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At least 973 records · Page 54Linked to original sources
PubMed1989

Brain abnormalities induced by murine cytomegalovirus injected into the cerebral ventricles of mouse embryos exo utero.

Murine cytomegalovirus (MCMV) was injected into the cerebral ventricle of mouse embryos on day 13 of gestation after exposing the embryos out of the uterus in the abdominal cavity of the mother. The embryos were allowed to develop to day 18 of gestation, then taken out from the abdominal cavity. Macroscopically, there were four expanded and three distorted brains out of 19 surviving embryos, whereas no brain abnormality was noticed in 13 embryos injected with culture medium instead of MCMV in the same way. Histopathological examination showed hydrocephalic lesions with strong dilatation of the ventricles and atrophy of the cerebral cortex, and inflammatory lesions with granulomatous proliferation of the ventricular walls with disappearance of the cortical zonation. Immunohistochemically, MCMV-induced nuclear antigen-positive cells were frequently observed in the wall of the ventricles and occasionally scattered in the cerebral cortex, white matter, and the nucleus basalis. Some fetuses injected with MCMV in the same way were recovered from the abdominal cavities on day 18 of gestation and transferred to foster nurse mothers. They showed massive cerebral necrosis after feeding for 9 days after birth. Brain abnormalities of mouse embryos after intraventricular injection with MCMV may provide an experimental model of brain damage induced by congenital cytomegalovirus infection.

Animals↗
PubMed2000

Effects of third ventricle injection of norepinephrine analogue on LH secretion of the non-laying SIJI goose.

The effect of norepinephrine analogue (NA) and norepinephrine antagonists on luteinizing hormone releasing hormone (LHRH) secretion in geese was investigated by monitoring serum levels of LH. Twenty non-laying geese were selected and randomly assigned to 4 groups of 5 each. The geese received a single intraventricular injection of saline (control), NA (12 microg/6 microl), phentolamine (1 microg/6l) plus NA or yohimbine (10 microg/6 microl). Phentolamine, a non-selective adrenoreceptor blocker was given 5 min before NA, but yohimbine, an alpha2-adrenoreceptor blocker, was delivered without NA injection. The results showed that serum levels of LH began to increase 20 min after injection of NA, and that high serum levels of LH were maintained until 105 min, followed by a decline to the basal level 125 min later. Significantly high levels of serum LH were observed at 50 and 105 min after the injection as compared with the respective control. Treatment with phentolamine completely blocked the stimulatory effect of NA on serum levels of LH in NA treated geese. Serum levels of LH increased by yohimbine treatment 5 min after the injection and the high levels of serum LH were maintained until 125 min later. Five out of 8 points were significantly high as compared with their respective control values. The present study also suggested that there is presynaptic modulation in the a-noradrenergic neural pathways which mediate the release of LHRH, and that this modulation may be carried out by alpha2-adrenoreceptor blocker.

Adrenergic alpha-Agonists↗
PubMed2000

Morphological changes following experimental intraventricular haemorrhage and intraventricular fibrinolytic treatment with recombinant tissue plasminogen activator.

Intraventricular haemorrhage (IVH) occurs in up to 50% of patients with primary intracerebral haemorrhage and aneurysmal subarachnoid haemorrhage. It is a significant and independent contributor to mortality and morbidity in these intracranial haemorrhages. Using a model of isolated IVH, we assessed the morphological changes induced by intraventricular bleeding and investigated the effects of intraventricular fibrinolytic treatment following IVH. IVH was induced in 32 pigs by intraventricular infusion of 10 ml autologous blood along with thrombin. The treatment group received an intraventricular injection of 1.5 mg (1 mg/ml) tissue plasminogen activator (tPA) following the injection of blood. The placebo group received the same volume of normal saline. Morphological examinations of the brains were carried out 7 days and 6 weeks following IVH. The ventricles were incompletely filled with blood and significantly enlarged in the placebo group 7 days after the IVH. In contrast, no residual intraventricular clots were visible in the animals treated with tPA, and the diameters of the lateral ventricles had returned to normal within 7 days. Marked losses of the ependymal covering of the ventricular walls were found in the placebo-treated animals, while the ependymal layer was largely intact in the animals treated with tPA. No haemorrhages induced by tPA were observed. The results indicate that intraventricularly administered tPA significantly enhances the lysis of intraventricular blood clots, accelerates the resolution of acute posthaemorrhagic hydrocephalus, and preserves the integrity of the ependymal layer.

