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PubMed1991

(D-Ala2)deltorphin II: D1-dependent stereotypies and stimulation of dopamine release in the nucleus accumbens.

In order to investigate the relative role of central delta- and mu-opioid receptors in behavior, the effects of (D-Ala2)deltorphin II, a natural delta-opioid peptide, and PL017, a beta-casomorphin derivative specific for mu receptors, were compared after local intracerebral and intraventricular administration. Intracerebral infusion of the two peptides was done bilaterally in the limbic nucleus accumbens and in the ventral and dorsal caudate putamen of freely moving rats through chronic intracerebral cannulas. After intra-accumbens infusion, the two peptides elicited marked but opposite behavioral effects: while (D-Ala2)deltorphin II evoked dose-dependent motor stimulation characterized by locomotion, sniffing, and oral stereotypies, PL017 elicited motor inhibition with rigidity and catalepsy. These effects were site specific because they could not be evoked from the ventral or from the dorsal caudate. Low doses of naloxone (0.1 mg/kg, s.c.) blocked the effects of PL017 but not those of (D-Ala2)deltorphin II, which instead were reduced by high doses of naloxone (1.0 mg/kg) and by the putative delta-antagonist naltrindole; this drug failed to affect the catalepsy induced by PL017. Therefore, while (D-Ala2)deltorphin II effects were delta-mediated, PL017 effects were mu-mediated. Blockade of dopamine D1 receptors by SCH 23390 abolished (D-Ala2)deltorphin II effects, while blockade of dopamine D2 receptors by raclopride or by haloperidol was without effect. Local application by reverse dialysis of (D-Ala2)deltorphin II (5 microM) to the accumbens resulted in a naloxone-sensitive increase of extracellular dopamine concentrations; these effects could not be evoked from the caudate, nor by PL017 in the accumbens. Intracerebroventricular administration of (D-Ala2)deltorphin II or of PL017 elicited behavioral effects qualitatively similar to those obtained from the accumbens.

Animals↗
PubMed1990

Proteolytic processing of beta-amyloid precursor by calpain I.

The beta-amyloid peptide is a core component of the neuritic plaques that accumulate in Alzheimer's disease. Since the beta-peptide resides within a family of precursor proteins (APPs), proteolytic processing of APP is required for beta-amyloid deposition into plaques. Here, we have examined the role played by the calcium-dependent cysteine protease calpain I in APP processing. Immunoblotting with a specific APP antiserum was used to assess the in vitro degradation of rat brain APP, which appears as a triplet of polypeptides of Mr 110-130 kDa. Both soluble and membrane-bound APP were extraordinarily sensitive to activated calpain I. APP contains at least 3 distinct calpain I cleavage sites. The most protease-sensitive site was located within the highly acidic structural motif called the PEST domain, a second site was upstream of the putative N-linked glycosylation sites, and a third generated a 16 kDa carboxy-terminal fragment that contains the beta-peptide. Based on light microscopic immunohistochemistry, APP and calpain I were extensively colocalized within large numbers of neurons distributed throughout the rat brain, with especially high levels of each in neocortical layer 5, subiculum, globus pallidus, entopeduncular nucleus, anterodorsal and reticular thalamic nuclei, motor trigeminal nucleus, deep cerebellar nuclei, and Purkinje cells. Both antigens were most prevalent within neuronal perikarya. Intraventricular kainate infusion, which is known to cause rapid activation of hippocampal calpain I, produced a 32% decline in APP levels after 24 hr, suggestive of in vivo degradation of APP by calpain I. Following kainate-induced neuronal loss, both APP and calpain I immunoreactivities appeared in the surrounding reactive astroglia. These results indicate that calpain I may be involved in the normal and, perhaps, pathological processing of APP, and that this processing could occur in either neurons or reactive astrocytes. Calcium influx and calpain I activation may provide a mechanism by which excitatory neurotransmission regulates APP metabolism.

