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PubMed1987

The effect of omega-phosphono-alpha-aminocarboxylic acids on seizures and brain amino acid levels in E1 mice.

The omega-phosphono-alpha-aminocarboxylic acids, e.g., 2-amino-5-phosphonopentanoate and 2-amino-7-phosphonoheptanoate, are known to act as potent and selective antagonists at N-methyl-D-aspartate receptors and to have a pronounced anticonvulsant action on a variety of animal models of epilepsy. In the present study, the effects of these omega-phosphono-alpha-aminocarboxylic acids on E1 mice were investigated. These mice are inbred mutant epileptic mice, which are highly susceptible to convulsive seizures upon throwing stimulation. 2-Amino-3-phosphonopropionate injected intraventricularly (at a dose of 1.04 mumol) had a marked anticonvulsant action, but at a lower dose (0.1 mumol), it induced running fits. 2-Amino-4-phosphonobutyrate induced transitory excitation just after the injection, followed by sedation. 2-Amino-5-phosphonopentanoate induced marked behavioral sedation. 2-Amino-6-phosphonohexanoate induced tonic-clonic convulsions and epileptic discharges in electroencephalograms. 2-Amino-7-phosphonoheptanoate showed a strong anticonvulsant action at a dose of 1.27 mumol, but it induced myoclonic seizures at a lower dose. Amino acid analyses of E1 mouse brain showed that 2-amino-3-phosphonopropionate increased the glutamine level, 2-amino-4-phosphonobutyrate decreased the aspartic acid level, 2-amino-5-phosphonopentanoate decreased the glutamic acid level, 2-amino-6-phosphonohexanoate decreased the glutamic acid, glutamine, gamma-aminobutyric acid, glycine and alanine levels, and 2-amino-7-phosphonoheptanoate decreased the glutamic acid label 1 hour after their injection. These findings suggest that the effects of omega-phosphono-alpha-aminocarboxylic acids on the E1 mouse brain are multiple and complicated, depending on the numbers of their carbon chain.

Amino Acids↗
PubMedDate not supplied

[Brain catecholamine participation in etimizol activation of the hypophyseal-adrenal cortex system].

In the experiments on rats the influence of aethimizol on the blood plasma 11-corticosteroids level and the brain catecholamines content was studied. It is established that an hour after the aethimizol injection (10 mg/kg) the blood corticosteroids concentration increases and the hypothalamic norepinephrine and dophamine levels decrease. The pituitary-adrenal system stimulating effect of aethimizol is blocked to a great extent by the intraventricular injection of 6-hydroxydophamine (250 microgram, twice), but is not prevented by the intraperitoneal reserpine treatment (1.5 mg/kg, twice). Aethimizol potentiates the behavioral effects of L-dioxyphenylalanine in mice. It is suggested that the stimulating action of aethimizol on the pituitary-adrenal system may be attributed to its activation of the catecholamines release and their uptake by the hypothalamus.

11-Hydroxycorticosteroids↗
PubMed1988

Reinnervation of dopamine neurons by regenerating serotonin axons in the rat medial zona incerta. A combined radioautographic and immunocytochemical ultrastructural study.

Cellular relationships between serotonin (5-HT) axons and tyrosine hydroxylase (TH)-containing neurons were examined by combined (3H)5-HT uptake radioautography and TH immunocytochemistry in the medial zona incerta (ZI) of adult rats, 7 and 50 days after an intracerebral injection of 5,7-Dihydroxytryptamine (5,7-DHT). Seven days post-lesion, only rare, scattered (3H)5-HT-labeled axon terminals were apparent in the zone of the medial ZI accessible to intraventricularly injected (3H)5-HT. In contrast, in sham-injected animals (3H)5-HT-labeled varicosities were numerous and often observed adjacent to TH-immunoreactive perikarya and dendrites. Fifty days post 5,7-DHT injection, the density of (3H)5-HT-labeled terminals approximated that seen in sham-treated animals. At the ultrastructural level, these regenerated 5-HT axons were similar in size, shape and content to those observed in sham-operated rats. Also, as in sham, some of the (3H)5-HT-labeled axons were directly apposed to TH-immunopositive labeled profiles. The latter included large dendritic shafts and dendritic spines, but only rare perikarya. In both sham- and 5,7-DHT-treated animals a few of the contacts between (3H)5-HT-labeled and TH-immunoreactive profiles exhibited an asymmetric synaptic differentiation. These results indicate that 5-HT fibers in the medial ZI, following regeneration, can reestablish normal relationships and even synapses with a given population of chemically identified cells.

