Intraventricular injection of antivasopressin serum blocks learned helplessness in rats.
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Animals↗
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Results for “Injections, Intraventricular”
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Suppressive effects of intraventricular injected dopamine and nomifensine on muricide induced by thiamine deficiency.
The effects of dopamine (DA) and nomifensine (NF) on muricide activity induced by thiamine deficiency were examined. The chronic administration of L-dopa and nomifensine during feeding of thiamine deficient diet attenuated the muricide activity. Moreover, acute administration of L-dopa or nomifensine (IP) and dopamine or nomifensine (ICV) suppressed the thiamine deficiency-induced muricide activity dose-dependently. Small doses of apomorphine inhibited the muricide response significantly. The suppressive effects of dopamine and nomifensine were antagonized by pretreatment with 6-hydroxydopamine, but were not changed by pretreatment with p-chlorophenylalanine. These results suggest that the dopaminergic system has an important role in the regulation to the thiamine deficiency-induced muricide response.
Aggression↗
Participation of the autonomic nervous system in lipolysis induced by intraventricular injection of carbachol in the pigeon.
The possible involvement of central cholinergic neurotransmission in lipomobilization in avian species was investigated by injecting carbachol into the brain lateral ventricle (i.c.v.) of conscious pigeons (N = 9 per experimental group). I.c.v. injections of carbachol (27 nmol in 1 microliter) induced an intense increase (nearly 91% above baseline levels) in the concentration of plasma free fatty acids (FFA). Previous intraperitoneal administration of hexamethonium (10 mg/kg) completely blocked the lipomobilizing effect of i.c.v. injections of carbachol. These results suggest that cholinergic neurons may be involved in central mechanisms controlling FFA mobilization in pigeons, and that this response is mainly mediated by activation of autonomic nervous system.
Acetylcholine↗
The histopathological, behavioral and neurochemical effects of intraventricular injection of ethylcholine mustard aziridinium (AF64A) in the neonatal rat.
This study investigated the histopathological, behavioral and neurochemical effects of bilateral injection of 2.0, 0.5 and 0.1 nmol/ventricle ethylcholine aziridinium (AF64A) on postnatal day (PND) 2. The rats showed a significant, but non-dose-related reduction of choline acetyltransferase (ChAT) in the hippocampus but not the cerebral cortex or the caudate nucleus when sacrificed on PND 16. No effect on ChAT was found in any region at PND 58. The group given 2 nmol/ventricle were hyperactive and showed a deficit in spatial learning when tested on the Morris water maze at PND 38-43. No such differences were observed for the rats injected with 0.1 or 0.5 nmol/ventricle AF64A. This spatial learning impairment in the 2 nmol group was associated with non-specific tissue damage seen only in animals from this group that were sacrificed at PND 40. This tissue damage was most evident in the left medial frontal cortex, the caudate nuclei and the anterior dorsal hippocampus.
Animals↗
Long-term alteration in tyrosine hydroxylase mRNA levels in rat locus coeruleus after intraventricular injection of 5,6-dihydroxytryptamine.
The time course variations in tyrosine hydroxylase (TH) activity and specific mRNA were measured in the rat locus coeruleus (LC) and substantia nigra after an intracerebroventricular (i.c.v.) injection of 5,6-dihydroxytryptamine (5,6-DHT), a neurotoxin known to selectively destroy serotoninergic neurons. In this study, the TH activity and TH mRNA were both analyzed from homogenates of single tissue samples (micropunches). TH mRNA was extracted and quantified by densitometry using a northern blot method and an artificial TH RNA as an external standard. 5,6-DHT injection led to a long-lasting increase in TH activity and TH mRNA in LC but not in substantia nigra. The elevation in LC was progressive and reached its maximum value (+75%) at day 4 and day 8 after 5,6-DHT. This effect on TH activity was accompanied by a parallel change in TH mRNA whose amplitude was +57%, +81% and +45% at day 2, 4, and 8 respectively after the neurotoxin injection. Return to normal values was observed at day 16. Variations in TH activity and TH mRNA in LC were of similar amplitude. These results suggest that serotonin could be a potent modulator of TH gene expression within noradrenergic LC neurons.
