

Comparison of acute effects of dynorphin and beta-endorphin on prolactin release in the rat.

The ability of dynorphin and beta h-endorphin (beta h-EP) to stimulate prolactin (PRL) release in male rats was examined. Rats were injected intraventricularly with either 1 or 10 microgram dynorphin, 1 or 10 microgram beta h-EP, 10 microgram dynorphin together with 20 microgram naloxone (NAL), or an equivalent volume (13 microliter) of saline. Dynorphin caused a dose-dependent release of PRL which was significant 10 min after injection but not at later sampling times. beta h-EP also increased serum PRL levels and maintained elevated PRL levels for at least 60 min. NAL, a specific opiate antagonist, completely blocked dynorphin-induced PRL release. These results indicate that dynorphin is a potent stimulator of PRL release, but its stimulatory activity is transient relative to the activity exhibited by beta h-EP. Furthermore, dynorphin's action is specific since NAL completely blocked dynorphin induced PRL release.

Animals↗
PubMed1983

Human growth hormone and somatomedin C suppress the spontaneous release of growth hormone in unanesthetized rats.

To investigate the feedback control of GH secretion, we examined the effects of human GH (hGH) and somatomedin C (SmC) on spontaneous GH secretory surges in unanesthetized, freely moving rats. Under pentobarbital anesthesia a right atrial catheter and an intracerebroventricular cannula were placed 7-10 days before the experimentation. For iv studies, hGH (0.3 U/ml.h) was infused for 6 h after an iv loading dose (0.3 U) at the beginning of the experiments. For intraventricular injections, hGH (0.1 U/10 microliter) or SmC (500 ng/10 microliter) were injected into the lateral ventricle 2 h before the experiments. The equivalent dose of crystalline BSA diluted in the same vehicle solutions was administered to the same rat as a control on a separate day. Venous blood samples were collected every 20 min for 6 h. Intravenous and intraventricular administration of crystalline BSA did not affect the typical rat GH (rGH) surges which appeared about every 3 h and reached peak values of more than 300 ng/ml. The iv infusion of hGH significantly inhibited the amplitude of rGH surges compared to controls (planimetric areas under the secretory profile 752 +/- 172 vs. 1921 +/- 183, P less than 0.01, n = 6). rGH secretion was similarly inhibited by intraventricular hGH (701 +/- 127 vs. 2208 + 225, P less than 0.01, n = 6) and by intraventricular SmC (537 +/- 70 vs. 1503 +/- 114, P less than 0.01, n = 6). These findings suggest that both GH and SmC are active in the feedback regulation of rGH secretion.

Animals↗
PubMed1975

Central site of the hypertensive action of bradykinin.

The intraventricular injection of 1 mug of bradykinin (BK) in rats anesthetized with urethane (1.5 g/kg i.p.) caused an increase in mean arterial blood pressure with little or no change in pulse pressure or heart rate. A similar hypertensive response followed the local administration of 0.5 mug of BK at the pars ventralis of the lateral septal area, whereas local application at other subcortical regions, known to be involved in cardiovascular regulation, caused no effect. Injections of 0.5 or 1 mug of synthetic substance P or 1 mug of 9-desarginine-bradykinin at the pars ventralis of the lateral septal area caused no change in blood pressure. In addition, bilateral electrolytical lesions placed in the lateral septal area either markedly reduced or completely blocked the pressor response to intraventricular BK. These results suggest that the pars ventralis of the lateral septal area is involved in the pressor action of BK in the central nervous system. They also indicate that this brain region responds fairly specifically to BK and that local vascular changes are unlikely to be involved in the mediation of the central action of BK.

Animals↗
PubMed1975

Demonstration of a pallido-nigral projection innervating dopaminergic neurons.

Afferents to the substantia nigra from the neostriatum and globus pallidus were studied in the rat by means of the autoradiographic tracing technique. 3H-leucine was injected stereotaxically into either the globus pallidus or neostriatum. Twenty-four hours later the axoplasmic transport of labelled proteins to the substantia nigra was studied by light and electron microscopic autoradiography. In animals used for electron microscopy, degeneration of dopaminergic cells in the substantia nigra was induced by intraventricular injection of 6-hydroxydopamine 72 hours before sacrifice. After neostriatal injections, light microscopic analysis revealed heavy labelling of the globus pallidus and entopeduncular nucleus, but only background labelling of the subthalamic nucleus. There was preferential labelling of the zone reticulata of the substantia nigra, with significantly less labelling of the zone compacta. After pallidal injections, light microscopic analysis showed very light labelling of those parts of the caudate-putamen in the vicinity of the injection site. There was intense labelling of the subthalamic nucleus and heavy labelling of the entopeduncular nucleus. The zona compacta of the substantia nigra was also heavily labelled. There was considerably less labelling of the zona reticulata. The electron microscopic analyses showed that after neostriatal injections, autoradiographic grains in the substantia nigra were located preferentially over boutons which terminated on normal dendritic processes. After pallidal injections, however, grains were preferentially located over boutons synapsing with degenerating dendritic processes. The degeneration produced in these dopaminergic processes by 6-hydroxydopamine was invariably of the dark type. Except for the different association with degenerating vs. non-degenerating dendrites, the subcellular distribution of autoradiographic grains in the substantia nigra was the same after injection into either the globus pallidue or caudate-putamen. Approximately 80 percent of the grains were over axons or boutons which invariably made symmetrical synaptic contacts. These observations demonstrate the existence of a pallido-nigral projection which terminates preferentially on dopaminergic cells in the pars compacta of the substantia nigra. They also confirm previous studies indicating that the strionigral projection terminates mainly in the pars reticulata. These terminations appear to be principally to non-dopaminergic cells.