5,7-Dihydroxytryptamine↗
PubMed1976

Aporphines. 15. Action of aporphine alkaloids on dopaminergic mechanisms in rat brain.

Of eleven aporphine analogues tested on striatal adenylate cyclase only (-)-apomorphine and (+/-)-N-n-propyl-norapomorphine (+/-(NPA)) were effective in stimulating the cyclase from rat brain. Inactive compounds included (+/-)-isoapomorphine, (-)-1,2-dihydroxyaporphine and (+/-)-10-hydroxy-N-n-propylnoraporphine. (+)-Bulbocapnine was an effective antagonist of the stimulating effects of dopamine or (-)-apomorphine on striatal adenylate cyclase. Injection of (-)-apomorphine into the lateral ventricle of rats with unilateral 6-hydroxydopamine-induced lesions of the nigro-striatal pathway caused the animals to rotate away from the side of the lesion. Intraventricular injection of 25 mug (+/-)-10-hydroxy-N-n-propylnorapomorphine was ineffective in producing rotation. The results are discussed in relation to the structural requirements for CNS dopamine receptor agonists.

Adenylyl Cyclases↗
PubMedDate not supplied

Delta sleep-inducing peptide (DSIP) stimulates growth hormone (GH) release in the rat by hypothalamic and pituitary actions.

To evaluate possible effects of delta sleep-inducing peptide on GH release, the peptide was micro-injected into conscious animals with third ventricular cannulae and blood samples were drawn from indwelling external jugular vein cannulae. Ovariectomized animals were used in order to eliminate gonadal steroid feedback. In the initial experiment, intraventricular injection of 5 micrograms of the peptide induced an elevation of GH which became significant by 30 min and persisted for the 120 min duration of the experiment after the injection. Diluent-injected animals showed a slight initial drop in GH and then no increase. The increase in plasma GH induced by the peptide was dose-related with a minimal effective dose of 0.1 microgram and a linear log-dose increase to a dose of 10 micrograms. This effect is presumably mediated hypothalamically via a dopaminergic mechanism since it could be blocked by pre-treatment of the animals with pimozide, a dopamine receptor blocker. Dispersed overnight, cultured pituitary cells from ovariectomized rats exhibited a dose-related increase in GH release in static incubations with DSIP. A response occurred with the lowest dose tested (10(-12) M) which increased to a maximum at 10(-10) M DSIP. The responses then declined at higher doses such that they were no longer significant at doses of 10(-7) and 10(-5) M. The increase even at the most effective dose was approximately 50% above the basal values. The results are consistent with the hypothesis that DSIP may be involved in GH release via a dopaminergic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

8-Hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) elicits eating in free-feeding rats by acting on central serotonin neurons.

A subcutaneous injection of 0.5 mg/kg 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a drug with high affinity for 5-hydroxytryptamine (5-HT1A) binding sites, substantially increased eating in non-deprived rats. Intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin for 5-HT neurons, also significantly increased eating in rats and antagonized the effect of 8-OH-DPAT. Microinjections of 8-OH-DPAT (0.5 and 1 microgram) in the nuclei dorsalis and medianus raphe also significantly increased eating in rats. 8-OH-DPAT appears to stimulate eating by acting on 5-HT-containing neurons. These results are compatible with the hypothesis that a decrease in central 5-HT function disinhibits feeding.

5,7-Dihydroxytryptamine↗
PubMed1987

Antinociceptive action of cholecystokinin octapeptide (CCK 8) and related peptides in rats and mice: effects of naloxone and peptidase inhibitors.

Cholecystokinin octapeptide (CCK 8) produced significant antinociception in the tail immersion test in the rat, paw pressure test in the rat and acetylcholine-induced writhing test in the mouse after subcutaneous (s.c.) administration. In the hot plate test, CCK 8 (s.c.) showed antinociceptive activity if the latency to lick was used as the end point but if the latency to jump was recorded the antinociceptive effects were not evident. Cholecystokinin tetrapeptide (CCK 4) was shown to be antinociceptive in the writhing but not in the hot plate test after subcutaneous administration and appeared to be less potent than CCK 8 when tested under the same conditions. Antinociception induced by CCK 8 in the hot plate test (lick) could also be demonstrated after direct intracerebroventricular (i.c.v.) injection and this observation was also made with the CCK-related peptide FMRF amide. Antinociception induced by CCK 8 (which did not appear to be associated with reduced locomotor activity) was evident 5 min after intraventricular injection and was maximal at 10 min, the effect lasting over a 30-45 min period. The antinociceptive effect of CCK 8 was antagonised by naloxone and was potentiated by simultaneous administration of the peptidase inhibitors bestatin, thiorphan and captopril.

