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PubMed1977

Beta-endorphin: stimulation of growth hormone release in vivo.

Two micrograms of beta-endorphin (beta-lipotropin61-91) injected intraventricularly in rats that had been treated with antiserum against somatostatin led to a 6- and 10-fold stimulation of the concentration of plasma growth hormone (somatotropin) measured 10 and 20 min after injection of the peptide, whereas 400 mug of methionine-enkephalin led to a 4- to 6-fold increase of levels of plasma growth hormone at 10 min with a rapid return to basal levels at later time intervals. At doses of 5 and 25 mug, beta-endorphin led to a 20- to 30-fold stimulation of levels of plasma growth hormone, the maximal effect being measured between 20 and 30 min after injection. These data suggest the possible role of the endogenous opiate-like peptides in the control of growth hormone secretion.

Animals↗
PubMed1994

Intracerebral microinjections of dermorphin: search for the epileptic induction thresholds.

To test the different sensitivity of several central structures to the epileptogenic action of mu opiate agonists, intracerebral microinjections of the selective mu agonist dermorphin were delivered into different areas of the rat dorsal and ventral hippocampus, septum, amygdala, entorhinal cortex, thalamus, striatum and neocortex. The dose of dermorphin (up to 6 nmol) necessary to trigger electrical epileptic events in each of these regions was studied. Epileptic discharges were triggered only in the ventral hippocampus (CA1 and CA3 areas), amygdala and entorhinal cortex. The epileptic induction threshold was the lowest in the CA1 area of the ventral hippocampus. The results suggest that when a mu opiate agonist is injected intraventricularly, the epileptic activity originates in the ventral hippocampus.

Animals↗
PubMed1985

Neuroendocrine effects of some amphibian peptides.

The effect of dermorphin and sauvagine, two new peptides originally isolated from amphibian skin, on the release of gonadotropins and prolactin was studied "in vivo" and "in vitro." The intraventricular administration of dermorphin to castrated male rats induces a significant decrease in serum LH, but not FSH, levels. Subcutaneous, as well as intraventricular, injections of dermorphin to normal male rats induce a statistically significant increase in serum prolactin levels, which is counteracted by naloxone. In the isolated and dispersed rat pituitary cell preparation, the addition of dermorphin to the media does not induce any alteration in prolactin output. Intraventricular administrations of sauvagine are ineffective in influencing the secretion of both LH and FSH. This peptide is also unable to modify it when tested "in vitro". On the contrary, subcutaneous injections of sauvagine to either normal male or lactating rats decrease serum prolactin levels. This prolactin inhibitory effect is also present "in vitro." These results suggest that dermorphin and sauvagine modulate the secretory activity of the anterior pituitary gland. However, the mechanism of control is different: dermorphin needs the mediation of brain structures, while sauvagine acts directly at the pituitary level.

Amphibian Proteins↗
PubMed2002

Intraventricular and intravenous treatment of a patient with refractory primary CNS lymphoma using rituximab.

The treatment of primary central nervous system lymphoma (PCNSL) with chemo- and radiotherapy is efficient in terms of tumor response. However, time to tumor progression often is of short duration and leptomeningeal relapse is common. We present a 66-year-old man in third relapse of a CD20-positive PCNSL. After treatment with intravenous and intraventricular administration of the chimeric anti-CD20 monoclonal antibody rituximab, a total clearing of lymphoma cells in the cerebrospinal fluid (CSF) was achieved. There was no change in the size of the parenchymal tumor mass but there was slight improvement of clinical symptoms after therapy. Rituximab infusions (375 mg/m2) were first given systemically on days 1 and 8. Intraventricular injections of rituximab via Ommaya reservoir were given on days 16 (10 mg), 17 (40 mg), 24 (25 mg) and 25 (25 mg). Reversible side effects such as nausea, chills and hypotension were observed only immediately after intraventricular administration of 40 mg rituximab. Antibody levels in CSF were measured at 7 timepoints during and after the treatment period. These data suggest that intraventicular treatment with rituximab is safe and feasible with a potential activity on leptomeningeal tumor manifestation. Efficacy and pharmacokinetics of rituximab in PCNSL should be investigated in future trials.

Aged↗
PubMed1984

Differential effects of baclofen, gamma-hydroxybutyric acid and muscimol on the protective action of phenobarbital and diphenylhydantoin against maximal electroshock-induced seizures in mice.

