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PubMed1971

Effects of adrenoceptor blocking agents on body temperature.

1. The effect on rectal temperature of adrenoceptor blocking agents, injected through a cannula chronically implanted into a lateral cerebral ventricle, was examined in unanaesthetized rabbits, cats and rats, kept at room temperature (19-22 degrees C).2. In rabbits, the alpha-adrenoceptor blocking agent phenoxybenzamine (50 or 100 mug) produced marked hypothermia when injected intraventricularly but not when injected intravenously. In some rabbits as little as 1 mug was effective on intraventricular injection. Phentolamine and ergotamine, the other alpha-adrenoceptor blocking agents examined, had a much weaker hypothermic action when injected intraventricularly, whereas the beta-adrenoceptor blocking agents propranolol, pronethalol and Trasicor had no effect.3. In rabbits in which the noradrenaline stores of the hypothalamus were depleted by intraventricular injections of reserpine, the hypothermic effect of phenoxybenzamine was abolished and remained abolished for a few days.4. In cats, an intraventricular injection of phenoxybenzamine (200 mug) produced long-lasting hyperthermia, but not in all cats, and only with the first, or the first two or three injections. Injected intraperitoneally, this dose had no effect on temperature. Phentolamine (100 or 200 mug) had a very weak hyperthermic effect and phentolamine (500 mug), a hypothermic effect, but only on intraventricular injection, whereas ergotamine (100 and 200 mug) had a weak hyperthermic effect both on intraventricular and intraperitoneal injection. Propranolol and Trasicor had no effect on temperature when injected intraventricularly.5. In rats, phenoxybenzamine (5 or 20 mug) produced long-lasting hypothermia on intraventricular injection.6. Some of the temperature effects produced by intraventricular injections of the alpha-adrenoceptor blocking agents are explained on the assumption that they prevent the effect on temperature produced by a continuous release of noradrenaline from adrenergic neurones innervating the anterior hypothalamus.

Amino Alcohols↗
PubMed1978

Modulation of acetylcholine metabolism in the hippocampal cholinergic pathway by intraseptally injected substance P.

Intraventricular injection of substance P induced a dose-dependent decrease of acetylcholine (ACh) turnover rate (TRACh) in the hippocampus of rats. The highest dose used (20 nmol) decreased the hippocampal TRACh to 40% of the control value. No changes in the ACh or choline content were detected in the various brain areas 40 minutes after injection, but after 70 minutes an increase in ACh content in diencephalon was significant. Local injection of substance P into the medial nuclei of the septum decreased significantly the hippocampal TRACh. Neither intraventricular injection nor injection into the periaqueductal grey of high doses of substance P (30 nmol) induced analgesia, whereas beta-endorphin (1 nmol) and morphine (15 nmol) were effective. No specific change in the electroencephalograph pattern recorded from either cortex or hippocampus could be detected within the first 2 hours after intraventricular injection of substance P.

Acetylcholine↗
PubMed1971

Hypothermia produced in mice by histamine acting on the central nervous system.

1. In mice 1-10 mug histamine injected intraventricularly produces hypothermia.2. This hypothermia was not antagonized by chlorcyclizine administered subcutaneously or intraventricularly, but chlorcyclizine injected intraventricularly was effective in antagonizing the hypothermia produced by a subcutaneous injection of histamine.3. Pretreatment with atropine was without effect on the hypothermia produced by an intraventricular injection of 10 mug histamine.4. Amphetamine and tranylcypromine not only effectively reduced the intensity of, or abolished, the hypothermia but also reversed the response to an intraventricular injection of 10 mug histamine so that hyperthermia was produced. Pargyline was without effect.5. Tolazoline strongly potentiated the hypothermia produced by the intraventricular injection of 10 mug histamine, but phentolamine did not.6. It is concluded that at least part of the hypothermia produced by a subcutaneous injection of histamine arises as a result of an action on the central nervous system.7. The possible mechanisms by which histamine acting on the central nervous system produces hypothermia and the suggestion that histamine may have a physiological role in thermoregulation are discussed in the light of these findings.

Amphetamine↗
PubMed1975

Transport of thyrotropin-releasing hormone from cerebrospinal fluid to hypophysial portal blood and the release of thyrotropin.

