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PubMed1991

Comparative study of certain antibiotics on epileptogenic property, including (1Rpi, 5S, 6S)-2-[(6,7-dihydro-5H-pyrazolo[1,2-a][1,2,4]triazolium-6-yl)] thio-6-[(R)-1-hydroxyethyl]-1-methyl-carbapenem-3-carboxylate (LJC10627), a carbapenem antibiotic with broad antimicrobial spectrum.

The epileptogenic effects of (1R, 5S, 6S)-2-[(6,7-dihydro-5H-pyrazolo[1,2-a][1,2,4]triazolium-6- yl)]thio-6-[(R)-1-hydroxyethyl]-1-methyl-carbapenem-3-carboxylate (LJC10627), a new derivative of carbapenem were studied in comparison with those of imipenem (imipenem/cilastatin), cefazolin and penicillin G. In intraventricular injection in rats, LJC10627 caused no epileptogenic activity at a dose of 32 micrograms. In contrast, imipenem, cefazolin and penicillin G showed dose-related seizure signs, continuous rhythmic spikes or high voltage spike-wave complexes and convulsive behaviors at doses higher than 10 micrograms. After intravenous injection of LJC10627, no epileptogenic signs on the electroencephalogram (EEGs) or in behavioral symptoms were observed, even at a dose of 500 mg/kg in rats and 300 mg/kg in rabbits, respectively. By contrast, imipenem/cilastatin provoked severe seizure patterns characterized by high voltage spikes-wave complex and convulsive behavior, both in rats and rabbits, using the same doses of LJC10627. Cefazolin and penicillin G also induced obvious epileptogenic signs in both rats and rabbits after intravenous injection. From these results, it was concluded that LJC10627, unlike imipenem (imipenem/cilastatin) and cefazolin, dose not elicit epileptogenic activity, and may therefore be safely used for clinical purpose.

Animals↗
PubMed1986

Influence of histamine and related compounds on the hypnotic effect of thiopental in mice.

Intraventricular injection of histamine (Hi) significantly prolonged thiopental sleeping time at doses of 0.5 microgram or larger. Both 1-methylHi and imidazole-4-acetic acid, however, did not affect thiopental narcosis. Pretreatment with alpha-fluoromethylhistidine diminished the effect of Hi, while histidine, metoprine and quinacrine prolonged thiopental narcosis. Injection with 2-methylHi did not affect thiopental sleeping time, while as in the case of Hi, 4-methylHi augmented the thiopental effect. In addition, H2-receptor blocking agents such as cimetidine, ranitidine and famotidine clearly antagonized Hi-induced prolongation of thiopental narcosis, while pyrilamine and chlorpheniramine had no effect. These results indicate that Hi-induced prolongation of thiopental narcosis appears to be exerted via H2-receptors and is, in some way, related to the Hi content in the brain.

Animals↗
PubMed1986

Pharmacological studies on ginger. III. Effect of the spinal destruction on (6)-shogaol-induced pressor response in rats.

(6)-Shogaol-induced pressor responses in blood pressure of rats were studied. Intraventricular injection of (6)-shogaol (0.1 to 0.5 microgram) caused a pressor response in a dose-dependent manner. (6)-Shogaol (0.5 mg/kg, i.v.)-induced pressor response was markedly reduced by a spinal destruction to the sacral cord level. However, norepinephrine (10 micrograms/kg, i.v.)-induced pressor response was not affected by the spinal destruction. In rats in which the spinal cord was destroyed to the thoracic cord level, (6)-shogaol-induced pressor response was reduced by hexamethonium (10 mg/kg, i.v.) and phentolamine (10 mg/kg, i.v.), etc. When the spinal cord was destroyed to the sacral cord level, the pressor response was not affected by these blockades. In the hindquarters of rats which were perfused with rats' blood, (6)-shogaol caused two pressor responses on the perfusion pressure. The first pressor response, which was accompanied by a rise in systemic blood pressure, was reduced by hexamethonium but was not entirely eliminated by phentolamine. However, the pressor response disappeared with spinal destruction to the sacral cord level. The second pressor response, which occurred about when the systemic blood pressure regained its original pressure, was not affected by hexamethonium, phentolamine or spinal destruction. Pressor response induced by the injection of (6)-shogaol (10 micrograms) into the perfusion circuit was not affected by phentolamine and spinal destruction. Furthermore, (6)-shogaol-induced peripheral pressor response disappeared with the combined treatment of [D-Arg1, D-Pro2, D-Trp7.9, Leu11]-substance P (0.5 mg/kg, i.v.), phentolamine and the section of the sciatic nerves.