This study was designed to compare the effects of baclofen (a GABAB agonist), muscimol (a GABAA agonist) and gamma-hydroxybutyric acid on the protective action of phenobarbital (PB) and diphenylhydantoin (DPH) against electroshock-induced convulsions. All drugs were given intraperitoneally, muscimol being also injected intraventricularly in a dose of 50 ng per mouse. It was found that both baclofen and gamma-hydroxybutyric acid potentiated the anticonvulsant activity of phenobarbital, being ineffective regarding the action of diphenylhydantoin. Conversely, muscimol injected by two different routes moderately enhanced the efficacy of diphenylhydantoin but remained without a significant effect upon the action of phenobarbital.

Animals↗
PubMed1989

The paradoxical stimulatory effect of morphine on LH secretion is dose-dependent and naloxone-reversible.

We previously observed that morphine stimulated luteinizing hormone (LH) secretion from ovariectomized rats when administered intravenously at a dose of 10 mg/kg body weight. The objectives of the present study were to determine: (1) if this paradoxical effect of morphine on LH secretion could be antagonized by naloxone; (2) whether beta-endorphin also stimulated LH secretion under similar conditions; (3) what influence, if any, the ovaries have on the expression of this opiate-induced LH secretion, and (4) whether this paradoxical effect of morphine extended to prolactin (PRL) secretion. An intravenous injection of morphine, 10 mg/kg body weight, to ovariectomized rats acutely increased both plasma LH and PRL concentrations. The LH and PRL responses were completely antagonized by the concurrent administration of the opiate antagonist naloxone (1 mg/kg body weight). In contrast, morphine suppressed LH concentrations and had no effect on PRL levels when injected at a dose of 1.0 mg/kg body weight. Intravenous injections of beta-endorphin, 1 mg/kg body weight, increased PRL concentrations to a level comparable to that observed following morphine, 10 mg/kg body weight, and produced a transient but insignificant inhibition of LH release. Intraventricular injections of much lower doses of beta-endorphin resulted in a dose-dependent suppression of LH release and a dose-dependent stimulation of PRL release in ovariectomized rats. Intravenous administrations of morphine (10 mg/kg), but not beta-endorphin (1 mg/kg), to normal female rats resulted in a 2-fold increase in LH concentrations similar to that observed in ovariectomized rats, whereas both treatments similarly increased PRL concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effect of cytidine on the modification of phospholipid metabolism induced by ischemia.

[1-14C-]Arachidonic acid was injected into the lateral ventricle of the gerbils (meriones unguiculatus) two hours before producing brain ischemia by the bilateral ligation of the carotid arteries. Ten minutes before the carotid ligation a group of animals received an additional intraventricular injection of cold cytidine (2.5 mumol/brain). Control animals with and without cytidine, together with the ischemic group, were decapitated directly into liquid nitrogen ten minutes after carotid ligation or sham surgery. Cytidine is able to both stimulate arachidonic acid incorporation into lipids and noticeably correct the release of this acid from polar lipids induced by ischemia. Based on these findings, it is possible to assume that cytidine exerts an effect on the biosynthesis of phosphoglycerides as well as on their catabolic activities.

Animals↗
PubMed1986

Stimulatory and inhibitory effects of the opioids on gonadotropin secretion.

In order to gain additional information on the role played by the opioids in the control of the secretion of anterior pituitary gonadotropins, morphine (an opioid agonist) and naloxone (an opioid antagonist) have been injected intraventricularly (i.v.t.) into normal or castrated male rats. The animals were killed by decapitation at different time intervals after treatment and serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin were measured by radioimmunoassay. Animals injected i.v.t. with 0.9% saline solution and sacrificed at the same time intervals served as controls. When morphine (at the dose of 200 and 400 micrograms/rat) and naloxone (at the dose of 7.5 and 15 micrograms/rat) were injected i.v.t. into normal male rats, a significant increase of serum levels of LH was observed 10 and 20 min after injection. There was no effect at 5, 40 and 60 min. Lower doses of morphine (6.25, 12.5, 25, 50 and 100 micrograms/rat) given i.v.t. were ineffective. When morphine (200 micrograms/rat) and naloxone (either in the dose of 7.5 micrograms/rat or of 15 micrograms/rat) were given simultaneously, serum LH was significantly higher than in the saline-treated controls both at 10 and 20 min. However, the increases of serum LH levels induced by the combined treatment were in both instances lower than those produced by the administration of either drug alone. Morphine (200 micrograms/rat) when administered i.v.t. to normal male rats significantly enhanced prolactin release at 10 and 20 min, and this effect of morphine was blunted by the concomitant i.v.t. administration of naloxone (7.5 and 15 micrograms/rat).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effect of intracerebroventricular injection of nicotinic acetylcholine receptor antibodies on ACTH, corticosterone and prolactin secretion in the male rat.