Animals↗
PubMed1979

Release of prolactin and LH and histamine-containing cells in brain.

The effects of histamine released from mast cells by the compound 48/80, a degranulating agent, on plasma prolactin and LH levels, were examined in rats. Compound 48/80 given systemically (s.c.) at a dose of 2 mg/100 g b.w. significantly increased at 15 and 60 min after injection, both prolactin and LH release in ovariectomized, steroid-primed rats. Prolactin but not LH was also augmented in the plasma of male rats following s.c. administration of compound 48/80. There were no modifications of plasma prolactin levels in male rats at 15, 30 or 60 min after intraventricular injection of 50 microgram compound 48/80. Results suggest that the hormone effects were due to histamine released from median eminence mast cells after systemic injection of compound 48/80.

Animals↗
PubMed1985

Neuropeptide Y immunoreactivity in the hamster geniculo-suprachiasmatic tract.

The distributions of neuropeptide Y (NPY) and avian pancreatic polypeptide (APP) immunoreactivity were examined in the suprachiasmatic nucleus and the geniculate area of male golden hamster brains. In some cases, colchicine was injected intraventricularly to aid in visualization of immunoreactive cell bodies. A group of hamsters were given bilateral or unilateral radiofrequency lesions of the geniculate area and neuropeptide Y immunoreactivity was examined in the suprachiasmatic nucleus after survival times varying between 8 and 300 days. Another group of hamsters received unilateral intraocular injections of anterograde tracers and the overlap of NPY-immunoreactive cells in the geniculate area and labeled retinal afferents was assessed. It was found that NPY- and APP-immunoreactive fibers formed a dense plexus in the ventro-lateral suprachiasmatic nucleus. NPY-immunoreactive cell bodies were observed in the intergeniculate leaflet as well as in the external lamina of the anterior portion of the ventral lateral geniculate nucleus. Unilateral lesions of the geniculate produced a relative reduction in neuropeptide Y immunoreactivity in the ipsilateral suprachiasmatic nucleus whereas bilateral lesions produced a reduction of neuropeptide Y immunoreactivity in both suprachiasmatic nuclei. All NPY-immunoreactive cells in the intergeniculate leaflet were overlapped by bilateral retinal afferents. In the ventral lateral geniculate nucleus, all NPY-immunoreactive cells were overlapped by contralateral retinal afferents; however, not all such cells were in areas receiving ipsilateral retinal afferents. These results indicate that the hamster geniculo-suprachiasmatic tract originates in part from NPY-immunoreactive cell bodies and that these cells lie in areas receiving direct retinal afferents.

Animals↗
PubMed1986

Morphine stimulates prolactin release in normal but not in castrated male rats.

Morphine (200 micrograms/rat) was injected intraventricularly (i.v.t.) into normal and into long-term castrated (4 weeks) adult male rats. Animals were killed 10, 20, 40 and 60 min after treatment. In normal animals, the treatment with morphine resulted in a significant increase of serum prolactin concentrations at all time intervals considered. However, the i.v.t. injection of 200 micrograms morphine/rat into castrated rats did not exert any significant effect on prolactin release at any time interval considered. When morphine (200 micrograms/rat) was administered i.v.t. together with the specific opioid receptor blocker naloxone (7.5 or 15 micrograms/rat) the stimulatory effect of morphine on prolactin release was diminished at 10 min, and totally blocked at 20 min. Naloxone given alone did not influence serum prolactin concentrations. The results suggest that the presence of endogenous androgens is essential to permit the stimulatory effect of morphine on prolactin release.

Animals↗
PubMed1980

Preferential neurotoxicity of colchicine for granule cells of the dentate gyrus of the adult rat.

Injections of 5-7 microgram (6-9 nmol) of colchicine into the dentate gyrus of the hippocampus of mature rats result in widespread destruction of dentate granule cells with little, if any, damage to other cell populations, including hippocampal pyramidal cells. Selective destruction of dentate granule cells is also observed after intraventricular injections. The destructive effects of colchicine appear as soon as 12 hr after the injection and lead to the disappearance of the granule cells over a period of days. Whereas the effects on nongranule cell populations in the hippocampus appear to be reversed by approximately 11 days after injection, the granule cells are almost completely absent at long intervals after injection. At the long postinjection survival intervals the disappearance of the granule cells is accompanied by elimination of their terminal projections, the mossy fibers, as revealed by Timm staining for heavy metals. Because the preferential neurotoxic effects of colchicine do not result in morbidity or obvious behavioral debilitation, the toxicity may prove useful for studying the functional consequences of removing specific cell populations in the central nervous system.

Animals↗