Alzheimer Disease↗
PubMed1988

Osmoreceptor mechanism for oxytocin release in the rat.

In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCl Locke solution (L.S.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCl or mannitol but not in the animals infused with hypertonic urea. The injection of 2 microliters of 0.6 M NaCl artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the blood-brain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCl infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCl L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osmoreceptors identical to those for vasopressin release.

Animals↗
PubMedDate not supplied

Effects of nerve growth factor infusion on behavioral recovery and graft survival following intraventricular adrenal medulla grafts in the unilateral 6-hydroxydopamine lesioned rat.

NGF was infused into the lateral ventricle of rats with unilateral 6-OHDA lesions of the substantia nigra along with adrenal medulla or control grafts. Treatment effectiveness, as measured by amphetamine-induced turning behavior, indicated that there were no significant differences between treated and control groups in spite of the survival of tyrosine hydroxylase (TH) immunoreactive grafts. Furthermore, adrenal medulla graft survival was not dependent on NGF infusion. These results indicate that TH-positive graft survival is not correlated with behavioral recovery as assessed by amphetamine-induced turning. These results differ from studies which utilized apomorphine-induced turning as a measure of behavioral recovery. We propose that adrenal medulla graft survival alone is not sufficient to promote behavioral recovery in the 6-OHDA lesioned rat.

Adrenal Medulla↗
PubMedDate not supplied

[The hypnogenic effects of delta sleep-inducing peptide (DSIP) analogs: a comparative study in rabbits and rats].

Hypnogenic effects of 3 DSIP analogs with a higher stability against aminopeptidase activity have been studied in rabbits and rats using intraventricular administration (injections and infusions). An analog (D-Ala-2) DSIP augmented slow wave and paradoxical sleep within the 5th, 8th and 11th hours of the recording period. An analog (D-Val-2) DSIP made the same within the 8th and 10th hours, and hexapeptide (D-Ala-2) DSIP (1-6) increased sleep during the 1st, 3rd, and 5th hours. Both nonapeptides augmented sleep in rabbits as well as in rats, though hexapeptide produced this effect in rabbits only, that might be related to some difference in distribution and colocalization of endogenous DSIP-like peptide in the pituitary of two rodent species. It may be suggested that hypnogenic activity of DSIP analogs is determined by the structure of administrated molecule, being mediated by such hormones as GRF and CLIP.

Aminopeptidases↗
PubMed1985

Vasoactive intestinal polypeptide effects a central inhibition of pulsatile luteinizing hormone secretion in ovariectomized rats.

Recent studies implicate vasoactive intestinal polypeptide (VIP) as a neurotransmitter or neuromodulator, and several observations suggest that VIP, originating within the brain, may alter the secretion of GnRH. We have tested the hypothesis that VIP acts as a central nervous system regulator of pulsatile GnRH secretion, as reflected in pulsatile LH release, by assessing the effect of intraventricularly administered VIP on several parameters of LH secretion in ovariectomized (OVX) rats. To examine the possibility that centrally administered VIP alters pituitary responsiveness to GnRH, we challenged OVX rats with GnRH and compared the LH response in VIP-treated animals with that in control animals. Finally, we tested the hypothesis that exposure of the animal to gonadal steroids alters VIP's effect on LH secretion by assessing LH release during central administration of VIP in OVX rats pretreated with estrogen and progesterone. Unanesthetized rats with external jugular cannulae were bled at 5-min intervals for 2 h before infusion and for 2 h during continuous intraventricular infusion of either VIP (1.8 nmol/h) or saline. Blood samples (300 or 400 microliter) were replaced with an equal volume of a blood replacement mixture. VIP infusion significantly reduced LH pulse frequency by 80% (P less than 0.002) and mean LH levels by 60% (P less than 0.002), but did not significantly affect LH pulse amplitude. In contrast, saline infusion produced no significant change in any of these parameters. The plasma LH response to 2 ng GnRH, iv, in VIP-treated animals did not differ significantly from that in control animals. Finally, VIP infusion had no discernible effect on LH secretion in OVX rats pretreated with estradiol benzoate (50 micrograms) and progesterone (25 mg). These results demonstrate that VIP can profoundly inhibit pulsatile LH secretion in the OVX rat and provide evidence to suggest that this effect is not due to diminished pituitary responsiveness to GnRH. Based upon these observations, we argue that VIP, originating within the brain, may be an important inhibitory regulator of pulsatile GnRH secretion.

