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PubMed1995

[Excitation of hypothalamic nucleus arcuatus neuron induced decrease of plasma sialic acid level in rats].

The effect of sodium glutamate (Glu) on plasma sialic acid (SA) level was studied by means of microinjection into the nucleus arcuatus (ARC) and ultraviolet spectrophotometry. The results indicate: (1) The plasma SA level was significantly decreased after microinjection of Glu into the ARC (P < 0.01). With increasing Glu concentration, the onset of the decrease occurred earlier. (2) When Glu was microinjected into ARC after intraventricular injection of apomorphine, the plasma SA level was significantly decreased (P < 0.01) and the time required to cause the decrease was shortened. (3) When Glu was microinjected into ARC after intraventricular injection of spiperone, no change was found in the plasma SA level (P > 0.05). The above results suggest that the mechanism underlying the decrease of plasma SA level is probably related to modulated dopamine (DA) release of hypothalamic dopaminergic neurons by DA-D2 receptor.

Animals↗

PubMedDate not supplied

Radioautographic localization of radioactivity in rat brain after intraventricular or intracarotid injection of 3H-L-prolyl-L-leucyl glycinamide.

Tritiated L-prolyl-L-leucyl-glycinamide was injected into the carotid artery or lateral ventricle of rats and the radioactivity localized by radioautography. After intracarotid administration, the radioactivity labeled the meninges, ependymal cells bordering the ventricles, and cells of the choroid plexus, as well as the median eminence and subfornical organ and thus may have reached the cerebrospinal fluid. After intraventricular injection, globus pallidus, indusium griseum, hippocampus, corpus callosum, and meninges. The results after intracarotid injection suggest that L-prolyl-L-leucyl-glycinamide may cross the blood brain barrier and the results after intraventricular injection suggest sites of localization which might be correlated with the previously reported effects of the tripeptide on the brain.

Animals↗

PubMed1982

Transmission and scanning electron-microscopic observations on tanycytes in the mediobasal hypothalamus and the median eminence of adrenalectomized rats.

Tanycytes in the median eminence (ME) of the rat exhibit morphological features suggesting their possible participation in transport phenomena. After adrenalectomy, which modifies the hypothalamo-hypophyseal axis, they undergo morphological changes characterized by an accumulation of lipid droplets, an increased number of bleb-like protrusions at their apex, as well as an increased pinocytosis of intraventricularly injected horseradish peroxidase (HRP). In addition, after adrenalectomy an increased number of vacuoles appears at the level of the tubero-infundibular sulci. Their intracellular location in the tanycytes is demonstrated by an intraventricular injection of HRP. The significance of these vacuoles is discussed in relation to the hydroelectrolytic modifications associated with the state of adrenalectomy.

Adrenal Glands↗

PubMed1994

An in vivo study of the effect of 5-HT and sympathetic nerves on transferrin and transthyretin mRNA expression in rat choroid plexus and meninges.

Brain expression of transferrin (Tf) and transthyretin (TTR) mRNA has been demonstrated in different species, TTR being found only in the choroid plexus. We report here that both these mRNAs are also expressed in the meninges. In vitro studies have shown that Tf secretion by the rat choroid plexus is stimulated by 5-hydroxytryptamine (5-HT) while sympathetic nerves regulate different transport functions in the same tissue. We have used various in vivo models to study the neuroendocrine regulation of Tf and TTR mRNA expression in the choroid plexus and meninges. Destruction of the serotonergic nerves in the brain by either raphe nuclei lesion or intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), which both decreased brain 5-HT levels significantly, did not affect Tf or TTR mRNA levels in choroid plexus and meninges, but increased TTR mRNA in liver. Intraventricular injection of 10 or 100 pmol 5-HT did not change the expression of these proteins in any of the tissues studied. Removal of the sympathetic innervation to the choroid plexus by cervical sympathectomy did not affect Tf or TTR mRNA levels in choroid plexus and liver, nor the incorporation of radioactive leucine into protein in various parts of the brain. In conclusion, our results do not support a regulatory role in vivo for neuronally derived 5-HT or sympathetic nerve activity on Tf and TTR mRNA expression in rat choroid plexus and meninges.