Animals↗
PubMed1977

Growth hormone release by gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) in the rat.

Effects of gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) on growth hormone (GH) release were investigated in the urethaneanesthetized male rat. An intraventricular injection of GABA and L-GABOB but not D-GABOB caused a significant increase in plasma GH. An intravenous injection of L-GABOB, at the dose which had no significant effect on basal plasma GH, remarkably enhanced plasma GH response to pentobarbital. These results suggest that GABA and L-GABOB stimulate GH release possibly via the central nervous system in the rat.

Aminobutyrates↗
PubMed1977

Effect of thyrotropin releasing hormone on heart rate and visual evoked potentials in rats.

The effect of injection of 0.3 microgram of thyrotropin releasing hormone (TRH) into the third ventricle on heart rate and photically evoked potentials in the midbrain reticular formation in urethane-anesthetized rats was studied. TRH increased the heart rate and amplitude of the visual evoked potentials within a few minutes following injection. The intraventricular injections of LHRH, consituent amino acids of TRH and intraperitoneal TSH did not exert any effect. This indicates that TRH is effective in the central nerveous system in inducing tachycardia in the rat.

Animals↗
PubMed1979

Central nervous system mediated stimulation by thyrotropin-releasing hormone of microcirculation in thyroid gland of rats.

The blood flow of thyroid, adrenal cortex and renal cortex in the pentobarbital anesthetized rat was assessed from hydrogen gas desaturation curve. The microcirculation of thyroid was markedly augmented within 2 min after an intraventricular injection of Thyrotropin-Releasing Hormone (TRH) while Met-Enkephalin (ENK) failed to influence. Both TRH and ENK stimulated the microcirculation of adrenal cortex moderately. ENK diminished the microcirculation of renal cortex whereas TRH did not exert any effect. The response of thyroid to TRH was abolished by vagotomy, thus the existence of a specific TRH-vagus -thyroid connection was indicated.

Adrenal Cortex↗
PubMed1999

Optimisation of polyethylenimine-based gene delivery to mouse brain.

Polyethylenimine (PEI) is proving to be an efficient and versatile vector for gene delivery in vivo. However, a limiting factor is the relatively short duration of gene expression in some sites. Given the particularly high levels of expression seen in the short term we postulated that loss of expression could result from overloading the nucleus with foreign DNA. To address this problem we first followed DNA delivery and localisation with digoxin-labelled plasmid DNA complexed with 22 kD linear PEI and used these complexes for intraventricular injection into brains of anaesthetised newborn mice. At 24 h post-injection, labelled DNA was found exclusively in the nuclear and perinuclear regions. We next carried out a dose response curve using decreasing amounts of DNA, either in a constant volume (2 microl) or at a constant concentration (500 ng/microl). In both conditions, transgene expression yield was maximum at 100 ng DNA per injection. Using this optimal amount of DNA increased yield of transgene expression significantly at 24 h and one week post-injection as compared to 1 microg DNA. A final point addressed was whether co-expressing an anti-apoptotic gene could enhance gene expression in the longer term. Co-expressing bcl-X(L) with luciferase or LacZ significantly increased expression of both these genes at one week post-injection.

Animals↗
PubMed1985

Hemodynamic effects of the intraventricular administration of angiotensin II and renin in awake dogs.

This study was undertaken to investigate the hemodynamic changes induced by intraventricular injections of angiotensin II (A-II), 1 to 100 ng/kg/min, and renin in doses of 0.025 to 0.3 units (u) in conscious instrumented dogs. Angiotensin II produced a dose-related increase in mean arterial pressure; however, only the highest dose produced a significant increase of 23 +/- 6 mmHg. In contrast, renin did not significantly alter mean arterial pressure in the doses administered but 0.1 and 0.3 u induced a significant increase in systolic arterial blood pressure of 10 +/- 2 and 17 +/- 4 mmHg, respectively. Neither A-II nor renin affected heart rate, dP/dt or carotid, coronary or renal blood flows. These data suggest that in conscious dogs, the threshold level of A-II necessary to induce substantial hemodynamic changes is greater than the amount of A-II that can be acutely generated by activation of angiotensinogen. In addition, the present data suggest that the magnitude of the response is dependent on the availability of the substrate rather than the dose of renin injected centrally into conscious dogs.

Angiotensin II↗
PubMed2001

Meningeal and perivascular macrophages of the central nervous system play a protective role during bacterial meningitis.