Animals↗
PubMed1975

Hemodynimic effects of systemic and central administration of clonidine in the monkey.

Systemic and regional hemodynamic changes were measured in restrained, conscious rhesus monkeys with indwelling arterial and venous catheters before and after clonidine (5 and 15 mug/kg) was slowly infused intravenously or smaller doses (2 mug/kg) were injected into a lateral cerebral ventricle. Dye-dilution cardiac outputs and the complete distribution of cardiac output were obtained intermittently with the use of the radioactive microsphere method. After the higher intravenous dose and the intraventricular injection, systemic arterial pressure was significantly lowered for 30-45 min. Both of these groups had similar changes in the redistribution of cardiac output and blood flow that outlasted the hypotensive period. Blood flow was maintained or increased in the hepatic and renal arteries at the expense of skin; flow to skeletal muscle and brain also decreased during the first hour. These data support previous studies that indicate that the primary action of clonidine is in the central nervous system and, in addition, add new information about the regional blood flow changes evoked by clonidine.

Animals↗
PubMed1993

Possible role of endothelin acting within the hypothalamus to induce the release of atrial natriuretic peptide and natriuresis.

Since endothelin has been localized in neurons in areas involved in water and electrolyte metabolism, areas which also contain atrial natriuretic peptide (ANP) neurons, we determined whether endothelin would release ANP and induce natriuresis. Endothelin-3 (ET-3) in doses ranging from 38 to 760 pmol was microinjected into the third ventricle (3V) of conscious, water-loaded male rats, and the effect on natriuresis and plasma ANP was determined. ET-3 evoked a dose-related natriuresis beginning within 20 min of injection. Even the lowest dose tested (38 pmol) was effective. At a dose of 95 pmol, it produced a rapid increase of plasma ANP within 5 min peaking at 20 min. A slight kaliuresis and antidiuresis was observed at the 2 highest doses of 380 and 760 pmol. The urinary changes following 3V injection of ET-3 were similar to those evoked by ANP, except for the antidiuresis with increased sodium concentration which followed injection of the 2 higher doses. These results suggest that these 2 higher doses also released vasopressin. Alternatively, activation of the sympathetic nervous system by these higher doses may have decreased glomerular filtration rate and been in part responsible for the antidiuresis. The results with 3V injection of ET-3 contrasted sharply with those obtained following intravenous injection of the 95-pmol dose injected intraventricularly. This intravenous dose of ANP induced a transient decrease in sodium and potassium excretion and urine volume, maximal at 20 min, and had no effect on plasma ANP concentrations at 5 or 20 min after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Interleukin-1 in cerebral ischemia.

During the past several years, it has become increasingly apparent that interleukin-1 (IL-1), particularly IL-1 beta plays an important role in brain injury during ischemia. Studies from various laboratories have shown that IL-1 beta mRNA and IL-1 beta protein are synthesized early in ischemia and that the injection of IL-1 beta into ischemic brain enhances edema formation. The most direct evidence that IL-1 beta contributes to ischemic injury, however, is the demonstration that infarct volume in focal ischemia is reduced following intraventricular injection of an endogenous interleukin-1 receptor antagonist (IL-1ra), or after IL-1ra is overexpressed in brain using an adenoviral vector to transfer IL-1ra cDNA to brain cells. Ischemic injury is also reduced in mice that fail to produce IL-1 beta because of an abnormal interleukin-1 beta converting enzyme gene (ICE knockout mice). At the present time, it is nuclear how IL-1 beta causes brain injury, but several possible mechanisms include 1) stimulation of an inflammatory response through the activation of glia or the induction of other cytokines and/or endothelial adhesion molecules and 2) release of free radicals through stimulation of arachidonic acid metabolism and/or nitric oxide synthase activity.

Animals↗
PubMed1972

Effects of catecholamines and adenosine derivatives given into the brain of fowls.

