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PubMed1976

Plasma renin activity following central infusion of angiotensin II and altered CSF sodium concentration in the conscious goat.

To study central influences on the renal release of renin, angiotensin II was infused into the lateral cerebral ventricle of conscious hydrated goats. CSF sodium concentrations was increased or lowered by similar infusions of hypertonic NaCl or of isotonic fructose solution. Infusion of angiotensin II in doses from 0.5 to 1 mug caused a drop in plasma renin activity (PRA) and elicited a rise in blood pressure, antidiuresis, natriuresis, and thirst. Intraventricular infusion of hypertonic NaCl also supressed PRA, induced antidiuresis, natriuresis, and an inconsistent rise in blood pressure. Lowering of CSF [Na+] by infusion of isotonic fructose caused a rise in PRA and was followed by a water diuresis in the non-hydrated animal. The fructose infusions caused some decrease in renal K+ excretion but no consistent change in renal Na+ excretion. The results indicate that angiotensin II and changes in sodium balance modulate renal renin release also via the central nervous system.

Angiotensin II↗

PubMed1992

Nerve growth factor affects 11C-nicotine binding, blood flow, EEG, and verbal episodic memory in an Alzheimer patient (case report).

Based on animal research suggesting that nerve growth factor (NGF) can stimulate central cholinergic neurons, the known losses of cholinergic innervation of the cortices in Alzheimer's disease (AD), and our experience of infusing NGF to support adrenal grafts in parkinsonian patients, we have initiated clinical trials of NGF infusions into the brain of patients with AD. Here we report a follow-up of our first case, a 69-year-old woman, with symptoms of dementia since 8 years. Intraventricular infusion of 6.6 mg NGF during three months resulted in a marked transient increase in uptake and binding of 11C-nicotine in frontal and temporal cortex and a persistent increase in cortical blood flow as measured by PET as well as progressive decreases of slow wave EEG activity. After one month of NGF, tests of verbal episodic memory were improved whereas other cognitive tests were not. No adverse effects could be ascribed to the NGF infusion. Taken together, the results of this case study indicate that NGF may counteract cholinergic deficits in AD, and suggest that further clinical trials of NGF infusion in AD are warranted.

Aged↗

PubMed1982

Regulation of sleep after neonatal locus coeruleus lesion: functional evidence of beta-adrenergic supersensitivity.

In the present report we analyzed the long-term effect of neonatal noradrenergic denervation on the regulation of paradoxical sleep in the rat. The locus coeruleus was destroyed bilaterally at 4 days of age by direct infusion of 6-hydroxydopamine into the nuclei. After they reached adulthood, the rats received either i.p. injections of a beta-blocker, propranolol, or the same treatment combined with intraventricular infusion of a beta-agonist, isoproterenol. Several doses of each drug were tested. The effects of propranolol, alone and together with isoproterenol, on paradoxical sleep (a decrease for the former drug and a restoration for the latter combination) were significantly more pronounced in the lesioned group than in age-paired controls. These data illustrate a functional aspect of the denervation supersensitivity phenomenon in beta-receptors.

Adrenergic beta-Antagonists↗

PubMed1976

Influence of prostaglandin E1 on cerebral mechanisms involved in the control of fluid balance.

The effects of infusions of PGE1 (30 ng/kg min-1) into the lateral cerebral ventricle were studied in the conscious, hydrated goat. The infusions caused release of antidiuretic hormone and increased renal sodium excretion. When PGE1 was infused together with hypertonic NaCl these effects became markedly enhanced and the infusion also induced drinking and a rise in the arterial blood pressure. Much weaker effects were obtained by the infusion of the hypertonic NaCl alone. This sodium-PGE1 interaction is discussed in relation to previously observed, central sodium-angiotensin II interaction. A more pronounced drinking effect was obtained in response to the intraventricular infusion of PGE1 + angiotensin II, than to the infusion of either substance separately. The PGE1 administered into the lateral cerebral ventricle did not induce any febrile response.

Angiotensin II↗

PubMed1997

Protection against quinolinic acid-mediated excitotoxicity in nigrostriatal dopaminergic neurons by endogenous kynurenic acid.