Animals↗
PubMed1975

Thermoregulation in the rabbit following intracranial injection of norepinephrine.

The release of norepinephrine (NE) from nerve terminals in the anterior hypothalamic/preoptic area (AH/POA) of the rabbit may serve to raise body temperature. To further examine the putative neurotransmitter role of NE, bilateral microinjections of 5 or 10 mug NE were made into or near the AH/POA of 44 conscious rabbits exposed to an ambient temperature of 15 degrees C. Microinjections into the AH/POS did not cause fever; they either had no influence on thermoregulation or rapidly induced ear vasocilation and increased ear temperature accompanied by slight falls in rectal temperature. The latter averaged 0.32 degrees C (range: 0.16-0.45 degrees C) in 18 rabbits in which the effects were prominent. In contrast, the injection of 100 or 250 mug NE into the lateral cerebral ventricles of conscious rabbits in the 15 degrees C environment caused mean fevers of 0.62 +/- 0.0, and 1.04 +/- 0.14 degrees C (+/- SE, n equals 6), respectively, within 70 min. The febrile response to intraventricular injection of NE may be due to an action of the drug at a site other than the AH/POA. Alternatively, the response may depend critically on the particular distribution of NE that results from its diffusion from the third ventricle into the AH/POA.

Animals↗
PubMedDate not supplied

Memory consolidation for contextual and auditory fear conditioning is dependent on protein synthesis, PKA, and MAP kinase.

Fear conditioning has received extensive experimental attention. However, little is known about the molecular mechanisms that underlie fear memory consolidation. Previous studies have shown that long-term potentiation (LTP) exists in pathways known to be relevant to fear conditioning and that fear conditioning modifies neural processing in these pathways in a manner similar to LTP induction. The present experiments examined whether inhibition of protein synthesis, PKA, and MAP kinase activity, treatments that block LTP, also interfere with the consolidation of fear conditioning. Rats were injected intraventricularly with Anisomycin (100 or 300 microg), Rp-cAMPS (90 or 180 microg), or PD098059 (1 or 3 microg) prior to conditioning and assessed for retention of contextual and auditory fear memory both within an hour and 24 hr later. Results indicated that injection of these compounds selectively interfered with long-term memory for contextual and auditory fear, while leaving short-term memory intact. Additional control groups indicated that this effect was likely due to impaired memory consolidation rather than to nonspecific effects of the drugs on fear expression. Results suggest that fear conditioning and LTP may share common molecular mechanisms.

Acoustic Stimulation↗
PubMed1984

The vasculature of experimental brain tumours. Part 3. Permeability studies.

The aim of this work was to elucidate the direction and time-course of transport processes which may affect the accumulation of oedema associated with experimental brain tumours. Astrocytomas were produced in BD-IX rats by intracerebral injection of cultured neoplastic glial cells. The cell line used was cloned from a culture of a primary mixed glioma induced by transplacental administration of N-ethyl-N-nitrosourea (ENU). At various times after cell injection the protein tracer horseradish peroxidase (HRP) was given to tumour-bearing rats, either intravenously or into the lateral ventricles of the brain. The movement of the HRP into tumours and surrounding brain either from blood or from ventricular cerebrospinal fluid (CSF) was studied by light and electron microscopy at various intervals after the injection of the tracer. The time-course of subsequent clearance of the HRP from the tumours and surrounding brain was also investigated. After intravenous injection, HRP rapidly penetrated all vascularized tumours and became evenly distributed within 10-20 min. The HRP remained present in sufficient quantity within the tumours to maintain this intensity for several hours, after which it gradually disappeared, showing no reaction product after 12 h. After intraventricular injection, HRP penetrated periventricular brain tissue up to a maximal distance 1-2 mm within 2 min, and the reaction product remained visible in this region for at least 20 min. In all tumour-bearing animals, HRP penetrated further into periventricular tumour tissue than into adjacent brain tissue. In large tumours HRP reaction product was seen up to 7 mm from the ventricular ependymal lining, although permeation to this distance took up to 10 min.

Animals↗
PubMed1986

Interaction of alpha-melanocyte-stimulating hormone with beta-endorphin to influence anterior pituitary hormone secretion in the female rat.