1. Adult fowls (Gallus domesticus) with cannulae chronically implanted into the IIIrd cerebral ventricle and various other sites of the brain received microinfusions or injections of catecholamines, adenosine, 3',5'-cyclic AMP or its dibutyryl derivative. The effects of these substances on behaviour, electrocortical activity and body temperature were studied.2. Behavioural and electrocortical sleep with fall in body temperature were obtained with intraventricular noradrenaline, alpha-methylnoradrenaline and isoprenaline; dopamine was ineffective. The doses required to elicit sleep were smaller than those affecting body temperature. Following mebanazine, the effects of noradrenaline were prolonged and doses of dopamine, previously ineffective, lowered body temperature and induced behavioural and electrocortical sleep.3. Noradrenaline, alpha-methylnoradrenaline, isoprenaline and dopamine infused into the hypothalamus induced sleep and lowered body temperature. Effective doses of noradrenaline, alpha-methylnoradrenaline and isoprenaline infused into the hypothalamus were one-twentieth to one-fifth those for intraventricular injection. Tachypnoea developed with isoprenaline and dopamine. Additionally with dopamine, there was deviation of the head to the contralateral side, together with repetitive jerking movements of the head. These effects were prolonged and intensified by mebanazine, whereas the involuntary movements with dopamine were greatly reduced by haloperidol.4. Involuntary movements, but without sleep, were induced by infusing dopamine into the paleostriatum augmentatum; noradrenaline infused into this site was ineffective.5. In three of five fowls pretreated with aminophylline, 3',5'-cyclic AMP infused into the hypothalamus induced behavioural and electrocortical sleep; without aminophylline pretreatment, 3',5'-cyclic AMP was ineffective. Adenosine infused into the hypothalamus, following pretreatment of fowls with aminophylline, consistently induced behavioural and electrocortical sleep. Dibutyryl cyclic AMP infused into the hypothalamus of intact fowls elicited behavioural arousal, followed by bursts of electrocortical spikes (6 Hz) over both cerebral hemispheres, spikes subsequently becoming regular at 1 Hz. Clonic limb and body movements occasionally accompanied the bursts of spike activity, infrequently developing into convulsions. In fowl encéphale isolé preparations, in which dibutyryl cyclic AMP was infused into the hypothalamus, spike activity was confined to the ipsilateral hemisphere.

Adenosine↗
PubMedDate not supplied

Evaluation of left ventricular function during roentgen contrast ventriculography.

Changes in the left ventricular (LV) function during direct ventriculography (contrast medium injected into LV cavity) and during intravenous left ventriculography (contrast medium injected into right atrium) were assessed in 22 normal subjects. During angiography the left ventricular pressure was continuously recorded by a microtip manometer catheter. LV images and pressure curves were analysed by a computer analysis system. The forceful intraventricular injection of contrast medium during the direct ventriculogram resulted in significant changes in the LV diastolic function, and increased LV pressure and LV working parameters. Mechanical efficiency of the LV contraction decreased. Acute volume overload of the left ventricle appears to be the main limitation of this method. To overcome this limitation, we recommend the use of intravenous biventriculography with simultaneous recording of LV pressure, instead of direct ventriculography. This modification with subsequent frame to frame analysis of the study results may be used successfully in clinical research trials.

Adult↗
PubMed1992

Evidence for upregulation of galanin synthesis in rat glial cells in vivo after colchicine treatment.

The localization of galanin (GAL) and GAL mRNA was studied in rat brain after colchicine or vinblastine treatment using in situ hybridization and immunohistochemistry. GAL-like immunoreactivity was found in glial cells, presumably activated microglia, in the cortex, caudate nucleus and septum, mainly on the injection side. GAL mRNA expression was found in small cells in the same areas with an overlapping distribution, including the adjacent white matter. The results suggest that the glial cells initiate synthesis of the peptide GAL in response to intraventricular injection of high doses of the 2 mitosis inhibitors.

Animals↗
PubMed1985

The effect of gastrin-releasing peptide on growth hormone secretion in the rat.

Several investigators have reported gastrin-releasing peptide (GRP)-like immunostaining in several regions of the rat brain. The objective of this study was to determine the possible effects of this peptide on GH release. Porcine GRP was injected intraventricularly (third ventricular) in a volume of 2 microliters into ovariectomized female rats. A significant decrease in basal GH release, as evidenced by decreased plasma GH levels, was observed within 10 min which lasted for 90 min after the injection of 2 micrograms (0.7 nmol) GRP (P less than 0.001). In addition, all GH pulses were abolished during this time. In subsequent experiments, varying doses of GRP were administered, and human pancreatic GH-releasing factor (GRF) was injected iv at a dose of 0.1 microgram/kg 20 min later to determine the responsiveness of the pituitary. The minimal effective dose of GRP to lower plasma GH was approximately 10 ng (3.6 pmol); however, the GH-releasing action of GRF was blocked by even the lowest dose of the peptide tested (5 ng; 1.8 pmol). To determine if GRP had any direct action on the pituitary, overnight-cultured pituitary cells from ovariectomized animals were incubated for 1 h with GRP in various concentrations. There was a slight dose-dependent stimulation of GH release with concentrations of GRP ranging from 10(-9)-10(-6) M; however, the GH-releasing action was much less than that of GRF. To confirm the direct stimulatory effect of GRP on GH release, dispersed pituitary cells were perifused with medium containing 2 X 10(-6) M GRP. An immediate increase in GH release was observed in the perfusate. Since GRP has a direct stimulatory action to release GH in the pituitary, but ivt injection of the peptide inhibits GH release and blocks the response to GRF, we suggest that GRP may act on periventricular structures to release somatostatin, which reduces GH release and blocks the response to GRF.