5,7-Dihydroxytryptamine↗

PubMed1981

[Hypnogenic properties of the vasoactive intestinal polypeptide in rats].

The intraventricular injection of 100 ng of vasoactive intestinal polypeptide (VIP) is followed by a significant increase of paradoxical sleep in the Rat. In P. chlorophenylalanine pretreated insomniac Rats which do not present spontaneous paradoxical sleep episodes, intraventricular injection of VIP induces normal quantities of this state of sleep.

Animals↗

PubMed1975

Neurochemical aspects of porphyria. Studies on the possible neurotoxicity of delta-aminolaevulinic acid.

It has been proposed that delta-aminolaevulinic acid (ALA), which is overproduced in the inherited hepatic porphyrias, may be responsible for the neurological manifestations of the acute attacks seen in these disorders. Studies were conducted in rats to test the neurotoxicity of ALA. It was found that, after intraperitoneal or subcutaneous injections, ALA is rapidly eliminated via the kidneys. In nephrectomised animals sustained elevation of blood ALA concentration was demonstrated, but despite this, brain uptake was extremely low. Experiments on incorporation of [4-14-C]-ALA into brain haem yielded similar information. After intraventricular injection of [4-14-C]-ALA, significant uptake by brain tissue occurred. The subsequent disappearance of ALA was moderately rapid and was virtually complete within 24 hours. Uptake of [4-14-C]-ALA was apparently significantly greater in the hypothalamus than in other brain areas. The subcellular distribution of radioactivity did not reveal any preferential uptake by nerve endings. Intraventricular injection of unlabelled ALA revealed definite but transitory neurotoxic effects in doses of 3 micromoles and greater. These include involuntary movements and ataxia. No effect of ALA administration on brain protein synthesis could be demonstrated. It is concluded that ALA does have effects on the nervous system in vivo, but the significance of these effects in relation to the pathogenesis of the neurological manifestations of acute porphyria is questionable.

Aminolevulinic Acid↗

PubMed2005

Glial overexpression of heme oxygenase-1: a histochemical marker for early stages of striatal damage.

The level of heme oxygenase-1 (HO-1) in the normal striatum is below the limit of immunodetection. However, HO-1 is overexpressed in both neural and non-neural cells in response to a wide range of lesions. We induced different types of lesions affecting the striatal cells or the main striatal afferent systems in rats to investigate if overexpression of HO-1 could be a useful histochemical marker of striatal damage. Thirty-six hours after intrastriatal or intraventricular injection of excitotoxins that affect striatal neurons (ibotenic acid) or of neurotoxins that affect striatal dopaminergic (6-hydroxydopamine) or serotonergic (5,7-dihydroxytriptamine) afferent terminals, or after surgical lesioning of cortico-striatal projections, there was intense induction of striatal HO-1 immunoreactivity (HO-1-ir). Double immunolabeling revealed that the HO-1-ir was located in glial cells. After intrastriatal injection of ibotenic acid, a central zone of neuronal degeneration contained numerous round and pseudopodic HO-1-ir cells, and was surrounded by a ring of HO-1-ir cells, most of which were immunoreactive for astroglial markers. Intraventricular injection of neurotoxins induced astroglial HO-1-ir cells which were more evenly distributed throughout the lesioned or denervated areas. HO-1-ir microglial cells were also observed in areas subjected to mechanical damage. The HO-1-ir was markedly lower or absent 1 week after lesion, and even more so 3 weeks after, although some HO-1-ir cells were still observed after intrastriatal injection of ibotenic acid or surgical corticostriatal deafferentation. The results indicate that determination of glial HO-1-ir is a useful histochemical marker for early stages of striatal damage.

5,7-Dihydroxytryptamine↗

PubMed1983

Electroencephalographic studies of chlorpromazine methiodide and somatostatin-induced barrel rotation in rats.