Meningeal (MM) and perivascular macrophages (PVM) constitute major populations of resident macrophages in the CNS that can be distinguished from microglial cells. So far, there is no direct evidence that demonstrates a possible role of MM and PVM in the CNS during normal or pathologic conditions. To elucidate the role of the MM and PVM during CNS inflammation, we have developed a strategy using a single intraventricular injection of mannosylated clodronate liposomes, which results in a complete and selective depletion of the PVM and MM from the CNS. Depletion of the MM and PVM during experimental pneumococcal meningitis resulted in increased illness, which correlated with higher bacteria counts in the cerebrospinal fluid and blood. This was associated with a decreased influx of leukocytes into the cerebrospinal fluid, which occurred despite an elevated production of relevant chemokines (e.g., macrophage-inflammatory protein-2) and a higher expression of vascular adhesion molecules (e.g., VCAM-1). In contrast, the higher bacterial counts correlated with elevated production of local and systemic inflammatory mediators (e.g., IL-6) indicating enhanced local leukocyte and systemic immune activation, and this may explain the worsening of the clinical signs. These findings show that the PVM and MM play a protective role during bacterial meningitis and suggest that a primary action of these macrophages is to facilitate the influx of leukocytes at the blood-brain barrier. More in general, we demonstrate for the first time that the PVM and MM play a crucial role during inflammation in the CNS.

Animals↗
PubMed1998

Effects of intraventricular norepinephrine on LH release in short- and long-term ovariectomized steroids-primed rats.

This study examined the noradrenergic mechanism in regulation of luteinizing hormone (LH) release in short- and long-term ovariectomized (OVX) steroids-primed rats. All rats were OVX on the diestrous day 1(D1) morning about 1000 h. After OVX, rats in the short-term OVX group were immediately primed with estradiol (E2, 0.1 mg/kg BW s.c.), fitted with atrial Silastic tubing, and a guide cannula in the right lateral cerebroventricle stereotaxically. Rats in the long-term OVX group received the same treatment (E2, atrial tubing and guide cannula implantation) three weeks later. Rats in both groups received progesterone (2 mg/rat s.c.) at 0930 h on the next day after E2. At 1000 h, intraventricular administration of norepinephrine HCl (NE, 0.01, 0.1, or 1.0 microgram in 2 microliters saline) was given. In short-term OVX-steroids-primed rats, NE did not alter LH levels in the peripheral plasma within 60 or 100 min. By contrast, in long-term OVX-steroids-primed rats, 1.0 microgram of NE gradually decreased plasma LH concentrations, which became significantly different from the initial value at the 60 min time point after treatment. On the other hand, intraventricular injection of 5 ng of the LH-releasing hormone (LHRH) elevated plasma LH concentrations within 10 min in both groups of rats, but at different efficacy: a brief release of LH in short-term OVX-steroids-primed rats and a prolonged release of LH in long-term OVX-steroids-primed rats. These results indicated that the interval after OVX plays a critical role in modulating the responsiveness to NE and LHRH in the steroids-primed OVX rats.

Adrenergic alpha-Agonists↗
PubMed2001

The p38 mitogen-activated protein kinase is involved in associative learning in rabbits.

This study examined the role of the mitogen-activated protein kinase (MAPK) family during acquisition of the rabbit's classically conditioned eye-blink response. Eye-blink conditioning produced a significant, bilateral activation of both extracellular signal-regulated protein kinases (ERKs) and p38 MAPK in the anterior cerebellar vermis. There was also a significant bilateral activation of ERKs in the dorsal hippocampus with no change in p38 MAPK. These changes were seen at 2 min after the last conditioning session, were maintained for at least 180 min, and occurred without any change in the protein expression of either ERKs or p38 MAPK. There were no changes in ERKs or p38 MAPK in frontal cortex, in cerebellar hemispheral lobule VI, or in a section of brainstem containing the inferior olive. Moreover, the stress-related protein kinase Jun N-terminal kinase (JNK), another subfamily of MAPKs, was not altered in any of the brain regions examined. Animals receiving explicitly unpaired presentations of a conditioned stimulus and an unconditioned stimulus did not acquire conditioned responses (CRs) and did not demonstrate any changes in ERKs, p38 MAPK, or JNK. The intraventricular injection of SB203580, a selective p38 MAPK inhibitor, significantly retarded CR acquisition and blocked the learning-related increases in p38 MAPK activity in the anterior vermis. PD98059, a selective MAPK kinase inhibitor, had a smaller and only marginally significant effect on CR acquisition, although it did block the learning-related increases in ERK activity in both the hippocampus and anterior vermis. These results indicate that p38 MAPK is activated during associative learning and may play a role in the transcriptional events that lead to memory consolidation.

