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PubMed1984

Behavioural and electrocortical spectrum power changes after intraventricular injection of patulin in rats.

The effects of patulin when given into the third cerebral ventricle of rats, on behaviour and electrocortical spectrum power have been investigated. Patulin (10 micrograms i.v.t.) produced behavioural sedation, hypoalgesia, tail rigidity, piloerection and postural changes. This symptomatology lasted approx. 3 h and was accompanied by slower frequency and larger amplitude potentials in the electrocorticogram (ECoG) and by an increase in total voltage power. A larger dose (50 micrograms) produced a more dramatic picture characterized by catatonic posture with kyphosis, loss of the righting reflex, tail rigidity and on a few occasions short-duration episodes of tonic-clonic convulsions. Such a symptomatology was accompanied by a flattening of ECoG activity with a significant fall in total voltage power, as well as in preselected bands (0-3, 3-6, 6-9, 9-12, and 12-16 Hz). A lower dose (1 microgram) of patulin, on the other hand, produced behavioural sedation without significant changes in ECoG spectrum power.

Animals↗
PubMed1985

Substantial reduction of noradrenaline in kitten visual cortex by intraventricular injections of 6-hydroxydopamine does not always prevent ocular dominance shifts after monocular deprivation.

Ten kittens had cannulas inserted into their lateral ventricles for daily injections of 6-hydroxydopamine (6-OHDA). At 5-6 weeks of age one eye was sutured shut, and one week later recordings were made from the visual cortex to assay the ocular dominance of a sample of cells. In six kittens the injections of 6-OHDA were continued until the day before recording, while in four kittens the injections were stopped around the time of eye suture, on the assumption that continued injections of 6-OHDA over several days has effects that are not specific to the noradrenaline (NA) system and that the two procedures might show different results. In all animals the concentration of NA in the visual cortex near the site of recording was reduced by approximately 90%. In all animals the ocular dominance histograms recorded from the visual cortex were shifted so that the majority of cells (83 +/- 13%) were dominated by the open eye. There were no substantial differences between the two groups of experimental animals or between the experimental animals and two control animals that had cannulas implanted and ascorbate alone injected without 6-OHDA. We conclude that the concentration of NA in the visual cortex can be reduced substantially by injections of 6-OHDA into the lateral ventricle without preventing the shift in ocular dominance that usually occurs after suturing shut the eyelids of one eye.

Animals↗
PubMed1992

Distribution of intraventricularly injected horseradish peroxidase in cerebrospinal fluid compartments of the rat spinal cord.

The circulation of the cerebrospinal fluid along the central canal and its access to the parenchyma of the spinal cord of the rat have been analyzed by injection of horseradish peroxidase (HRP) into the lateral ventricle. Peroxidase was found throughout the central canal 13 min after injection, suggesting a rapid circulation of cerebrospinal fluid along the central canal of the rat spinal cord. It was cleared from the central canal within 2 h, in contrast with the situation in the brain tissue, where it remained in the periventricular areas for 4 h. In the central canal, HRP bound to Reissner's fiber and the luminal surface of the ependymal cells; it penetrated through the intercellular space of the ependymal lining, reached the subependymal neuropil, the basement membrane of local capillaries, and appeared in the lumen of endothelial pinocytotic vesicles. Furthermore, it accumulated in the labyrinths of the basement membrane contacting the basolateral aspect of the ependymal cells. In ependymocytes, HRP was found in single pinocytotic vesicles. The blood vessels supplying the spinal cord were classified into two types. Type-A vessels penetrated the spinal cord laterally and dorsally and displayed the tracer along their external wall as far as the gray matter. Type-B vessels intruded into the spinal cord from the medial ventral sulcus and occupied the anterior commissure of the gray matter, approaching the central canal. They represented the only vessels marked by HRP along their course through the gray matter. HRP spread from the wall of type-B vessels, labeling the labyrinths, the intercellular space of the ependymal lining, and the lumen of the central canal. This suggests a communication between the central canal and the outer cerebrospinal fluid space, at the level of the medial ventral sulcus, via the intercellular spaces, the perivascular basement membrane and its labyrinthine extensions.

Animals↗
PubMed1982

Accumulation, elimination, release and metabolism of pipecolic acid in the mouse brain following intraventricular injection.

Following i.c.v. (intracerebral ventricular) injections of D,L-[3H]pipecolic acid (PA), it is reabsorbed from the ventricles and redistributed to various brain regions. The highest accumulation is found in three brain regions ipsilateral to the injection site, hippocampus, neocortex, striatum, and in the diencephalon. Following preloading in vivo, the radioactivity is released from hippocampus slices in the perfusion medium after depolarization induced by high K+. During perfusion with a Ca++ free medium containing EGTA, a significant reduction of release is observed. The radioactivity of D,L-[3H]PA in the brain shows a more rapid phase of decrease from 0 to 2 hours and a slower phase from 2 to 5 hours. At 5 hours, only 28% radioactivity, represented mainly by PA, is left in the brain. Kidney secretion represents the major route of elimination of the injected PA. The presence of alpha-aminoadipic acid both in brain and urine was observed. Probenecid (200 mg/kg) significantly increases the accumulation of i.c.v. injected D,L-[3H]PA in brain and kidney. The presence of a regional accumulation of PA in certain brain regions, its metabolism in brain, its enhanced retention following probenecid administration and its Ca++ dependent release following high K+ stimulation, all constitute indirect evidence for a neuronal localization of this brain endogenous aminoacid.