The capacity of the medium eminence to transport thyrotropin-releasing hormone (TRH) from cerebrospinal fluid (CSF) to hypophysial portal blood, and the ability of TRH when introduced into a lateral ventricle to stimulate TSH release from the pituitary gland were investigated. Male rats were injected either intraventricularly or intravenously with 0, 1, 10, or 100 ng of TRH, and plasma TSH concentrations were determined at various times thereafter. TRH administration via both routes resulted in substantial release of TSH. Following intraventricular injection of TRH, there was a delay in reached maximal TSH concentration when compared with the faster elevation and faster decline in TSH concentrations which followed intravenous injection of the same dose of TRH. In a second experiment, 7 muCi of [3H]TRH were introduced intraventricularly or intravenously, and hypophysial portal and arterial blood were simultaneously collected and examined for the presence of radioactivity. The intraventricular injection of [3H]TRH resulted in a peak of radioactivity in portal blood within minutes, which was maintained for 20--30 min and then declined. The concentration of radioactivity in arterial blood from the same animals was considerably lower than that in portal blood. The intravenous administration of [3H]TRH resulted in radioactive peaks in both portal and arterial blood with a higher concentration of radioactive substances in arterial blood. However, the level of radioactivity in portal blood following intravenous injection of [3H]TRH comprised no more than 5--10% of that found following intraventricular administration of the saem dose. The data support the view that TRH is able to cross the medium eminence from CSF into hypophysial portal blood and that it is capable of stimulating the pituitary gland to release TSH.

Animals↗
PubMed1991

Levels of morphine and metabolites in CSF during respiratory depression after intraventricular morphine injection.

We report a case of respiratory depression after intracerebroventricular morphine administration of a dose inadvertently 10 times greater than the typical daily dose. At the time of the respiratory dysfunction, the concentrations of morphine and its metabolites in cerebrospinal fluid (CSF) and plasma samples were determined. On comparison of these results with previous clinical studies in which there was no respiratory depression, no relationship was found between the occurrence of respiratory depression and the concentration of morphine or its metabolites in the CSF. The occurrence and characteristics of respiratory depression may be related to the concentrations of morphine and its metabolites in bulbar tissue.

Adenocarcinoma↗
PubMed1988

Memory enhancement with posttraining intraventricular glucose injections in rats.

Recent findings suggest that peripheral epinephrine enhancement of memory storage may be mediated in part by an increase in circulating glucose levels subsequent to epinephrine release or injection. Because glucose, unlike epinephrine, has ready access to the central nervous system, it is possible that glucose acts directly on central processes to enhance memory. To test this possibility, rats were trained on a one-trial inhibitory avoidance task and received immediate or delayed injections of glucose in artificial cerebrospinal fluid. On retention tests 24 hr after training, animals that received 3 or 5 micrograms glucose (in 1 microl cerebrospinal fluid over 3 min) had significantly enhanced performance of the learned response. These findings are consistent with the view that glucose can regulate the storage of new information by acting on central processes. Whether there are additional peripheral contributions to glucose effects on memory remains to be determined.

Animals↗
PubMed2004

Life span extension and reduced neuronal death after weekly intraventricular cyclosporin injections in the G93A transgenic mouse model of amyotrophic lateral sclerosis.

OBJECT: The authors investigated whether cyclosporin A (CsA), a cyclophilin ligand with mitochondrial permeability transition pore-blocking and calcineurin-inhibiting properties, affects motor function, neuronal death, and life span in the G93A transgenic mouse model of familial amyotrophic lateral sclerosis (FALS). METHODS: The G93A mice received weekly intracerebroventricular injections of CsA (20 microg/mouse/week) starting at the age of 65 days, and physical performance on an exercise wheel was monitored beginning at 84 days of age. Mice were allowed to survive for clinical observation of body weight, hindlimb weakness, and life span or until a defined end stage or were killed at 110 days of age for histological analysis. CONCLUSIONS: Treatment with CsA significantly delayed the onset of hindlimb weakness and also extended the time from its onset to paralysis. The overall life span of CsA-treated G93A mice was significantly extended, by 12% compared with vehicle-treated transgenic littermates. The CsA also prolonged physical performance on the exercise wheel and delayed weight loss. Histologically, there was significant preservation of both cervical and lumbar spine motor neurons and also tyrosine hydroxylase-positive dopaminergic substantia nigra neurons in 110-day-old CsA-treated mice compared with their transgenic littermates. The local administration of CsA directly into the brain ventricles is an effective means of central nervous system drug delivery (because CsA does not readily cross the blood-brain barrier), which in this study ameliorated clinical and neuropathological features of FALS in G93A mice. The remarkably low intrathecal CsA dose required for neuroprotection reduces potential adverse effects of systemic immunosuppression or nephrotoxicity seen with chronic systemic delivery of the drug.

Age Factors↗
PubMed1990

[Effects of extracts of different parts of the brain of kindled animals on seizure activity of recipient rats].