5,6-Dihydroxytryptamine↗
Blockade of the hypothalamic-pituitary-adrenal response to stress by intraventricular injection of dexamethasone: a method for studying the stress-induced peripheral effects of glucocorticoids.
Interest in the mechanisms whereby stressors can influence behavior and physiological functioning has involved the use of a variety of methods to prevent the stress-induced release of glucocorticoids, an important and commonly studied stress hormone. We examined the effect of intracerebral ventricular dexamethasone (ICV DEX) on the stress-induced release of adrenocorticotropic hormone (ACTH), corticosterone, plasma epinephrine (E), and plasma norepinephrine (NE). Male Sprague-Dawley rats were stereotaxically implanted with third ventricle ICV cannulae, administered DEX or vehicle, and exposed to 100 1.6-mA tail shocks. Stress hormones were assessed from blood taken during and after the cessation the shock. We report an ICV DEX injection protocol (10 microgram given four times) that results in blocking the stress-induced release of ACTH and corticosterone, and attenuating the stress-induced release of plasma E and NE. We hypothesize that ICV DEX reduces hypothalamic corticotropin releasing hormone (CRH) synthesis and/or release. This method would be especially useful for those studying the effect of pituitary-adrenal hormones on steroid sensitive peripheral targets, such as the immune system.
Adrenocorticotropic Hormone↗
Radioprotection in rat spinal cord with WR-2721 following cerebral lateral intraventricular injection.
The capacity of WR-2721 to provide radioprotection in central nervous system (CNS) tissue was assessed in F-344 rats irradiated with Cs-137 to the cervical spinal cord 45 min following injection of either 0.33 mg (0.60 X LD50) of WR-2721 or carrier solution in the right lateral cerebral ventricle. The radiation dose groups were 20, 26, 32, or 38 Gy; the dose rate was 1.48 Gy/min. Following irradiation, the time in weeks to forelimb and hindlimb paralysis was measured and statistical significance was assessed by means of the log rank sum test. The median times in weeks to forelimb paralysis in control vs. WR-2721-treated rats were, respectively, 20 vs. 22 at 38 Gy, 19 vs. 31 at 32 Gy (p less than 0.01), 23 vs. 28 at 26 Gy (p less than 0.01), and 49 vs. 60 at 20 Gy (p less than 0.01). The median times to hindlimb paralysis in control vs. WR-2721-treated rats were respectively, 20 vs. 29 at 38 Gy (p less than 0.001), 20 vs. 35 at 32 Gy (p less than 0.01), 23 vs. 34 at 26 Gy (p less than 0.001), and 58 vs. 65 at 20 Gy (p less than 0.01). From these results, we calculated the DMF for forelimb paralysis to be 1.3 and for hindlimb paralysis, 1.6. Histological studies from selected spinal cords from symptomatic killed rats showed petechial hemorrhages, rare microvascular thrombi, and scattered microinfarcts in both gray and white matter. In the white matter columns, there were scattered microfoci of demyelination. The histological findings did not differ between the control and WR-2721-treated groups, but were worse in the higher dose groups. These data indicate that WR-2721 has the capacity to be radioprotective in CNS tissues, when it is administered by a route that bypasses the blood-brain barrier.
Amifostine↗
Autoradiographic studies with a behaviorally potent 3H-ACTH4--9 analog in the brain after intraventricular injection in rats.