Animals↗
PubMed1997

Intraventricular injection of NGF, but not BDNF, induces rapid motor activation that is inhibited by nicotinic receptor antagonists.

The acute and subacute effects of intracerebroventricularly (ICV) administered nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF) on locomotor activity were evaluated in awake adult rats. Immediately after ICV injection through an implanted cannula, locomotor activity was measured by a computerized system using infrared photocells, which allowed us to record locomotion, motility, and rearing simultaneously. A single dose of 5 microg mouse beta-NGF produced significant increases in horizontal ambulatory components of locomotor activity (locomotion and motility), but not vertical movement (rearing) 30-45 min after ICV administration. These increases lasted for at least 3-4 h. Systemic injection of 2.0 mg/kg mecamylamine, a central nicotinic receptor antagonist, inhibited the hyperactivity induced by NGF. Systemic injection of 0.5 mg/kg scopolamine, a muscarinic receptor antagonist, did not interfere with the NGF effects. Thus, while scopolamine induced marked increases in all three measures of behavior in both NGF and cytochrome-c-treated animals, locomotion and motility remained significantly higher in the NGF group. Immunohistochemistry demonstrated that NGF diffused readily from the ventricular space into brain parenchyma on the injected side and could be visualized 1 h after ICV injection. These results suggest that ICV administration of NGF increases locomotor activity by inducing acetylcholine release, and that nicotinic receptors are involved in the hyperactivity induced by NGF. ICV administration of 5 microg recombinant human BDNF had no significant effect on locomotor activity during the 0- to 4-h period after ICV injection. However, it produced significant decreases in locomotion, motility, and rearing 24-26 h later. Hence ICV administration of BDNF has entirely different effects on animal behavior from those evoked by NGF. While NGF elicits increases in ambulatory behavior within hours, BDNF causes delayed decreases in ambulatory behavior.

Animals↗
PubMed1977

Specific uptake of a behaviorally potent [3H]ACTH4-9 analog in the septal area after intraventricular injection in rats.

Distribution within the brain of a behaviorally potent [3H]ACTH4-9 analog 2 h after intraventricular injection in rats was studied in the presence and absence of behaviorally and structurally similar peptides, to explore the significance of earlier found preferential uptake of the [3H]ACTH4-9 analog in the septal area. Hypophysectomy resulted in significantly enhanced uptake of radioactivity in the septum as compared to normal rats. No increase in this brain area of hypophysectomized rats was observed after intraventricular injection of [3H]Phe. Elevated circulating ACTH levels after adrenalectomy seemed too low to compete with the septal uptake of the ACTH4-9 analong. Subcutaneous substitution of hypophysectomized rats with sustained release zinc phosphate preparations of the behaviorally equipotent peptides ACTH1-24 and ACTH4-10 decreased the accumulation of the [3H]ACTH4-9 analog in the septum, whereas treatment with the behaviorally inactive fragment ACTH11-24 is not effective. Retreatment of hypophysectomized rats with neuropeptides, differing structurally from natural ACTH peptides (7-D-Phe-ACTH4-10, BETA-LPH61-76 and 9-desglycinamide, 8-Lys-vasopressin), did not change the uptake of the ACTH4-9 analog in any of the investigated brain areas. These results give evidence for specific uptake of the ACTH4-9 analog in the septal region, because competitive displacement occurs only with peptides which both behaviorally and structurally are closely related to the ACTH4-9 analog.

Adrenalectomy↗
PubMed1981

Formation and degradation of deamido-TRH (pyroglutamyl-histidyl-proline) in rat brain after intraventricular injection of TRH.

Thyrotropin-releasing hormone (TRH) injected into the lateral ventricle of the rat's brain was rapidly metabolized to deamido-TRH (DA-TRH). Brain levels of TRH decreased with a half-life of 7 min, while the DA-TRH formed from its disappeared with a half-life of 2.5 min. To prevent the post-mortem degradation of DA-TRH it was necessary to sacrifice rats by directing focused microwave irradiation towards the brain. The short half-lives determined for TRH and DA-TRH in vivo were much shorter than those obtained using in vitro techniques. The in vivo formation and accumulation of DA-TRH was inhibited by bacitracin and unaffected by probenicid.

Animals↗
PubMed1983

Reduced hypothalamic thermosensitivity following intraventricular injection of pyrogen in conscious rabbits.

Hypothalamic temperature thresholds for vasodilatory and respiratory reactions were determined before and after i.c.v. injection of pyrogen in rabbits. During the rising phase of fever the increases in the hypothalamic thresholds for vasodilatory and respiratory reactions differed from those found in the pre-pyrogen preoptic anterior hypothalamic area (POAH) heating by 2.1 +/- 0.2 degrees C and 1.89 +/- 0.31 degrees C, respectively. During the plateau phase of fever the threshold for vasodilatory reaction was further increased (by 0.7 +/- 0.23 degrees C), whereas that for panting remained at the same level. It is concluded that pyrogen exerts a depressive action on POAH thermosensitivity.

Animals↗