The peptide-containing fraction was emitted from the hippocampal and ventral mesencephalic region tissue of rats kindled with subconvulsant doses of corazol. Extracts were prepared by the help of hot acetic acid on the stage of generalized clonic-tonic seizure development. The intraventricular injection of VMR-extracts in relatively high dose increased seizure reactions which were induced in intact recipient rats by intraperitoneal corazol injection. The intraventricular injection of the extract in relatively low dose (100 times less) suppressed corazol-induced seizures in recipients. Data are discussed from the point of view of pathological epileptic system formation and the role played by peptides in supporting it's activity during pharmacological kindling.

Animals↗
PubMed1979

Effects of cerebral intraventricular magnesium injections and a low magnesium diet on nonspecific excitability level, audiogenic seizure susceptibility and serotonin.

Cerebral intraventricular injections of 17 and 50 microgram magnesium in artificial cerebrospinal fluid progressively depressed the Non-specific Excitability Level of permanently cannulated 150--200 g rats fed a low magnesium diet for 21 days. Compared with control diet, a low Mg diet caused an increase in brain serotonin. Weanling rats fed a low Mg diet for 2 weeks, then injected with 25 microgram Mg via acute cannulations, displayed reduced audiogenic seizure susceptibility compared with sham-injected controls.

Acoustic Stimulation↗
PubMed1988

The role of M2 muscarinic receptors in the posterior hypothalamus in the pressor response to intracerebroventricularly-injected neostigmine.

Injection of neostigmine into the lateral cerebral ventricle of urethane-anesthetized rats increases arterial blood pressure. Prior injection of atropine or the muscarinic M2 antagonist 4-DAMP into the posterior hypothalamic nuclei inhibited the pressor response to neostigmine by up to approximately 56%. The same maximum degree of inhibition was elicited by bilateral electrical lesions of the posterior hypothalamic nuclei. The response was not modified by intrahypothalamic injection of pirenzepine or intraventricular injection of hexamethonium, but was prevented by intraventricular injection of 4-DAMP. The results indicate that about half of the pressor response to intraventricular injection of neostigmine was mediated through M2 muscarinic receptors in the posterior hypothalamic nuclei, and the remainder through M2 muscarinic receptors in other regions of the brain.

Animals↗
PubMed1975

[Role of brain biogenic amines in the central thermoregulatory mechanism of the rat (author's transl)].

Changes in rectal and skin temperatures following intraventricular injection of biogenic amines and related substances were investigated in rats. Intraventricular injection of norepinephrine in a small dose (6 mug) produced a slight elevation of rectal temperature, but in larger amounts (25-50 mug) resulted in a dose-dependent hypothermia which was associated with a marked rise of skin temperature. No change was observed in plasma free fatty acid and glucose levels and oxygen consumption after intraventricular injection of norepinephrine (25 mug). Intraventricular injection of imipramine and safrazine produced a slight fall in the rectal temperature. Norepinephrine-induced hypothermia was more pronounced in rats pretreated with safrazine and less in rats pretreated with alpha-methyl-p-tyrosine, as compared with that in controls. Intraventricular injection of 6-hydroxydopamine (0.75-250 mug) brought about a marked dose-dependent hypothermia. The second injection of 6-hydroxydopamine 5 days after the first injection had no effect on the body temperature. Norepinephrine injection 2 days after the second injection of 6-hydroxydopamine produced a more pronounced hypothermia than the change in control rats without pretreatments. Haloperidol did not affect the hypothermia induced by 6-hydroxydopamine. Intraventricular injection of dopamine and L-DOPA showed less effect that norepinephrine had. Intraventricular injection of phenoxybenzamine prior to norepinephrine blocked the hypothermia and skin temperature elevation which are normally observed following norepinephrine injection, while propranolol given in the same way showed less or no effect. Intraventricular injection of phenylephrine produced a dose-dependent hypothermia, whereas no dose-response relationship was obtained by isoproterenol. These results suggest that in the rat the hypothermic effect of norepinephrine injected intraventricularly is mediated by an action of central alpha-receptor. At high and low ambient temperatures hypothermia was similarly observed following intraventricular injection of 5-hydroxytryptamine (25 mug) as at normal room temperature. On the other hand, norepinephrine (25 mug) produced a rise in rectal temperature at high ambient temperature and a marked fall at low ambient temperature. The hypothermic effect of norepinephrine was not different between cold-adapted ones at room temperature. From the results the role of norepinephrine and other biogenic amines in the brain in thermoregulatory processes was discussed.

Adaptation, Physiological↗
PubMed1991

Receptor-mediated retrograde transport in CNS neurons after intraventricular administration of NGF and growth factors.