Autoradiographic studies aimed at identifying target cells in the brain for ACTH-like peptides were performed using (3H-7-Phe)-4-Met(O2),8-D-Lys, 9-Phe-ACTH4--9, a behaviorally potent analog of ACTH4--9. The 3H-peptide was injected into the lateral ventricle of hypophysectomized rats that were sacrificed 5, 30, 60, 180, and 240 min later. Dry-mount autoradiograms of brain showed the highest density of silver grains in the ventricular lumen and choroid plexus. In addition, radioactivity penetrated brain tissue as far as 100 microns from the ventricles, and was distributed predominantly over neuropil. Within 5 min after the injection, an intracellular concentration of radioactivity above background levels was observed in a small proportion of cells near the ventricles in the septum, caudate-putamen, preoptic area, hypothalamus, thalamus, amygdala, and hippocampus. The cellular labeling decreased in intensity at greater distances from the injection site and at longer survival intervals, and was no longer evident 4 hr after the injection. The labeled cells were usually small, dark, and often elongated, suggesting that ACTH peptides may act preferentially upon a morphologically distinct class of cells in the brain.
Adrenocorticotropic Hormone↗
Hyperthermic response of the cat to intraventricular injection of the opioid delta-receptor agonist D-Ala2-D-Leu5-enkephalin.
The delta opioid receptor agonist D-Ala2-D-Leu5-enkephalin was injected into the third cerebral ventricle of cats to determine its effects on core temperature for comparison with other peptide and non-peptide opioids that act on a variety of receptors to alter thermoregulation. Like other opioid peptides that have been studied in this species, D-Ala2-D-Leu5-enkephalin (5-25 micrograms) induced a dose-related hyperthermia. This response was undiminished in cats tolerant to morphine and was found to consist of two components. One component of the hyperthermic response was inhibited by pretreatment with low doses of opioid antagonists (25 micrograms naloxone; 5-15 micrograms naltrexone) and may be mediated by the v2-receptor that mediates this response to D-Ala2-Met-enkephalinamide. The other component, which was prevented by 100 micrograms naltrexone but still only partially inhibited by 250 micrograms naloxone, is attributed to delta-receptor stimulation. In tests over a range of environmental temperatures, the hyperthermic response to 10 micrograms D-Ala2-D-Leu5-enkephalin was less in a 4 degrees C environment than at the usual laboratory temperature of 22 degrees C. Responses in 22 and 34 degrees C environments were similar. No increase in respiratory rate occurred to indicate activation of compensatory heat-loss mechanisms so that the hyperthermia was indicative of an increase in the level about which body temperature is regulated.
Animals↗
Cardiovascular effects of intraventricular injection of FMRFamide, Met-enkephalin and their common analogues in the rat.
The molluscan neuropeptide, Phe-Met-Arg-Phe-NH2 (FMRFamide), the mammalian opioid peptide met-enkephalin, and their common analogues, met-enkephalin-Arg6-Phe7 (YGGFMRF) and Tyr-Gly-Gly-Phe-Met-Arg-Phe-amide (YGGFMRFamide), were injected into the lateral ventricle of the rat; the cardiovascular effects were studied. FMRFamide caused a rapid, transient elevation in blood pressure accompanied by a great increase in pulse pressure. These effects were followed by secondary increases in blood and pulse pressures. Met-enkephalin produced an initial reduction in blood pressure which was followed by a gradual increase at the higher of two test doses (300 nmole). Injection of YGGFMRF resulted in a gradual increase in blood pressure. This response resembled that to met-enkephalin. The initial response to YGGFMRFamide was similar to that to FMRFamide: increases in both blood and pulse pressures after injection. However, the secondary effect of YGGFMRFamide, a prolonged reduction in blood pressure, was not produced by FMRFamide. These results suggest that the initial excitatory cardiovascular responses may be due to the presence of the C-terminal amide. All of the cardiovascular effects of injecting these peptides into the lateral ventricle were abolished by pre-treatment with naloxone in a dose that, itself, produced no cardiovascular changes. In conclusion, these peptides seem to act via the naloxone sensitive opiate receptors in the rat brain.
Animals↗
Sequence of forebrain activation induced by intraventricular injection of hypertonic NaCl detected by Mn2+ contrasted T1-weighted MRI.