It has been reported that intraventricular injection of chlorpromazine methiodide (CPZMI), a quaternary ammonium derivative of chlorpromazine, in rats induces abnormal, twisting postures which may serve as an experimental model of the human movement disorder dystonia. We have shown elsewhere that the behavior induced by intraventricular CPMZI is identical to what has been called "barrel rotation," first observed to follow intraventricular injection of somatostatin (SRIF), which consists of twisting about the long axis, with repetitive lateral rolling. The suitability of barrel rotation, induced by CPZMI or SRIF, as an experimental model for dystonia depends on its physiologic basis. Human dystonia is clinically not a convulsive phenomenon. SRIF-induced barrel rotation has been reported to be associated with epileptiform activity recorded by the electroencephalogram (EEG). The purpose of this study was to investigate EEG activity during CPZMI- and SRIF-induced rotation. We found that CPZMI barrel rotation was not associated with epileptiform activity in cortex, amygdala, or hippocampus, and contrary to prior reports, neither was SRIF rotation. Both CPZMI and SRIF injected in high doses could induce epileptiform activity, but this was associated with clonic motor phenomena and not barrel rotation. We conclude that electroencephalographic criteria do not exclude either CPZMI- or SRIF-induced rotation as models for movement disorders, but their validity as such requires further study.

Animals↗

PubMed1987

Interactions between neuropeptide Y and adrenergic systems in the stimulation of luteinizing hormone release in steroid-primed ovariectomized rats.

Intraventricular injection of neuropeptide Y (NPY) stimulates LH release in estradiol benzoate- and progesterone-primed (EBP) ovariectomized rats. Because adrenergic neurotransmitters, norepinephrine (NE) and epinephrine (E), show intraneuronal coexistence with NPY in certain brain regions of the rat and there are similarities in the effects of NPY and NE/E on LH release, we investigated the possible interaction of NPY and adrenergic receptor systems in the stimulation of LH release in EBP-treated ovariectomized rats. The experiments were designed to determine whether NPY exerted its effects via adrenergic receptors and whether combined administrations of NPY and NE can act synergistically or in an additive manner to enhance the LH release response. Permanent stainless steel cannulae were placed in the third ventricle of the brain, and the rats were ovariectomized. Two weeks after surgery, rats were injected with EB (30 micrograms/rat) and P (15 mg/rat). Two days later, the effects of either vehicle alone (control) or various adrenergic and dopaminergic receptor antagonists and an opiate receptor agonist on stimulation of LH release by NPY were assessed. Intraventricular injection of 0.47 nmol NPY increased plasma LH levels at 10, 20, and 30 min in control rats. The NPY-induced LH response was not blocked by pretreatment with any of the following drugs: the alpha-adrenoreceptor antagonist phenoxybenzamine, the alpha 1-adrenoreceptor antagonist prazosin, beta-adrenoreceptor antagonist propranolol, the dopamine receptor antagonist pimozide, or the opiate receptor agonist morphine. All of these drugs affect LH release in other circumstances. On the other hand, the alpha 2-adrenoreceptor antagonist yohimbine significantly attenuated the NPY-induced LH increments. In the second study dealing with the possible synergistic or additive interactions between NPY and NE, we observed that when doses of NPY and NE that separately were only minimally effective in stimulating LH release were administered together, the amounts of LH secreted were greater than the sum of the individual responses. However, when NE and NPY were given together in doses that alone had either no stimulatory or maximal stimulatory effects, there were no additive or synergistic effects on LH release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1982

[Effect of the "memory peptide" ACTH 5-10 on the self-stimulation reaction of rabbits].

Experiments on rabbits were made to study variation in the frequency of the self-stimulation reaction from the lateral hypothalamus under the effect of the corticotropin fragment ACTH5-10. Intraperitoneal administration of the peptide in a dose of 50 micrograms/kg that causes the improved training in different behavioral models produces no significant effect on the mechanism of intracranial positive reinforcement. Intraventricular injection of 5 microliters of 0.9% NaCl leads to a short-term suppression of the self-stimulation reaction. Administration of 50 pcM/kg ACTH5-10 in the same volume of physiological saline completely abolishes the inhibitory action of the intraventricular injection itself.