Acoustic Stimulation↗
PubMed2001

Roles of the telencephalic cells and their chondroitin sulfate proteoglycans in delimiting an anterior border of the retinal pathway.

The axons of the retinal ganglion cells run on the diencephalotelencephalic boundary on their way to the tectum; however, they do not invade the telencephalon anteriorly. To investigate the mechanisms that prevent the retinal axons from entering the telencephalic territory, the effects of the telencephalic cells were examined on the outgrowth of the retinal axons in vitro; the retinal outgrowth was selectively inhibited by the cellular substrate derived from the telencephalon. The responsible factor for the selective inhibition was, furthermore, found in the telencephalic membranes and the fraction of peripheral membrane molecules from the telencephalon. Because the inhibitory effect was destroyed by chondroitinase ABC but not by heat, this inhibition was attributable to the carbohydrate chains of chondroitin sulfate proteoglycans (CSPGs) adhering to the membranes of the telencephalic cells. To understand the function of the telencephalic CSPGs on the retinal pathfinding in vivo, their carbohydrate chains [chondroitin sulfate glycosaminoglycan (CS-GAG)] were removed from the embryonic brains by intraventricular injection of chondroitinase ABC; the removal of CS-GAG resulted in an anterior enlargement of the optic tract. The results indicate that the telencephalic cells delimit the anterior border of the optic tract with their CSPGs and prevent the retinal axons from aberrantly entering the anterior territory.

Animals↗
PubMed1975

Changes in labeling of soluble and solubilized rat brain proteins using (3H)-leucine as precursor during a learning experiment.

This paper deals with an electrophoretic study on soluble and solubilized rat brain proteins during a brightness discrimination. After intraventricular injection of L-[3H]-leucine the most pronounced increase in relative specific activity was found for several soluble acidic protein-band complexes as well as for solubilized slow-migrating non-myelin proteins obtained from hippocampus of trained animals over the data obtained for active and passive controls.

Animals↗
PubMed1975

[The relationship between temperature adaptation and the effect of noradrenaline on central control of thermoregulation].

In rats cold--adapted (1--3 degrees C) or warmth--adapted (26--28 degrees C) for 4--5 weeks, the body temperature, oxygen uptake, electric muscle activity were continuously recorded before and after intraventricular injection of noradrenaline (NA) at a total volume of 5--8 mcl. At the ambient temperature of 25 degrees C, extremely small doses (5--8 mcg) of NA raised the body temperature due to shivering. Injections of NA were more effective in the cold--adapted rats. Injections of NA at a low ambient temperature (10 degrees C) evoked greater thermoregulatory responses in the warmth-adapted rats.

Adaptation, Physiological↗
PubMed2002

Beta-endorphin suppresses release of thyrotropin-releasing hormone in rat hypothalamus during acute hypoxia exposure.

AIM: To study the influences of beta-endorphin (beta-EP) on the responses of thyrotropin-releasing hormone (TRH) in median eminence (ME) and paraventricular nucleus (PVN) of hypothalamus to acute hypoxia in conscious rats. METHODS: Brain TRH, serum T3 and T4 were measured by radioimmunoassay. The male Wistar rats were exposed in a simulated hypobaric chamber at 7000 m altitude (8.2 % O2) for 2 h. beta-EP was given by intraventricular injection (icv) before hypoxia. RESULTS: beta-EP (0.1 or 1 micromol/L, icv) elevated TRH levels of ME by 12 % (P <0.05) and 15 % (P < 0.05) in treated groups comparing with saline control group (4.8+/-0.3) microg/g protein, and enhanced TRH of PVN by 24 % (P <0.05) and 44 % (P < 0.01) in treated groups comparing with control group (180+/-21) ng/g protein during hypoxia. Meanwhile, serum T3 and T4 were significantly decreased (P < 0.05 or P < 0.01). Naloxone 10 micromol/L abolished the effects of beta-EP (0.1 micromol/L) on TRH in ME (P <0.01) and PVN (P < 0.01) as well as T3 and T4. Naloxone (10 micromol/L, icv) alone reduced contents of TRH in ME and PVN (P <0.05 or P <0.01), but increased the levels of serum T3 and T4 (P <0.01). CONCLUSION: beta-Endorphin was involved in the modulation of hypothalamic TRH release of rats during hypoxia, through an inhibitory mechanism of TRH release in ME and PVN of hypothalamus.