In order to define the sequence of forebrain activation involved in osmoregulation, central activation in response to intracerebroventricular injection of NaCl solution (10 microl of 0.15, 0.5, or 1.5 M) was detected using manganese-contrasted magnetic resonance imaging (MRI) in anesthetized rats. Changes in renal sympathetic nerve activity (RNA) were also measured, and the time courses of forebrain activation and RNA changes compared. NaCl injection resulted in rapid activation of the subfornical organ (SFO), organum vasculosum lamina terminalis (OVLT), and periventricular regions and the lateral hypothalamic area (LHA), then of the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON). The delay in activation in the PVN and SON showed a wide variation from 0 to 5.78 min, and the average delay in the PVN (2.88+/-0.34 min) and SON (2.90+/-0.39 min) was significantly greater than that in the SFO (0.40+/-0.10 min) and OVLT (0.74+/-0.13 min). NaCl (1.5 M) injection elicited a rapid, large increase in RNA, which consisted of two components, an early rapid increase at 99 s after injection (160+/-27%) and a slower increase at 9 min after injection (209+/-34%). These results suggest that the PVN and SON are activated not only by the afferent input from the SFO and OVLT but also by diffusion of the hypertonic stimulus to these regions and probably by their intrinsic osmosensitivity. The PVN might be responsible for the second slower component of the RNA response, but cannot be responsible for the first component.
Animals↗
Locomotor effects of ethanol and acetaldehyde after peripheral and intraventricular injections in Swiss and C57BL/6J mice.
Several studies have suggested that acetaldehyde, the first product of ethanol metabolism, is involved in the locomotor stimulant effects of ethanol in mice, although it has never been formally tested whether acetaldehyde injected directly into the brain of mice has stimulant properties. Recently, it was also shown in rats that both ethanol and acetaldehyde can induce opposite locomotor effects according to the route of administration. Whereas peripheral administrations of ethanol and acetaldehyde induced locomotor depressant effects, their infusions directly into the brain produced locomotor stimulation. The aim of the present study was to characterize in mice the locomotor effects of ethanol and acetaldehyde injected either peripherally by the intraperitoneal route or centrally into the brain ventricles. Additionally, the effects of ethanol and acetaldehyde were compared in two strains of mice known for their differential sensitivity to the locomotor effects of ethanol, namely Swiss and C57BL/6J mice. Ethanol induced a biphasic effect on locomotor activity in Swiss mice, with stimulant effects at low to moderate doses and depressant effects at higher doses. Such a profile of effects was observed whatever the route of administration, peripheral or central. In C57BL/6J mice, ethanol only induced monophasic depressant effects. In this mouse strain, no evidence of the stimulant effects of ethanol was found after either an i.p. or an i.c.v. administration of ethanol. In contrast to ethanol, acetaldehyde yielded only depressant effects in both strains of mice after both peripheral and central administrations. These results indicate that the route of administration does not alter the locomotor effects of ethanol and acetaldehyde in mice. Additionally, the present study shows that the stimulant properties of acetaldehyde, even after direct infusion into the brain, are not as obvious as previously speculated.
Acetaldehyde↗
Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain.
To study the role of neurotrophin-responsive neurons in brain growth and developmental resistance to seizure-induced injury, we infused saporin-conjugated 192-IgG (192 IgG-saporin), a monoclonal antibody directed at the P75 neurotrophin receptors (p75(NTR)), into the ventricles of postnatal day 8 (P8) rat pups. 7-10 days after immunotoxin treatment, loss of p75(NTR) immunoreactivity was associated with depletion of basal forebrain cholinergic projection to the neocortex and hippocampus. Kainic acid (KA)-induced seizures on P15 resulted in hippocampal neuronal injury in the majority of toxin-treated animals (13/16), but only rarely in saline-injected controls (2/25) (P < 0.001). In addition, widespread cerebral atrophy and a significant decrease in brain weight with preserved body weight were observed. Volumetric analysis of the hippocampal hilar region revealed a 2-fold reduction in perikaryal size and a 1.7-fold increase in cell packing density after 192 IgG-saporin injection. These observations indicate that neurotrophin-responsive neurons including basal forebrain magnocellular cholinergic neurons may be critical for normal brain growth and play a protective role in preventing excitotoxic neuronal injury during development.