Amino Acid Sequence↗
PubMed1987

Nerve growth factor receptor-mediated transport from cerebrospinal fluid to basal forebrain neurons.

Recent data indicate that the neurons of the cholinergic basal forebrain (CBF) respond to nerve growth factor (NGF) with increased survival under experimental conditions and have NGF receptors which mediate the binding and retrograde transport of NGF from axon terminals to somata. Focal intraparenchymal injections of retrograde tracing agents into neuropil demonstrate that the distribution of axons from cholinergic nuclei to cortex and hippocampus is topographically restricted and largely ipsilateral. Monoclonal antibody 192, a well-characterized antibody which recognizes only the rat NGF receptor, was labelled with 125I and injected into a lateral ventricle of adult rats. Highly specific bilateral transport to numerous neurons of the CBF system was demonstrated by autoradiography. This result directly demonstrates that suitably targeted antibodies can be taken up by specific neuronal populations following intraventricular injection and implies that CBF neurons may be influenced by relatively high molecular weight substances injected into cerebrospinal fluid.

Animals↗
PubMed1986

Failure to kindle seizures after repeated intracerebral administration of arginine vasopressin.

In an attempt to kindle seizures with arginine-vasopressin (AVP), we injected AVP into the amygdala or hippocampus of rats. Although behavioral and electrographic alterations were sometimes observed, seizures failed to develop, even in rats that had previously been kindled with electrical stimulation. This and previous failures to kindle seizures by intraventricular injections of AVP call into question the possibility of AVP kindling.

Amygdala↗
PubMed1986

Immunocytochemical evidence for stimulatory control by the ventral noradrenergic bundle of parvocellular neurons of the paraventricular nucleus secreting corticotropin releasing hormone and vasopressin in rats.

The regulation, by catecholaminergic innervation, of parvocellular neurons of the paraventricular nuclei (PVN) secreting corticotropin releasing hormone (CRH) and vasopressin (Vp) was studied by immunocytochemical visualization of both neurohormones in control rats and in rats given discrete injections of 6-hydroxydopamine in the ventral noradrenergic ascending bundle (VNAB). In both groups, the changes in immunostaining intensities observed in axon terminals of the external median eminence and in PVN perikarya 48 h after a blockade of axoplasmic transport by intraventricular injections of colchicine, served as an index for hormonal release and synthesis. In controls, this treatment induced a strong decrease in CRH and Vp immunoreactivity within the terminals, together with intense labeling of PVN perikarya containing CRH. By contrast, bilateral VNAB lesions strikingly inhibited both the colchicine-induced reduction of the CRH and Vp immunoreactivity in axons and the accumulation of CRH in the perikarya. Unilateral VNAB lesions induced similar alterations but these were restricted to the ipsilateral PVN and median eminence. Comparison of these immunocytochemical data with earlier physiological observations on the effects of VNAB lesions on ACTH secretion indicates that the catecholaminergic afferents to the PVN conveyed by the VNAB stimulate the release and the synthesis of CRH and Vp by parvocellular neurons projecting into the external median eminence.

Afferent Pathways↗
PubMed1976

Antinociceptive and stimulant effects of morphine after chemical sympathectomy.

The modifications produced by 6-hydroxydopamine (6-OHDA) on the analgesic and toxic effects of morphine have been studied in mice and cats. After intracerebral injections of 6-OHDA, mice had a lower threshold for morphine-induced convulsions. Morphine analgesia assayed by the phenylquinone test was apparently antagonized in the 6-OHDA pretreated mice, but the 6-OHDA mice showed more reactivity to the phenylquinone. Intraventricular injection of 6-OHDA in cats produced an acute syndrome with mydriasis, bradycardia, bradypnea, hypothermia and EEG slowing, which subsided after several days, 6-OHDA was successful in blocking the morphine mania, but the animals died within 24 h.

Amines↗