The aim of the present study was to investigate the involvement of CNS nicotinic receptors for acetylcholine in the secretory activity of the hypothalamo-hypophyseal-adrenal axis and prolactin (PRL). Adult male rats received a daily intraventricular injection of partially purified nicotinic acetylcholine receptor antibodies (anti-AChR) obtained from a female patient with myasthenia gravis, for 5 consecutive days. Control animals were treated similarly with immunoglobulins obtained from a healthy woman. Blood samples were withdrawn either under basal conditions or following ether stress. Treatment with anti-AChR increased basal ACTH and corticosterone (CS) levels (by approximately two-fold) but completely inhibited the responses of these hormones and PRL to ether stress. In control animals, normal basal and stress-induced responses of ACTH, CS and PRL were observed. This study demonstrated the importance for nicotinic acetylcholine receptors in the mediation of basal and stress-induced adrenocortical activity as well as for the mediation of PRL secretion in response to stress.

Adrenocorticotropic Hormone↗
PubMed1988

In vivo voltammetric study of 6-hydroxydopamine-induced neuronal degradation.

Freely moving rats were injected intraventricularly with 200 micrograms of 6-hydroxydopamine (6-OHDA) and examined for transport of this substance to the striatum, degradation of dopamine (DA) neurons, and functional recovery through microcomputer-controlled in vivo voltammetry. Approximately 6 min after the injection, 6-OHDA began to appear in the extracellular fluid of the contralateral striatum. It increased linearly and began to decrease exponentially with the termination of the injection. Two hours after the injection with 6-OHDA, a peak began to appear at the same potential as the peak of DA in the differential pulse voltammogram. It persisted for approximately 3 days. When the rats were injected intraperitoneally with L-3,4-dihydroxyphenylalanine (L-Dopa), the conversion of L-Dopa to DA was not found 1 week after the 6-OHDA injection, but was clearly recognized 5 months after the injection. When the rats were examined for behavioral changes arising from the L-Dopa injection, they were found to be clearly less hyperactive 5 months after the 6-OHDA injection than 1 week after.

Animals↗
PubMed1984

Immature rabbit hippocampus is damaged by systemic but not intraventricular kainic acid.

Intraventricular injection of kainic acid produced a characteristic necrosis in the hippocampal CA3 region of adult rabbits. Neurons in immature rabbit hippocampus were relatively insensitive to the intraventricular neurotoxin, even though these injections caused seizures. In contrast, the immature hippocampus was highly sensitive to kainate delivered systemically. Systemic kainate preferentially killed neurons in the CA1 region, not the CA3 region, of immature animals. Kainate injections also caused cellular damage in brain regions other than hippocampus. In immature rabbits, the pattern of extra-hippocampal damage was similar regardless of the route of kainate delivery. This pattern of extra-hippocampal damage was distinctly different than that seen in adults following intraventricular kainate. These data suggest that kainate-induced damage in the CA3 and CA1 regions of the hippocampus are mediated by different mechanisms. Furthermore, the dissimilar patterns of extra-hippocampal damage in immature and adult rabbits suggest that mature and immature animals have differential sensitivity to kainate, different types of kainate binding sites, and/or different distributions of kainate receptors.

Animals↗
PubMed1994

Involvement of angiotensin receptor subtypes in osmotically induced release of vasopressin.