The interaction of alpha MSH and beta-endorphin on the secretion of PRL, GH, and LH was determined in the ovariectomized rat. The potent stimulatory effect on PRL release of injection of 20 ng (5.8 pmol) beta-endorphin into the third cerebral ventricle was completely blocked by 100 ng (60 pmol) alpha MSH. The same dose of alpha MSH partially blocked the effect of 150 ng (44 pmol) beta-endorphin on PRL secretion. Intraventricular injection of either 20 ng beta-endorphin or 100 ng alpha MSH had no effect by itself on plasma LH. However, coinjection of these doses of beta-endorphin and alpha MSH suppressed plasma LH levels significantly within 15 min. beta-Endorphin (150 ng) produced a significant suppression of plasma LH levels. Furthermore, coadministration of 100 ng alpha MSH with 150 ng beta-endorphin lowered plasma LH for a longer period of time than this dose of beta-endorphin alone. Low doses of beta-endorphin (20 ng) or alpha MSH (100 ng) alone or in combination did not alter plasma GH levels. A higher dose of 150 ng beta-endorphin produced a slight elevation of plasma GH. This effect was potentiated 5-fold when 150 ng beta-endorphin were injected in combination with 100 ng alpha MSH. These results indicate that alpha MSH acts as an antagonist to beta-endorphin in regard to the secretion of PRL, whereas it potentiates the effect of beta-endorphin in stimulation of GH and inhibition of LH secretion.

Animals↗
PubMed1981

Analgesia following intraventricular administration of 2-deoxy-D-glucose.

The glucose analogue, 2-deoxy-D-glucose (2-DG) elicits hyperphagic and analgesic responses in rats. The former response appears to be mediated by central processes since overeating is elicited following intraventricular administration of 2-DG at low (3.5 and 5.0 mg/kg) doses. The present study examined whether flinch-jump threshold would increase 30, 90 and 180 min following intraventricular injections of 2-DG at low (3.5, 5.0 and 10.0 mg/kg) doses and compared these effects with systemically-applied 2-DG doses of 350 and 500 mg/kg. Intraventricular 2-DG administration increased jump thresholds for up to 180 min across all test doses. Flinch thresholds were also increased, but in a manner dissociated from jump thresholds. Animals with cannulae located near, but not in the lateral ventricle, displayed delayed analgesic effects. The magnitude of intraventricular 2-DG analgesia was not at potent as the 100-fold higher systemic injections. It appears that central mechanisms mediated intraventricular 2-DG analgesia at the low dose range since higher, systemic 2-DG doses have previously failed to increase flinch-jump thresholds.

Analgesia↗
PubMed2003

Anti-kindling effect of slow repetitive transcranial magnetic stimulation in rats.

The cerebrospinal fluid (CSF) of animals exposed to electroconvulsive shock (ECS) has anticonvulsant properties when injected into naive animals. The present study investigated whether the CSF of humans exposed to 1 or 10 Hz repetitive transcranial magnetic stimulation (rTMS) has similar properties. Using a 4 day rat flurothyl kindling seizure model we found that the kindling rate was significantly decreased by intraventricular injection of CSF from depressed patients exposed to 1 Hz rTMS. The CSF from patients that underwent 10 Hz rTMS showed a trend toward an increased kindling rate. These results support the similarity of ECS and rTMS and suggest that 1 Hz and 10 Hz rTMS produce distinct physiologic changes.

Adult↗
PubMed1978

In vivo enzyme activity of purified human brain renin.

Cerebrospinal fluid (CSF) of rats contains high angiotensinogen concentrations. When 3500-fold purified renin from human brain was injected into the brain ventricles of rats, angiotensin I concentrations increased from undetectable levels to 147.9 +/- 18.8 fMol per ml CSF. In parallel, mean arterial blood pressure increased from 93 +/- 2.4 mm Hg to 107 +/- 3.7 mm Hg. The increase in blood pressure could be abolished by intraventricular administration of saralasin, a blocker of angiotensin II receptors. Intraventricular injection of cathepsin D had no effect on arterial blood pressure and the agiotensin I concentration in CSF remained below detection limits of the radioimmunoassay. We conclude that brain renin acts on endogenous brain angiotensinogen under physioloical in vivo conditions to form angiotensin I. The latter is converted to angiotensin II and leads to biological effects, i.e. increase of blood pressure.

Angiotensin I↗
PubMed1984

A possible role of prostacyclin to stimulate prolactin and growth hormone release by hypothalamic and pituitary actions, respectively.