Adrenocorticotropic Hormone↗

PubMed1989

Paraventricular and supraoptic bursting oxytocin cells in rat are locally regulated by oxytocin and functionally related.

1. Oxytocin was pressure injected through a glass micropipette into a supraoptic (SON) or paraventricular nucleus (PVN) while recording the electrical activities of oxytocin cells in a contralateral nucleus, to see whether oxytocin acts locally in the magnocellular nuclei to control their bursting activity and whether the oxytocin cells of the four magnocellular nuclei were functionally interconnected during suckling. To test the rapidity of these relations, similar intranuclear injections were realized with acetylcholine, known to rapidly increase the background activity of oxytocin cells. The effects of intranuclear injections of oxytocin and acetylcholine were tested before and after interhemisphere sections of various dimensions. 2. Injecting oxytocin (1 ng in 100 nl) into a magnocellular nucleus (5 times into the PVN and 15 times into the SON) facilitated the occurrence and increased the amplitude of bursts of the oxytocin cells in both the contralateral PVN and SON. This facilitatory effect was similar to that induced by intraventricular injection of the same dose of oxytocin, though slightly delayed and lower. 3. Injecting acetylcholine (0.6 microgram in 100 nl) into the SON (7 times) induced a rapid and sustained increase in the background activity of oxytocin cells in both the contralateral PVN (2 times) and SON (5 times) within the same delay (less than 15 s). This excitatory effect was similar to that induced by an intraventricular injection of 5 micrograms acetylcholine. The effects on bursting activity were not considered in this study. 4. Neither the injections of oxytocin or acetylcholine outside but near the magnocellular nuclei (200-500 microns), nor the intranuclear injection of 100-200 nl of cerebrospinal fluid-like medium, modified the background activity, the frequency and amplitude of bursts of the oxytocin cells in the nucleus contralateral to the injection site. 5. After interhemisphere sections most oxytocin cells were silent, bursts occurred in an erratic manner, and their amplitude was attenuated and irregular (more than the 20% variation normally recorded in non-operated rats). Moreover, the amplitudes of successive bursts of pair-recorded supraoptic-supraoptic (SO-SO) oxytocin cells, highly related in control conditions (correlation coefficient, r = 0.68 to 0.98) were no longer correlated after interhemisphere section (r = 0.24 to -0.61), but all bursts remained synchronized.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗

PubMed2002

Early neonatal 192 IgG saporin induces learning impairments and disrupts cortical morphogenesis in rats.

We have shown previously that neonatal intraventricular injections of the selective cholinergic immunotoxin 192 IgG saporin on postnatal day 7 (pnd 7) induce marked cholinergic loss in hippocampus and neocortex and a learning impairment on pnd 15. In the present study, we analysed the behavioural, morphological and neurochemical effects of earlier intraventricular injection of the immunotoxin 192 IgG saporin (pnd 1 and 3). We hypothesised that these earlier lesions would interrupt a critical stage in neocortical maturation, and impair behavior more profoundly than the later lesions. Passive avoidance (PA) learning and locomotor activity during the PA test were assessed on pnd 15. Retention of the PA task was assessed on pnd 16. Reactivity to spatial and object novelty was assessed on pnd 180 in a spatial open field test with five objects. Choline acetyltransferase (ChAT) activity was measured in basal forebrain targets on pnd 20 and pnd 180. Neonatal administration of 192 IgG saporin resulted in a slower acquisition of the PA task in females; retention and locomotor activity were not affected. On pnd 180, reaction to spatial novelty was mildly impaired in lesioned rats of both sexes. There was a marked reduction of ChAT in the hippocampus and neocortex of lesioned rats of both sexes, at both ages. Morphological analysis of the somatosensory cortex of lesioned rats revealed alterations in cortical development with sex specific variations in total cortical thickness. These results suggest that interrupting cholinergic basal forebrain innervation of neocortex and hippocampus during the first postnatal days affects the development of cognitive behaviour, neurochemistry and cortical organisation in a sex specific manner. Furthermore, the alterations in cortical organization are more profound than those noted after a lesion later in postnatal development. These behavioural and morphological abnormalities could be considered a model for several neurodevelopmental disorders associated with mental retardation.