We have previously shown that AT1 and AT2 angiotensin II (Ang II) receptors mediate the release of arginine vasopressin (AVP) to central injections of Ang II. In this study we have tested the hypothesis that Ang II, acting at AT1 and AT2 receptors in the brain, is involved in mediating osmotically stimulated AVP release. Adult Sprague-Dawley rats were fitted with intraventricular (i.v.t.) cannulas and catheters in the carotid artery and the femoral vein. Intraventricular injections of Ang II receptor antagonists specific to different subtypes of the receptor (AT1 and AT2) were given before a 30 min infusion of hypertonic (2.5 M) saline. Arterial blood samples were collected 5 min before and at two time points after (+15 min and +30 min) beginning the saline infusion. We found that both losartan (AT1 specific) and CGP42112A (AT2 specific) significantly reduced osmotically induced release of AVP. PD123319 (AT2 specific) had no effect of osmotically stimulated AVP release. A combined treatment of losartan + PD123319 was no more effective than losartan in blocking the AVP response. Since losartan was the most rapid and effective antagonist of osmotically stimulated AVP release, we conclude that AT1 receptors are directly involved in the response. However, but since CGP42112A was also an effective antagonist and since, AT2 receptors are located at sites distant from the hypothalamus, such as the locus ceruleus, they may also contribute to this response. We conclude that brain Ang II receptors are involved in osmotically stimulated AVP release.

Angiotensin II↗
PubMed1981

Effects of intracerebral administration of atropine and morphine on the caudate stimulation-induced caudate spindle in rats.

The electrical stimulation of the caudate nucleus could induce a caudate spindle in the rat as in case of the cat and monkey. The spindle was enhanced by atropine (3-10 mg/kg, i.v.) or morphine (3-10 mg/kg, i.v.) and the effect of these drugs were completely abolished by eserine (0.3 mg/kg, i.v.), but not by methysergide (1 mg/kg, i.v.), PCPA (400 mg/kg, i.p. for 3 days) or reserpine (3 mg/kg, i.p. for 2 days). An intraventricular injection of atropine (5-10 microgram/rat) or morphine (10 microgram/rat) exerted a facilitatory action on the spindle, while an intrathalamic and intracaudate injection of atropine (5-50 microgram/rat) showed a suppressive action. The spindle was also markedly enhanced by the microinjection of atropine (15-30 microgram/rat) or morphine (30 microgram/rat) into the reticular formation, and these actions were completely antagonized by eserine (0.3 mg/kg i.v.), but only partially by methysergide (4 microgram/rat, intraventricular administration.) These results suggest that the cholinergic system may play an important role in the regulation of the caudate spindle.

Animals↗
PubMed2002

Adeno-associated virus-mediated gene transfer to the neonatal brain.

For many metabolic diseases, early treatment is necessary to prevent irreversible developmental damage. This is particularly true for childhood diseases that affect the central nervous system (CNS). The development of effective techniques for gene transfer to the neonatal brain would provide a new set of therapeutic options for many of these disorders. Vectors based on adeno-associated virus (AAV) have shown promise as agents for neonatal CNS transduction. In preclinical animal models, a single treatment with AAV vectors at birth has been shown to produce persistent CNS expression of transduced genes into adulthood. Transduction of the neonatal brain has been accomplished by a variety of methods, including direct intraparenchymal injection, intraventricular infusion, and intravenous administration. Of these methods, intraparenchymal injection provides the highest levels of localized activity, while intraventricular infusion results in a more widespread distribution of activity when performed in the neonate. Here we describe a method for direct, intraparenchymal injection of AAV into the neonatal brain. This technique provides a method for investigators to evaluate the effects of in vivo expression of exogenous genes on the process of early brain development.

Adenoviridae↗
PubMed2004

Postischemic intraventricular administration of FGF-2 expressing adenoviral vectors improves neurologic outcome and reduces infarct volume after transient focal cerebral ischemia in rats.

Fibroblast growth factor (FGF)-2 is a potent neurotrophic and angiogenic peptide. To examine possible protective effects of FGF-2 gene expression against transient focal cerebral ischemia in rats, a replication defective, recombinant adenovirus vector expressing FGF-2, was injected intraventricularly 2 hours after middle cerebral artery occlusion (MCAO). The treatment group showed significant recovery compared with the vehicle-treated groups in terms of serial neurologic severity scores over the 35 days after MCAO. Further, 2,3,5-triphenyltetrazolium chloride staining showed that FGF-2 gene transfer decreased infarct volume by 44% as compared with that in the vehicle-treated groups at 2 days after MCAO. The same tendency of gene transfer effects on infarct volume was confirmed at 35 days after MCAO with hematoxylin/eosin staining. Enzyme-linked immunosorbent assay revealed that FGF-2 concentration was increased significantly at 2 days after MCAO, not only in cerebrospinal fluid but also in cerebral substance in the lesioned and treated animals. These results suggested that FGF-2 gene transfer using these adenoviral vectors might be a useful modality for the treatment of occlusive cerebrovascular disease even after the onset of stroke.