Endogenous excitotoxins have been implicated in the degeneration of dopaminergic neurons in the substantia nigra compacta of patients with Parkinson's disease. One such agent quinolinic acid is an endogenous excitatory amino acid receptor agonist. This study examined whether an increased level of endogenous kynurenic acid, an excitatory amino acid receptor antagonist, can protect nigrostriatal dopamine neurons against quinolinic acid-induced excitotoxic damage. Nigral infusion of quinolinic acid (60 nmoles) or N-methyl-D- aspartate (15 nmoles) produced a significant depletion in striatal tyrosine hydroxylase activity, a biochemical marker for dopaminergic neurons. Three hours following the intraventricular infusion of nicotinylalanine (5.6 nmoles), an agent that inhibits kynureninase and kynurenine hydroxylase activity, when combined with kynurenine (450 mg/kg i.p.), the precursor of kynurenic acid, and probenecid (200 mg/kg i.p.), an inhibitor of organic acid transport, the kynurenic acid in the whole brain and substantia nigra was increased 3.3-fold and 1.5-fold respectively when compared to rats that received saline, probenecid and kynurenine. This elevation in endogenous kynurenic acid prevented the quinolinic acid-induced reduction in striatal tyrosine hydroxylase. However, 9 h following the administration of nicotinylalanine with kynurenine and probenecid, a time when whole brain kynurenic acid levels had decreased 12-fold, quinolinic acid injections produced a significant depletion in striatal tyrosine hydroxylase. Intranigral infusion of quinolinic acid in rats that received saline with kynurenine and probenecid resulted in a significant depletion of ipsilateral striatal tyrosine hydroxylase. Administration of nicotinylalanine in combination with kynurenine and probenecid also blocked N-methyl-D-aspartate-induced depletion of tyrosine hydroxylase. Tyrosine hydroxylase immunohistochemical assessment of the substantia nigra confirmed quinolinic acid-induced neuronal cell loss and the ability of nicotinylalanine in combination with kynurenine and probenecid to protect neurons from quinolinic acid-induced toxicity. The present study demonstrates that increases in endogenous kynurenic acid can prevent the loss of nigrostriatal dopaminergic neurons resulting from a focal infusion of quinolinic acid or N-methyl-D-aspartate. The strategy of neuronal protection by increasing the brain kynurenic acid may be useful in retarding cell loss in Parkinson's disease and other neurodegenerative diseases where excitotoxic mechanisms have been implicated.

Alanine↗

PubMed1970

The spontaneous release of prostaglandins into the cerebral ventricles of the dog and the effect of external factors on this release.

1. Prostaglandins E(1), E(2), F(1alpha) and F(2alpha) have been identified in perfusates of the cerebral ventricles of anaesthetized dogs.2. Infusions of serotonin into the lateral ventricle caused a four-fold increase in the release of prostaglandins E into the ventricles and this increase was dissociated from the hyperthermic action. Intraventricular infusions of adrenaline and noradrenaline had no effect on the level of prostaglandin release.3. Neither electrical stimulation of a hind foot pad nor the intraperitoneal administration of chlorpromazine, amphetamine, tranylcypromine or imipramine had any consistent effect on the amounts of prostaglandins released into the cerebrospinal fluid.4. When prostaglandin E(1) was added to the fluid perfusing the ventricular system, respiratory changes were observed but almost all the added prostaglandin was recovered from the perfusate leaving the cisterna.

Amphetamine↗

PubMed1993

Central nervous system effects of intrathecal muscle relaxants in rats.