Prostacyclin (PGI2) (1-5 micrograms in 3 microliters 0.05 M Tris/HCl buffer, pH 7.5) and its stable metabolite, 6-oxo-PGF1 alpha, were microinjected into the third ventricle of ovariectomized rats, and plasma FSH, GH, PRL, and TSH levels were measured by RIA. Control animals received 3 microliters buffer. Injection of 5 micrograms PGI2 dramatically elevated plasma PRL values (4- to 5-fold) at 5 and 15 min, whereas the same dose of 6-oxo-PGF1 alpha produced a significant but smaller (2-fold) stimulatory effect. A delayed increase (1.5-fold) in plasma GH occurred after intraventricular PGI2 at 30 and 60 min. 6-Oxo-PGF1 alpha failed to alter GH levels. There were no alterations in plasma FSH and TSH after intraventricular injection of PGI2. Dispersed, overnight cultured cells from anterior pituitaries of ovariectomized rats were tested with 10(-4)-10(-7) M PGI2 and its metabolite. After 15 min of incubation, 3 X 10(-5) PGI2 produced a highly significant elevation in GH release (P less than 0.001), whereas there was no alteration in PRL levels. Only pharmacological doses of 6-oxo-PGF1 alpha (10(-4) M) stimulated GH release. There was no alteration in PRL release by the cultured cells even in the presence of 10(-4) PGI2. These results suggest that PGI2 stimulates PRL release by a hypothalamic action either to increase the release of PRL-releasing factor, or to decrease release of PRL-inhibiting factor, or by both mechanisms. The delayed stimulatory effect of PGI2 on the release of GH may be exerted via an effect on the anterior lobe itself, since PGI2 was effective in stimulating GH release by the incubated pituitary cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

[Oxytocin as a putative factor in the control of periodic and synchronized neurosecretory bursts of oxytocinergic cells (author's transl)].

During suckling, the intramammary pressure and the electrical activity of oxytocinergic cells in the paraventricular nucleus were recorded simultaneously in urethane-anaesthetized Rats. Injection of an oxytocin antagonist (1 microliter d(CH2)5OVT 10(-3) or 10(-4) M) into the 3rd ventricle, inhibited both frequency and amplitude of neurosecretory bursts and milk-ejections. The same effect was observed when the milk-ejection reflex was previously activated by the intraventricular injection of oxytocin (1 microliter--10(-6) M). Thus, oxytocin might regulate the frequency and amplitude of oxytocinergic cells' neurosecretory bursts and could be involved in their synchronism.

Animals↗
PubMed1980

Effects of intraventricular gamma-acetylenic-GABA on GABA concentrations, GABA-T and GAD in several areas of the chick brain.

The great interest in new compounds able to increase GABA concentration in the brain as potential antiepileptic drugs has led to the synthesis of powerful inhibitors of GABA transaminase (GABA-T) e.g. gamma-acetylenic GABA (GAG) and gamma-vinyl-GABA. Present experiments were aimed to study behavioral, electrocortical and biochemical effects of GAG after its intraventricular injection. It has been shown that in chicks the microinjection of GAG into the third cerebral ventricle produced a biphasic behavioral and electrocortical syndrome : an initial phase of behavioral and electrocortical sleep followed by a paradoxycal increase in motor activity and a very intense behavioral and ECoG arousal pattern. In addition intraventricular GAG (0.8 mumol) produced a significant increase 1 and 2 h later in GABA concentration in the diencephalon and brain-stem whereas no changes occurred in other brain areas e.g. cerebral hemispheres, optic lobes. Higher doses (1.6 mumol), produced after 1 h, concomitantly to the increased GABA concentration, a significant GABA-T inhibition and a profound inhibition of glutamate-decarboxylase in the diencephalon and brain-stem. Present experiments may explain the paradoxical behavioral, motor and electrocortical stimulation observed at the time of GABA increase concentration and suggest that a small functional neuronal pool of GABA, more than the whole absolute levels of GABA in a given area of the brain, seems to be involved in the control of GABAergic mediated inhibitory mechanisms.

4-Aminobutyrate Transaminase↗
PubMed1976

The effects of neurally active amino acids on pituitary gonadotropin secretion.

Several neurally excitant amino acids were injected into the third ventricle of anesthetized male rats, and plasma levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured. LH levels increased following injections of 2.0 mum glutamate, lysine, or beta-alanine. Glycine (2.0 mum), alpha-alanine (2.0 mum), and 0.9% saline were ineffective in altering LH levels. None of the amino acids tested significantly altered FSH levels. Of the 3 amino acids which raised blood LH levels following an intraventricular injection, i.e., glutamate, beta-alanine, and lysine, only lysine caused a significant increase in LH levels following injection into the pituitary. The present study provides evidence for a possible role for certain neurally excitant amino acids in the neuronal control of LH secretion.