Adenoviridae↗
PubMed1994

Injection of an aromatase inhibitor after the critical period of sexual differentiation.

We have investigated the possible role of the second week of life in the differentiation of sexually dimorphic behaviours, dependent on the androgenic aromatization, and its possible relationship with the serotonergic systems. For this purpose, 5 mg/kg of a suspension of an aromatase inhibitor, LY43578, has been intraventricularly injected to males on day 12 of life. Studies have been made in adulthood on exploratory and motor activities, anxiety, sexual motivation, and sexual performance. Indoleamine levels in the hypothalamus and corpus striatum have been measured. Sexual behaviour, exploration, and serotonergic metabolism were not affected by the treatment. Sex partner preference and anxiety in the plus-maze showed a feminized tendency in the treated group that, however, did not reach statistical significance. From these results we have confirmed the restriction of the critical period of androgenic aromatization for the organization of reproductive and exploratory behaviour.

Animals↗
PubMed1975

The fate of N-dansyl-L-phenylalanine in the cerebrospinal fluid after intraventricular and intracisternal injection: a comparative fluorescence microscopic and analytical study.

Absorption, accumulation and release of N-Dansyl-L-phenylalanine (DPA) through the ependyma, plexus choriodei and brain parenchyma after intraventricular and intracisternal injection was examined at different postinjection intervals by fluorescence microscopy. The following results were obtained: 1. After intraventricular injection, DPA is rapidly absorbed from the ependyma and plexus choriodei in all ventricles and subsequently disappears from the various points of the ventricles at different times. DPA is no longer evident in the ependyma after 40 min and the plexus after 90 min. Aborption and storage occur primarily in the dopaminergic centers of the brain. This stage begins 5 min p.i. attains a maximum after 40 min and is maintained up to 180 min p.i. 2. If DPA is administered intracisternally, fluorescence is initially restricted to the ependyma and choroid plexus of the fourth ventricle and to the wall of the aquaeduct. Only at 5-10 min p.i. are rostral ventricular portions labelled. Passage of the amino acid out of the ventricle only occurs to a limited extent. 40 min after intracisternal injection, DPA is no longer demonstrable in the ependyma and plexus or brain parenchyma. 3. Intrathecally administered DPA appears in the periglomerular tubules of the kidney as well 2.5 min p.i. and is stored there for up to 40 min. The kidney medulla remains free of fluorescence. 4. DPA injected into the CSF is protein-bound.

Animals↗
PubMed1988

Ganglioside interactions with the dopaminergic system of rats.

The effects of ganglioside treatment on changes in dopaminergic function following 6-hydroxydopamine (6-OHDA) or repeated exposure to haloperidol were studied in male Fischer-344 rats. Rats were injected sc with 30 mg/kg of a mixed ganglioside preparation (GM) at the time of the surgery and for 13 days after receiving an intranigral injection of 6-OHDA. GM treatment attenuated 6-OHDA depletion of striatal dopamine (DA) and DOPAC. Another group of rats was implanted with chronic indwelling cannulas in the lateral cerebroventricles at the time of 6-OHDA administration into the substantia nigra. Daily intraventricular injection of 25 or 50 micrograms GM attenuated depletions of striatal DA and DOPAC. A separate experiment sought to determine the effects of GM1 on the development of receptor supersensitivity produced by repeated exposure to a dopamine receptor antagonist. Rats were injected sc with 1 mg/kg haloperidol for 8 or for 16 days; some rats were coadministered 20 mg/kg GM1 sc. Four days after the last dose, the rats were challenged with 1 mg/kg apomorphine, and activity was counted for 60 min. Treatment with GM1 decreased the behavioral supersensitivity to apomorphine induced by repeated exposure to haloperidol. These experiments suggest that treatment with GM can have a protective effect against 6-OHDA-induced depletion of dopamine if treatment with GM begins at the time of lesioning. These studies also support receptor binding data from other laboratories indicating that treatment with GM1 can affect up-regulation of dopamine receptors.

3,4-Dihydroxyphenylacetic Acid↗