Animals↗

PubMed1983

Effect of prostaglandin E1 on vasoactive intestinal polypeptide release from the hypothalamus and on prolactin secretion from the pituitary in rats.

In order to elucidate the mechanisms by which prostaglandin (PG) affects PRL secretion, the effect of PGE1 on vasoactive intestinal polypeptide (VIP) release from the rat hypothalamus was examined by determining plasma VIP levels in rat hypophysial portal blood in vivo and VIP release from the perifused hypothalamus in vitro. Intraventricular injection of PGE1 (1 and 5 micrograms/rat) caused a 2- to 3-fold increase in the concentration of plasma VIP in hypophysial portal blood in anesthetized rats. The flow rate of portal blood was slightly increased after the injection of PGE1. VIP release from the perifused rat hypothalamus was stimulated by high potassium levels (56 mM). The infusion of PGE1 (10 microM) resulted in a significant increase in VIP release from the hypothalamus in vitro. Both these responses were calcium dependent. The intraventricular injection of PGE1 (1 and 5 micrograms/rat) resulted in a dose-related increase in peripheral plasma PRL levels in the rat. These findings suggest that PGE1 plays a stimulatory role in regulating VIP release from the hypothalamus into hypophysial portal blood and causes PRL secretion from the pituitary in rats.

Alprostadil↗

PubMed1984

Alteration of striatal glutamate release after glutamine synthetase inhibition.

The effect of the glutamine synthetase (GS) inhibitor, methionine sulfoximine (MSO), on glutamate levels in, and glutamate release from, rat striatal tissue was examined. Tissue levels of glutamate were unchanged 24 h after an intraventricular injection of MSO, but tissue glutamine levels were decreased 50%. Calcium-dependent, potassium-stimulated glutamate release was diminished in tissue prisms from animals pretreated with MSO compared to controls. The decreased release of glutamate correlated over time with the inhibition of GS following an intraventricular injection of MSO. The maximum diminution of calcium-dependent, potassium-stimulated glutamate release (50%) and the maximum inhibition of GS activity (51%) were observed 24 h after MSO. The addition of 0.5 mM glutamine to the perfusion medium completely reversed the effects of MSO pretreatment on calcium-dependent, potassium-stimulated glutamate release. Since GS is localized in glial cells and the measured glutamate release is presumed to occur from neurons, the data support the contention that astroglial glutamine synthesis is an important contributor to normal neuronal neurotransmitter release.

Animals↗

PubMed1976

Effects of intraventricular 6-hydroxydopamine injections on serum prolactin and LH levels: absence of stress-induced pituitary prolactin release.

The drug 6-hydroxydopamine (6-OHDA) has been reported to reduce hypothalamic norepinephrine (NE) content after administration into the lateral ventricle without altering the dopamine content of tubero-infundibular neurons. Serum prolactin levels in male rats injected with 2 X 250 mug 6-OHDA were significantly higher than in untreated control rats. Intraventricular injection of male rats with artificial cerebrospinal fluid resulted in elevated mean prolactin levels similar to those observed in 6-OHDA-treated animals. Further experimentation on animals decapitated at different times after removal from the animal quarters, indicates that prolcatin levels in 6-OHDA-treated rats are continuously elevated whereas they rise from basal levels to extremely high levels in CSF-treated rats, thus resulting in similar mean values. The CSF-treated controls ate hypersensitive to the stress of being removed from their normal environment. Such an effect was not observed in 6-OHDA-treated nor in untreated, and thus stress-inexperienced rats. In a long term study, serum prolactin and luteinizing hormone (LH) levels were followed over a period of 71 days after 6-OHDA treatment. Prolactin levels increased within one day after treatment and stayed at a high level for 15 days. Subnormal prolactin values were measured 37 days after 6-OHDA treatment. Serum LH levels were below normal 3 h and one day and were increased 37 and 71 days after 6-OHDA treatment. These results suggest that NE is important in the transmission of stressful stimuli to hypothalamic prolactin regulating centers. They further suggest functional recovery of LH and prolactin regulating mechanisms after 6-OHDA treatment.

