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In rats dehydrated for 48 h and injected intraventricularly with L-cysteine-35S-hydrochloride, the specific activity of TCA-precipitable material, both in the hypothalamus and neurohypophysis, was found to diminish under reserpine treatment.
Ricin, a protein from the seeds of Ricinus communis which inhibits protein synthesis by eukaryotic ribosomes, is highly toxic when injected intraventricularly to rats, the LD50 being 0.241 micrograms/rat at 72 hr and 0.084 micrograms/rat at 7 days. Poisoned animals showed signs of central depression; they did not die before 20 hr of intoxication. Incorporation of amino acids in vivo into brain total protein and into brain ribosomes was impaired, as was protein synthesis in vitro by microsomes isolated from the brain of poisoned rats.
A peptide material with opiate-like activity in the guinea-pig ileum was extracted from porcine pituitaries using a hot glacial acetic acid extraction method and was partially purified by gel filtration. When injected intraventricularly in rats, these purified peptides induced strong analgesia, catelepsy, respiratory depression and other opiate-like effects, which lasted for several hours.
Glutamate and GABA content in different regions of adult female rat brain were determined at 10 and 30 min following intraventricular injection of LHRH or somatostatin. Cerebral cortex, cerebellar and hypothalamic glutamate levels were significantly elevated at 30 min following injection of 1 micrograms somatostatin, whereas hypothalamic glutamate levels were elevated at 10 min following a 0.5 micrograms dose. LHRH at a dose of 1 micrograms elevated cerebellar and brain stem glutamate levels at 10 and 30 min, whereas a 0.5 micrograms dose significantly elevated cerebral cortex, cerebellar and hypothalamic glutamate levels at 30 min. Third ventricular injection of 1 micrograms somatostatin produced a significant decrease in hypothalamic GABA levels at 10 and 30 min, whereas a 0.5-microgram dose decreased brain stem GABA levels at 10 min. LHRH at a dose of 0.1 microgram significantly increased cerebral cortex and cerebellar GABA levels at 10 min and brain stem GABA levels at 10 and 30 min following injection. Intraventricular injection of LHRH at a dose of 0.5 microgram significantly elevated cerebral cortex, cerebellar and brain stem GABA levels at 30 min. Hypothalamic GABA levels were elevated at 10 and 30 min following 0.5 and 1 microgram intraventricular LHRH injection. The implications of these results are discussed in relation to probable interaction between these neuroactive amino acids and neuropeptides in the rat brain.
1. Cholinergic synapses in the hypothalamus may transmit information in those thermoregulatory pathways which function to raise body temperature. The effect of atropine, administered intracranially, on the febrile response to intravenous leucocyte pyrogen or intracranial prostaglandin E1 was therefore examined in conscious rabbits. 2. In rabbits exposed to a thermoneutral environment, micro-injections of PGE1, into the anterior hypothalamus, intraventricular injections of PGE1, and intravenous injection so leucocyte pyrogen all caused fever accompanied by vasoconstriction in the ears and reduced respiratory rate. Intraventricular injection of 200 mug atropine during such fevers attenuated their development. This was due to the activation of heat loss mechanisms through vasodilatation in the ears and an increase in the frequency of respiration. This suggests a similarity in the pattern of neuronal activity evoked by PGE1 and leucocyte pyrogen, at least at the site(s) where atropine directly or indirectly exerted its effect and in the efferent pathways from this site. 3. In rabbits exposed to a cold environment, intraventricular injection of PGE1 caused fever through the activation of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shievering and a decrease in O2 consumption so that temperature ceased to rise and returned to normal. 4. During fever, reversal by atropine of the increased heat conservation of rabbits in a neutral environment, and of their increased heat production in a cold environment adds further support to the concept that cholinergic synapses provide an important link in central temperature-rasising pathways.
In adult fowls intravenous but not intraventricular injection of diazoxide produced hypotension and a rise in blood glucose concentration. Since noradrenaline microinfused into the hypothalamus produced a fall in blood pressure, it does not seem that hypotensive effects of diazoxide are mediated through release of noradrenaline in areas of the luain accessible from the ventriculus tertius cerebri. Present experiments also indicate that the hyperglycemic effects of diazoxide is unlikely to be due to an action on central adrenergic receptors.
Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light:dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of gamma-amino-butyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.
In rats, intraventricularly injected antimelatonin antibody caused the appearance of transitory epileptiform abnormalities. Epileptic activity arose from and was limited to the cortical mantle of the hemisphere ipsilateral to the injection side. The occasional occurrence of lateralized seizures has also been observed. Control injection of saline, of the vehicle (rabbit serum), or of antibody saturated with melatonin induced flattening and desynchronization of the electroencephalogram but not epileptiform activity. Repeated antimelatonin injections caused reappearance of the same type of epileptic abnormalities that lasted slightly longer than the first time. Melatonin may play an inhibitory role in neuronal excitability.
Intraventricular injection of 6-hydroxydopamine does not modify the states of alertness in the Kitten, if it is performed in the first week of postnatal life. At three weeks of age, it induces the same sleep impairments as those observed in the adult Cat. Therefore, in the immediate postnatal period, sleep control is not achieved through the monoaminergic systems.
The metabolism of connective tissue biopolymers in the blood serum and in the aorta under repeated intraventricular injections of P-substance, L-enkephalin and B-endorphine was studied in chronic experiments on rabbits. The alternations of the central neurochemical processes, caused by prolonged intraventricular injections of neuropeptides were proved to lead to intensification of metabolic processes in the connective tissue characterized by the accumulation of its biopolymers in the aorta wall. The injection of P-substance, in contrast to opioid peptides, is accompanied by more marked alternations.
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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.
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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.
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