Animals↗
PubMed1992

A comparative study on the convulsant activity of carbapenems and beta-lactams.

Beta-lactams are well known to have potent convulsant activity. Imipenem, the first carbapenem antibiotic introduced in the clinical field, has been reported to induce convulsions. The neurochemical mechanism of the convulsions induced by carbapenems and cephalosporins were studied. Intraventricular injection of cefazolin, cephaloridine and imipenem, and of panipenem (a new carbapenem), induced convulsions in a dose-dependent manner in mice. They inhibited the receptor binding of gamma-aminobutyric acid (GABA), an inhibitory transmitter in the mammalian central nervous system. These in-vitro and in-vivo results suggest that carbapenems and cephalosporins might induce convulsions through the inhibition of GABA receptor binding when they are accumulated in the central nervous system.

Animals↗
PubMed1992

[Effect of intraventricular administration of histamine and its receptor agonists on pentagastrin-induced gastric acid secretion in rats].

The present study shows the dual effects of intraventricularly injected histamine (0.25-2.0 micrograms/5 microliters) on pentagastrin-induced gastric acid secretion. Male Wistar rats weighing 200-300 g were anesthetized with intraperitoneal sodium pentobarbital. Gastric acid was continuously washed out with 37 degrees C saline solution by means of a perfusion pump. On the background of continuous intravenous infusion of pentagastrin [7.5 micrograms/(kg.h),] histamine (0.25 microgram/5 microliters) or 2-pyridylethylamine (PEA, 10 micrograms/5 microliters), a H1-receptor agonist, was injected into the third ventricle through a chronically implanted canula. The acid output decreased 10 min after injection and did not recover at 90 min. When the dose of histamine was increased to 1.0 micrograms or 2.0 micrograms, dual effects appeared. The acid output decreased respectively in 73% or 50% of the animals, while in the rest 27% and 50% of the animals, the acid output increased. H2-receptor agonist dimaprit (10 micrograms/5 microliters, i.c.v.) or impromidine (0.1 micrograms/5 microliters, i.c.v.) had no pronounced effect on pentagastrin-induced acid secretion. Pretreatment with diphenhydramine (16 micrograms/0.2 ml or 32 micrograms/0.2 ml, i.m.) abolished the inhibitory effect of histamine and PEA on acid secretion. These results suggest that histamine may be involved in the central regulation of gastric acid secretion, and the inhibitory effect may be mediated by H1-receptors in the brain. The mechanism underlying the production of the dual effects of histamine is unknown.

Animals↗
PubMed2005

Norepinephrine attenuates hypoxia-inhibited thyrotropin-releasing hormone release in median eminence and paraventricular nucleus of rat hypothalamus.

OBJECTIVE: We have previously found that chronic hypoxia inhibited thyrotropin-releasing hormone (TRH) mRNA expression in rat paraventricular nucleus (PVN). This study presented the effects of hypoxia on TRH secretion in rat hypothalamus, and the norepinephrine (NE) involvement in the modulation of TRH secretion during acute hypoxia exposure. SETTING AND DESIGN: Hypoxia was simulated at altitudes of 5 km (10.8% O2) or 7 km (8.2% O2) in a ventilated hypobaric chamber, and control group was set at local altitude of 2.3 km (15.8% O2). The duration of hypoxia exposure was designed acutely and chronically for 0.5, 2, 24 h, 5, 10, and 30 d, respectively. TRH levels were measured by specific radioimmunoassay. RESULTS: The results showed that hypoxia of 5 km or 7 km significantly enhanced TRH levels of the ME and PVN, and reduced serum T3 levels in most hypoxia-exposed groups. Intraventricular injection (icv) of NE (4 nmol/L) induced a decrease in TRH levels in the median eminence (ME) and PVN, and an increased serum T3 levels following hypoxia of 7 km exposure for 2 h, compared with icv saline control, indicating TRH release increased. The stimulating effect of NE on the TRH secretion was abolished by icv antagonist of adrenergic alpha2-receptor, yohimbine (40 nmol/L). CONCLUSIONS: We conclude that acute and chronic hypoxia exposure produces an inhibition of hypothalamic TRH secretion from the ME and PVN. Central adrenergic system may play a stimulating role through alpha2-receptor in the acute hypoxia-modulating TRH release from rat hypothalamus.

Adrenergic alpha-Agonists↗