When given for a sufficient time and dose intravenously, neuromuscular blocking drugs eventually can enter the cerebrospinal fluid (CSF). To study the potential pharmacologic consequences of neuromuscular blocking drugs in the CSF, a model was developed in the rat by using an intrathecal infusion of these drugs. A cannula was stereotaxically implanted in a lateral cerebral ventricle of anesthetized male Sprague-Dawley rats (250-300 g). Several days later, the effects of an intraventricular infusion (5 microL/min) of atracurium (0.804 mumol/mL), pancuronium (0.172 mumol/mL), and vecuronium (21.978 mumol/mL) were studied in unanesthetized rats. These rats (n = 6 in each group) exhibited dose-dependent hyperexcitability, during drug infusion, with seizures occurring at threshold doses of (mean), 0.12, 0.26, and 0.065 +/- 0.010 and 3.32 mumol/kg of atracurium, pancuronium, and vecuronium, respectively. The neuromuscular ED50 (intravenous dose required to produce a 50% depression of twitch tension) in rats determined by other investigators are 0.408, 0.115, and 0.352 mumol/kg for atracurium, pancuronium, and vecuronium, respectively. Therefore, seizure threshold doses were not related to the potencies of these drugs as neuromuscular blocking drugs. Based on these data, central nervous system effects were studied over the subseizure dose range approximating 1/100, 1/10, and 1/5 of the cumulative dose causing seizures for each drug (n = 5 for each dose). At 1/100 of seizure dose, decreased locomotor activity and piloerection occurred. At 1/10 to 1/5 of seizure dose, agitation, shivering, splayed limbs, and whole body shaking resulted.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1980

Increased sensitivity to intracerebroventricular infusion of serotonin and deaminated indoles after lesioning rat with dihydroxytryptamine.

Rats were prepared with a chronic intracerebroventricular cannula, and treated with intracisternal 5,7-dihydroxytryptamine (DHT) after i.p. desmethylimipramine or control vehicle. After recovery, they were tested behaviorally by direct observation and electronic monitoring of motor activity. Intraventricular infusion of a placebo or 5-hydroxyindoleacetic acid (5-HIAA) had little effect, but serotonin (5-HT) decreased, and norepinephrine increased locomotor activity in intact rats. Following pretreatment with 5,7-DHT, a small increase in locomotor activity was noted which was not altered by intracranial infusion of vehicle. In contrast, infusions of 5-HT produced a striking dose-dependent (ED50 = 5 micrograms/min) pattern of hyperactivity, 'myoclonic' jerking movements, postural changes, and autonomic responses. Norepinephrine increased locomotor activity in the DHT-lesioned rats (but not significantly more than in controls), but failed to produce the myoclonic syndrome. The deaminated indoles, indoleacetaldehyde and 5-HIAA were more potent than 5-HT in producing the myoclonic response; tryptamine when infused at an equimolar dose had no effect. The putative serotonin antagonists, cyproheptadine and methiothepin (i.p.), were more effective in blocking responses to infused 5-HT than to equipotent doses of deaminated indoles. These behavioral responses may represent exaggerated ex"itatory effects mediated by serotonin in the brain stem and spinal cord, possibly modified by altered forebrain mechanisms. A neurophysiologic or neuropharmacologic role for deminated indoles should be reconsidered as they may not merely be inactive metabolites.

5,7-Dihydroxytryptamine↗

PubMed1987

Neurochemical and behavioral effects of N-ethyl-acetylcholine aziridinium chloride in mice.

N-ethyl-choline aziridinium (ECA) and N-ethyl-acetylcholine aziridinium (EAA) were shown to be inhibitors of high affinity choline uptake in vitro (IC50 = 0.4 microM and 1.5 microM, respectively), and intraventricular administration showed that EAA was more selective in its inhibition of hippocampal choline uptake in vivo. EAA significantly reduced the activity of choline acetyltransferase in the hippocampus 3 to 28 days following intraventricular infusion, but not in the striatum or parahippocampal cortex. Neither muscarinic receptor binding nor glutamic acid decarboxylase activity were affected in any of the three brain regions. EAA (12 or 16 nanomoles, intraventricular) significantly impaired memory performance of mice in a radial arm maze when tested two weeks after treatment. A subgroup analysis implicated long-term reference memory as the mechanism disrupted.

Animals↗

PubMed2001

Both cerebral GABA(A) receptors and spinal GABA(A) receptors modulate the capacity of isoflurane to produce immobility.