Animals↗
Loss of striatal dopaminergic fibers after intraventricular injection of tetrahydrobiopterin in rat brain.
We have reported previously that tetrahydrobiopterin (BH4), an obligatory cofactor for dopamine synthesis, exerts preferential toxicity on dopamine producing cells. We report in the present study that BH4 injection into the lateral ventricle leads to degeneration of the dopaminergic terminals in the striatum, evidenced by a loss of tyrosine hydroxylase (TH) immunopositive fibers, a decreased amount of TH protein, and decreased dopamine content. Thus, the results of our study further provide evidence that BH4, the molecule endogenously present in the dopaminergic neurons, may participate in the nigrostriatal degeneration as in Parkinson's disease.
Animals↗
Induction of cerebrospinal fluid eosinophilia in rats by the intraventricular injection of Angiostrongylus cantonensis antigen.
Resistance to Angiostrongylus cantonensis is contingent upon the generation of an eosinophilic response in the CSF of infected hosts. We have studied the parameters required for the generation of this CSF eosinophilia in normally permissive rats. We initially induced a marked peripheral eosinophilia in rats by infection with either Mesocestoides corti or Angiostrongylus cantonensis or the surgical transfer of A. cantonensis young adult worms (YA) into their pulmonary arteries. Next, we injected various antigens into the ventricles of these rats. A. cantonensis-preinfected rats demonstrated significant CSF eosinophilia following injection of A. cantonensis egg antigen, 1st-stage larval (L1) antigen, or M. corti antigen, but not following YA antigen inoculation. A. cantonensis egg and M. corti antigens were potent chemoattractants for eosinophils in an in vitro chemotaxis assay. These data indicate that peripheral eosinophilia, meningeal stimulation by A. cantonensis infection and the presence of potent chemoattractants, e.g., egg and L1 antigens are prerequisites for CSF eosinophil accumulation in permissive rat hosts.
Angiostrongylus cantonensis↗
Repeated intraventricular injections of ACTH 1-24: the effects of home or novel environments on excessive grooming.
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Adrenocorticotropic Hormone↗
Intraventricular injection of neuropeptide Y antisera curbs weight gain and feeding, and increases the display of sexual behaviors in obese Zucker female rats.
Obese Zucker rats are hyperphagic, overweight, and infertile. It has been postulated that neuropeptide Y (NPY) overproduction may contribute to obesity and infertility in these animals. To test this hypothesis, ovariectomized, adult obese Zucker rats were implanted with cannulae in the third ventricle and subsequently injected with NPY antisera or normal rabbit sera (NRS) 6, 4 and 2 h before experimental observation. Steroid-treated females injected with NPY antisera were significantly more receptive and were more likely to show proceptive behaviors than after treatment with NRS (e.g., lordosis quotient: NPY antisera, 65.5+/-6.9%; NRS, 30.9+/-11.6%, P < 0.02; 91% displaying proceptivity after NPY antisera injection vs. 36% after NRS, P < 0.03). Injection of NPY antisera also curbed food intake and weight gain (24 h food intake: NPY antisera, 10.5+/-2.1 g; NRS, 20.5+/-1.7 g, P < 0.01; 24 h weight gain: NPY antisera, -5.4+/-2.2 g; NRS, 5.8+/-0.7 g, P < 0.01). Locomotor activity was similar after NRS and NPY antisera treatment (P > 0.5) suggesting that general malaise was not responsible for the effects of NPY antisera on food intake or body weight. These data suggest that endogenous neuropeptide Y contributes to excessive feeding and weight gain, and suppressed reproductive behaviors in obese Zucker female rats.
Animals↗
Pressor-depressor blood pressure responses in the cat after intraventricular injection of drugs.
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Animals↗