Alanine↗
PubMed1983

The central actions of glycine and strychnine on prolactin and LH secretion.

Unanesthetized diestrous female rats were tested for the prolactin response following an intraventricular injection of several doses of the neuroinhibitory amino acid glycine, and the antagonist strychnine. Glycine in doses of 1.0 or 0.1 mumoles increased pituitary prolactin release, significantly elevating plasma hormone levels. Direct pituitary effects for glycine were not observed. Strychnine, a glycine antagonist, was effective in blocking the prolactin release caused by glycine in doses as low as 5 nmoles. Intraventricular glycine administration did not alter pituitary LH release significantly. These studies suggest a central stimulatory role for the neuroinhibitory amino acid glycine in provoking prolactin secretion, and that this effect is strychnine sensitive.

Animals↗
PubMed1983

[Effects of dimaprit, an H2 receptor agonist, on blood levels of corticosterone in the rat].

These experiments were performed in order to further clarify the role played by hystamine in the control of hypothalamus-hypophisis-adrenal axis. To this aim we evaluated the effect of Dimaprit, a H2 agonist on plasma corticosterone levels. This drug was administered intraperitoneally or i.c.v. at the doses of 25, 50 and 100 mg/kg or 100 gamma/animal respectively. The administration i.p. at the dose of 100 mg/kg increased plasma-corticosterone levels whereas Dimaprit, injected intraventricularly did not modify plasma-corticosterone levels. These results seem to suggest that Dimaprit stimulates corticosterone secretion at a peripheral level.

Animals↗
PubMed1981

Central nervous system toxicity of intraventricularly administered gentamicin in adult rabbits.

To determine whether daily intraventricular injection of gentamicin sulfate would cause neurologic or morphologic abnormalities of the central nervous system, adult male rabbits were given gentamicin sulfate, 2 mg/kg, intramuscularly twice a day plus saline, 0.2 ml (group 1), or gentamicin, 0.05 mg/kg (group 2), 0.25 mg/kg (group 3), or 0.5 mg/kg (group 4), given as the sulfate intraventricularly once a day. The majority of the animals in group 4 developed neurologic abnormalities which progressed to death in animals that were not euthanized; neuropathologic studies revealed chemical ventriculitis and meningitis that were associated with high levels of gentamicin in the cerebrospinal fluid and tissue of the central nervous system. Similar neurologic and morphologic changes were seen in most animals of group 3 but not in rabbits of groups 1 and 2. The ototoxicity and nephrotoxicity of gentamicin are well known; these data indicate that it may be toxic to the central nervous system as well.

Animals↗
PubMed1991

Limited distribution of pertussis toxin in rat brain after injection into the lateral cerebral ventricles.

In vivo administration of pertussis toxin is often used to study the involvement of guanine nucleotide binding proteins in signal transduction. Especially when it is administered in the brain the effect is often poor. This could be due to the fact that pertussis toxin does not reach the area of interest. To evaluate the extent to which pertussis toxin is distributed in rat brain after intraventricular injection, different techniques were used. Immunohistochemical studies with an antibody against pertussis toxin showed that immunoreactivity was limited to periventricular brain structures less than 0.5 mm from the lumen. The highest immunoreactivity was seen 16-24 h after injection. After 96 h the labeling was very weak. The proportion of guanine nucleotide binding proteins that were ADP-ribosylated by in vivo injection of pertussis toxin into the ventricles as assessed by in vitro [32P]-back-ADP-ribosylation was very low 48 h after the injection, in all regions studied. Direct injection of pertussis toxin into the brain caused a marked ADP-ribosylation localized to the region injected that was maximal at 72 h after injection. At 96 h there were also effects after control injections, indicating non-specific effects. Synaptosomal membranes and other membranes were equally affected by pertussis toxin. The results suggest that in studies regarding the effect of pertussis toxin treatment on signal transduction, the toxin must be injected very close to the brain region of interest and, furthermore, that the rats should be killed 48-72 h after injection. In case of lack of effect on the response of interest one should examine whether the ADP-ribosylation of pertussis toxin-sensitive guanine nucleotide binding proteins in the area of concern has been affected.

Adenosine Diphosphate Ribose↗