We previously demonstrated that intrathecal administration of the noncompetitive gamma-aminobutyric acid type A (GABA(A)) receptor antagonist picrotoxin increased isoflurane MAC (the minimum alveolar concentration of anesthetic producing immobility in 50% of animals) by a maximum (ceiling effect) of approximately 40%. We also found that IV administration of picrotoxin increased MAC by more than 60%, without evidence of a ceiling effect. The larger increase with IV administration suggested a role of cerebral GABA(A) receptors. Accordingly, in this study we examined the effect of intracerebroventricular administration of picrotoxin in rats, finding that picrotoxin infusion into the third ventricle increased isoflurane MAC by a maximum of approximately 40%, without finding a ceiling effect. In addition, we concurrently infused picrotoxin into the intrathecal and intracerebroventricular spaces, producing an increase in MAC in excess of 70%, also with no evidence of a ceiling effect. The dose-response relationship for the intrathecal-intraventricular infusion paralleled that of the IV infusion but was shifted to the left by an order of magnitude. We conclude that both cerebral and spinal GABA(A) receptors modulate the capacity of inhaled anesthetics to produce immobility. Because other studies have shown that the spinal cord, and not the brain, mediates the capacity of inhaled anesthetics to produce immobility, these results call into question the relevance of GABA(A) receptors to the immobilizing action of isoflurane.

Anesthetics, Inhalation↗

PubMed1985

[Induction of paradoxical sleep (PS) by infusion of cerebrospinal fluid from PS-deprived rats].

In the rat, alpha-Methyldopa (alpha-MD, 50 mg/kg i.p.) induced during 8 hrs. an important reduction of paradoxical sleep (PS) and an increase of light slow waves sleep (SWS1). These effects were reversed by intraventricular infusion of cerebrospinal fluid (CSF) from PS-deprived donor rats, and PS restauration depended directly on the duration of the deprivation in the donor. It is probable that hypnogenic substances accumulate in the CSF during PS-deprivation, and that these factors can by-pass the noradrenergic step in the chain of biochemical events normally leading to the appearance of PS.

Animals↗

PubMed2003

A ligand of the p65/p95 receptor suppresses perforant path kindling, kindling-induced mossy fiber sprouting, and hilar area changes in adult rats.

Kindling, an animal model of epilepsy, results in an increased volume of the hilus of the dentate gyrus and sprouting of the mossy fiber pathway in the hippocampus. Our previous studies have revealed that chronic infusion of neurotrophins can regulate not only seizure development, but also these kindling-induced structural changes. Kindling, in turn, can alter the expression of neurotrophins and their receptors. We previously showed that intraventricular administration of a synthetic peptide that interferes with nerve growth factor stability and thus its binding to TrkA and p75(NTR) receptors suppressed kindling and sprouting. However, the precise involvement of TrkA, p75(NTR), and downstream signaling effectors of neurotrophins on kindling, sprouting and hilar changes are unknown. One of these downstream effectors is Ras. In the present study, we find that intraventricular infusion of the synthetic peptide Reo3Y, which binds to p65/p95 receptors and causes a rapid inactivation of Ras protein, impairs development of perforant path kindling, reduces the growth in afterdischarge duration, blocks kindling-induced mossy fiber sprouting in area CA3 of hippocampus and in inner molecular layer of the dentate gyrus, and prevents kindling-induced increases in hilar area. These results are consistent with a mediation of neurotrophin effects on kindling, hilar area, and axonal sprouting via Trk receptors, and suggest important roles for Ras in kindling and in kindling-induced structural changes.

Animals↗

PubMed1988

Intra-ventricular infusion of the NMDA antagonist AP5 impairs performance on a non-spatial operant DRL task in the rat.

Rats were trained to lever press on a differential reinforcement of low rates (DRL-18 s) schedule. They were then allocated to four treatment groups. These were: hippocampal aspiration lesions [HIPP]; implantation of osmotic minipumps for intraventricular infusion of either (a) the NMDA receptor antagonist 30 mM D, L-2-amino-5-phosphonopentanoic acid [AP5] or (b) vehicle [VEH]; and an unoperated control group [UNOP]. In subsequent DRL testing, the HIPP group showed a profound and enduring loss of efficiency, resulting from an increased tendency to respond too early; the AP5 group showed a qualitatively similar, but less severe, impairment followed by full recovery once the minipumps had expired; the VEH and UNOP groups both maintained their pre-operative levels of efficiency. We conclude that AP5 infusion disrupts temporary memory storage in the hippocampus, and that the hippocampus is concerned with the retention of memories outside the purely spatial domain.

2-Amino-5-phosphonovalerate↗

PubMed1991

The effects of central norepinephrine infusions on drinking behavior induced by angiotensin after 6-hydroxydopamine injections into the anteroventral region of the third ventricle (AV3V).