Radiolabel tracer techniques were used to follow the distribution of nerve growth factor (NGF) and other neuromodulatory factors after intraventricular injection. Autoradiography showed that shortly after intraventricular injection of radio-iodinated NGF (125I-NGF), substantial amounts of radioactivity had penetrated the ventricular wall surfaces; this binding was transient and nonspecific. The 125I-NGF was progressively cleared from the central nervous system (CNS), presumably via the flow of cerebrospinal fluid (CSF) into the blood. A relatively small proportion of the injected 125I-NGF was taken up by NGF receptor-positive neurons in the CNS. Retrograde accumulation of radiolabel was observed within the basal forebrain cholinergic neurons at 5 hours after intraventricular injection. Labeling intensity was maximal at 18 hours and much reduced by 30 hours. This labeling was blocked by co-injection of an excess of unlabeled NGF. Specific and saturable retrograde labeling was also observed within other NGF receptor-bearing neurons, including the prepositus hypoglossal nucleus and the raphe obscurus nucleus. When epidermal growth factor (EGF), transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-AA (PDGF-AA), PDGF-BB, leukemia inhibitory factor (LIF), insulin-like growth factor-I (IGF-I), or IGF-II was radiolabeled and injected intraventricularly, specific labeling of neurons was observed for 125I-IGF-II and 125I-LIF within separate subpopulations of the dorsal and medial raphe. No retrograde accumulation within neurons was observed for EGF, TGF-beta 1, PDGF-AA, PDGF-BB, or IGF-I. This study describes an in vivo method for identifying putative neuromodulatory factors and their responsive neurons.

Animals↗
PubMed1987

The effects of the cholecystokinin antagonist, proglumide, on prolactin secretion in the rat.

Since cholecystokinin produced important effects on prolactin secretion following its intraventricular injection in ovariectomized rats, we have evaluated the effects of the cholecystokinin antagonist, proglumide, to assess the physiologic significance of CCK in the control of prolactin release. Conscious rats of either sex were used following implantation of third ventricular and/or intravenous cannulae for the administration of proglumide. Blood samples were drawn from conscious animals at various times after injection of the compound. Intraventricular injection of 1 or 10 micrograms of proglumide produced a dramatic decline in plasma prolactin levels in either castrate or intact male rats. Similar results were found following the intravenous injection of 10 or 100 micrograms of the drug. These results contrasted sharply with the findings in ovariectomized females in which the intraventricular injection of the same two doses of proglumide used in males produced a dose-related elevation of prolactin which was opposite to the delayed lowering of prolactin following the intravenous injection of the same doses of the compound used in males. These results indicate that proglumide can lower prolactin in male rats and suggests a physiologically significant role of CCK in the control of prolactin secretion in the male. There appears to be a sex difference in the response since the results contrasted sharply in ovariectomized female rats. The results in the females are puzzling and it is apparent that further studies are needed to determine whether or not CCK has a physiologically significant role to play in prolactin secretion in the female. Since previous results have shown that CCK has no effect on the release of prolactin by the pituitary directly these interactions are presumably taking place in the hypothalamus.

Animals↗
PubMed2003

Intraventricular brain injection of adeno-associated virus type 1 (AAV1) in neonatal mice results in complementary patterns of neuronal transduction to AAV2 and total long-term correction of storage lesions in the brains of beta-glucuronidase-deficient mice.

Inherited metabolic disorders that affect the central nervous system typically result in pathology throughout the brain; thus, gene therapy strategies need to achieve widespread delivery. We previously found that although intraventricular injection of the neonatal mouse brain with adeno-associated virus serotype 2 (AAV2) results in dispersed gene delivery, many brain structures were poorly transduced. This limitation may be overcome by using different AAV serotypes because the capsid proteins use different cellular receptors for entry, which may allow enhanced global targeting of the brain. We tested this with AAV1 and AAV5 vectors. AAV5 showed very limited brain transduction after neonatal injection, even though it has different transduction patterns than AAV2 in adult brain injections. In contrast, AAV1 vectors, which have not been tested in the brain, showed robust widespread transduction. Complementary patterns of transduction between AAV1 and AAV2 were established and maintained in the adult brain after neonatal injection. In the majority of structures, AAV1 transduced many more cells than AAV2. Both vectors transduced mostly neurons, indicating that differential expression of receptors on the surfaces of neurons occurs in the developing brain. The number of cells positive for a vector-encoded secreted enzyme (beta-glucuronidase) was notably greater and more widespread in AAV1-injected brains. A comprehensive analysis of AAV1-treated brains from beta-glucuronidase-deficient mice (mucopolysaccharidosis type VII) showed complete reversal of pathology in all areas of the brain for at least 1 year, demonstrating that the combination of this serotype and experimental strategy is therapeutically effective for treating global neurometabolic disorders.

Animals↗