Animals↗

PubMed1989

Hypothyroidism enhances carbachol-induced hypothermia in the rat.

We studied cholinergic regulation of body temperature in hypothyroid rats. Thyroidectomy caused a progressive decrease in core temperature. Intraventricular injection of carbachol in a dose of 10 nmol did not change core temperature of the normal rat, whereas the same dose of carbachol significantly decreased the temperature of thyroidectomized rats. One hundred nmol carbachol decreased to a greater extent core temperature of the thyroidectomized rats than that of normal rats. Intraventricular injection of atropine significantly increased core temperature of thyroidectomized rats. The present data indicate that brain cholinergic mechanisms participate in controlling temperature in the hypothyroid status and thyroid hormones play a significant role in the brain cholinergic regulation of body temperature.

Animals↗

PubMed1980

Autoradiography of GABA in the rat hypothalamic median eminence.

Light microscopy autoradiographs of the rat hypothalamic median eminence were prepared after injection of high specific activity tritiated GABA and GABA structural analogs. Following intracardiac injection of labeled GABA with short (15 min) survival time, a dense accumulation of silver grains was observed over the external layer of the median eminence. The silver grains appeared much less numerous and randomly scattered over the internal layer. No conspicuously labeled cells could be detected in the median eminence. A similar pattern of labeling was observed after 10 min in vitro incubation of the median eminence with a low concentration (2.5 x 10(-7) M) of labeled GABA. Clusters of silver grains were also visible over the external layer following intraventricular injection of labeled GABA. In this latter case, however, other sites of labeling were revealed over the internal and ependymal layers. The dense labeling over the external layer with tritiated GABA was partially reduced by a simultaneous intracardiac injection of a 50-fold excess of non-radioactive cis-aminocyclohexane carboxylic acid--a reported preferential substrate for GABA neuronal uptake--but it was not displaced by a 2000-fold excess of non-radioactive beta-alanine--a reported specific substrate for GABA glial uptake. Intracardiac injection of triated beta-alanine led to a faint and even labeling over the entire median eminence with no preferential accumulation of silver grains over the various layers. Following intraventricular injection of labeled beta-alanine the tanycytes and their processes as well as numerous glial cells appeared heavily labeled. These results suggested that there exist cell elements in the external layer of the hypothalamic median eminence which are capable of accumulating exogenous GABA according to its neuronal uptake characteristics. Although the exact nature of these cells is not readily apparent at this stage of our investigations, these findings led us to speculate that there might be a subpopulation of GABAergic nerve endings in the vicinity of the primary plexus capillaries.

Alanine↗

PubMed1990

The NMDA receptor mediates cortical induction of fos and fos-related antigens following cortical injury.

Cortical cavity lesions and lateral ventricular injections of quinolinic acid, a NMDA receptor agonist, induce Fos and Fos-related antigens (FRAs) throughout ipsilateral adult rat brain cortex in similar patterns. c-fos mRNA, assessed using in situ hybridization, was induced by 1 h and disappeared between 3 and 8 h following cortical lesions. Fos proteins, detected using a specific monoclonal antibody, were induced by 1 h and disappeared by 4 h after cortical lesions. FRA proteins, detected using polyclonal antibodies, were induced between 1 and 4 h and persisted for at least 72 h following focal cortical injury. Intraventricular injections of CPP, a competitive NMDA receptor antagonist, completely blocked the induction of these nuclear proteins in cortex ipsilateral to the focal cortical lesions--except around the injury site itself. Intraventricular injections of quisqualate, a non-NMDA glutamate analogue, induced Fos in hippocampus but not in cortex. These data show that NMDA receptors mediate the induction of Fos and FRAs following cortical injury. It is proposed that local cortical injury releases excitatory amino acids that act at NMDA receptors to initiate spreading depression and that the resultant depolarization induces Fos in neurons throughout the cortex. Since Fos and FRAs are proteins that regulate the expression of target genes, they could mediate long-term biochemical adaptations in neurons following cortical injury.

Animals↗