Adult male Sprague-Dawley rats were injected with either 6-hydroxydopamine (6-OHDA) or vehicle in the median preoptic nucleus and the organum vasculosum of the lamina terminalis. The subjects were tested for drinking responses to intraventricular angiotensin II (ANG II) or saline during either saline or norepinephrine intraventricular infusions. Rats injected with 6-OHDA into the ventral lamina terminalis initially failed to show drinking responses to ANG II injections. However, norepinephrine infusion in combination with ANG II injection restored the drinking response to ANG II in rats with catecholamine depletions of the lamina terminalis region.

Angiotensin II↗

PubMed1981

In vivo high-affinity uptake and axonal transport of D-[2,3-3H]aspartate in excitatory neurons.

D-[2,3-3H]aspartate ([3H]D-Asp) at microM concentrations in Krebs' solution was infused intracerebrally in rats, mice and hamsters. Neuropil sites in the hippocampal formation, septum and neostriatum, known to receive excitatory nerve inputs with glutamate and aspartate as putative transmitters, showed strong autoradiographic labeling after intraventricular infusions. There was evidence for retrograde axonal transport to pyramidal cell bodies in hippocampus CA3 and neocortex. Infusions into the hilus fasciae dentatae led to anterograde axonal transport of [3H]D-Asp in the mossy fibers.

Animals↗

PubMed1981

Functional recuperation of the serotoninergic innervation in the rat locus coeruleus.

1. 5,6-dihydroxytryptamine (5,6-DHT) or a lesion of the raphe centralis superior (RCS) cause significant decreases in the serotonin (5-HT) content and significant increases in the tyrosine hydroxylase activity in the locus coeruleus (LC) of the rat. This suggests that noradrenaline (NA) synthesis is controlled by serotonin-containing neurons in the raphe system via their terminals in the LC. 2. Radioautography after intraventricular infusion of tritiated serotonin (3H-5-HT) and biochemical determinations of endogenous 5-HT content showed an almost complete disappearance of serotoninergic axonal varicosities and content in the LC region 10-15 days after intraventricular administration of 75 micrograms of 5,6-DHT. Two to 4 months after neurotoxin administration, 5-HT fibers had regrown in the LC but, contrary to the normal innervation pattern, the majority of them invaded the medial most portion of the nucleus and the adjacent subependymal region. The LC region regained almost all of its endogenous 5-HT content in the same time period. 3. Functional recuperation of these 5-HT fibers was demonstrated by the fact that the RCS had, after regeneration, the same functional control on NA synthesis as in the normal animal.

5,6-Dihydroxytryptamine↗

PubMed1983

Calmodulin infused intracerebroventricularly enhances food intake in the cat.

In the fasted cat, calmodulin (CaM) infused into the cerebral ventricle produces an increase in the normal intake of food in a dose-dependent manner. The enhancement of feeding by CaM seems to be functionally specific since the response was: (1) abolished by the simultaneous intraventricular infusion of calcineurin, a specific CaM antagonist; (2) not mimicked by another calcium binding protein, troponin C; and (3) independent of the CaM's lack of effect on body temperature and water intake. This finding opens up the dual possibility that this Ca2+ binding protein may affect receptors other than intracellularly and that CaM is involved in specific functions controlled by the brain.

Animals↗

PubMed1990

Alterations of ventricular pH alter water intake and food consumption in rats.

The pH of third ventricular CSF was altered by infusing acidic or alkaline solution of artificial cerebrospinal fluid (aCSF) through chronically implanted stainless steel cannula. In two separate group of rats (n = 18 each) water and food consumptions were recorded 30 min, 1 hr, and 24 hr after intraventricular infusions of the modified aCSF solutions having pH 6.0, 8.0 and 7.4 (control). On raising the CSF pH, water intake increased in all three observations. Feeding was not affected in the observations taken after 30 min and 1 hr, but significantly reduced food consumption was observed 24 hr after the infusions. Lowering of pH had no effect either on dipsogenic or feeding response. The CSF pH correlated positively with drinking in all three observations. Since dipsogenic and feeding responses are centrally regulated by ion sensitive cells, it may be presumed that altered CSF pH influenced the activities of the sensors by altering ionic conductance across their membranes.

Acetates↗