Animals↗
PubMed1987

Effects of intraventricularly injected isoosmolar glycerol on brain water and electrolytes in the rat.

The infusion of isoosmolar glycerol (0.35 mol/dm-3) into the ventricles of laboratory rats for 120 minutes led to an increase in the serum osmolality by 11 mosm/kg and to hypernatremia. The brain water content of the cerebral hemispheres decreased by 0.9% (P less than 0.05). A corresponding intraventricular infusion of saline or d-glucose did not cause significant changes in these parameters. These findings support the view that glycerol, even in a dose incapable of creating a major osmotic gradient between plasma and brain, could have a beneficial effect in the control of intracranial volume-pressure perturbations. It is hypothesized that, besides acting as an osmotic dehydrating agent in certain concentrations, glycerol influences the central neuroendocrine system responsible for brain ion and volume homeostasis. By its presumed reduction of central and peripheral vasopressin release through lowering the cerebrospinal fluid sodium concentration, it may help in decreasing the brain water content.

Animals↗
PubMed1982

Central administration of arginine vasotocin: effects on exploratory behavior in the rat.

Synthetic arginine vasotocin (AVT) was infused into rat brains either by intraventricular administration or by local infusion on the pineal body. Subsequently, exploratory behavior was analyzed in a hole board. The behavioral effects induced by this peptide were dependent on the time of day, i. e. the light or the dark phase. High intraventricular doses (0.4 microgram) administered during the light phase altered exploratory activity such that the number of hole visits was increased, while the duration of each visit was decreased; lower doses produced no effect. In contrast, during the dark phase peripineal infusion of AVT (10(-4) pg) attenuated the number of hole visits and increased the mean duration of the visits. The strongest effects were obtained with peripineal applications during the dark phase. This treatment also resulted in significantly lowered levels of pineal melatonin.

Animals↗
PubMed1993

Catecholamine infusion versus intraaortic counterpulsation at the initial phase of left intraventricular balloon pumping in the fibrillating animal heart.

This experimental study compares the effect of catecholamine infusion to the effect of intraaortic counterpulsation (IABP) while initiating intraventricular balloon pumping (IVBP) in the fibrillating heart. In 12 dogs IVBP started immediately after the induction of ventricular fibrillation. Intravenous adrenaline or noradrenaline (at a progressively increasing infusion rate until the systolic aortic blood pressure was 120 mm Hg) was interchanged with IABP. The systolic aortic pressure, the aortic flow and the mean left atrial pressure were, respectively, 120.4 +/- 0.5 mm Hg, 42 +/- 4 ml kg-1 min-1 and 18.7 +/- 1.2 mm Hg (x +/- SEM) ten min after initiating catecholamine infusion and 97 +/- 5 mm Hg (with a 131 +/- 4 mm Hg diastolic wave), 69.6 +/- 4 ml kg-1 min-1 and 16 +/- 1.5 mm Hg ten min after initiating IABP. The difference in aortic flow was significant (p < 0.001). The results indicate that a better aortic flow may be obtained by combining IVBP and IABP than IVBP and vasoconstrictive agents in the fibrillating heart. If IVBP, IABP and catecholamines are combined, both AF and AP may increase.

Animals↗
PubMed1989

Presence of a distinct 24-hour melatonin rhythm in the ventricular cerebrospinal fluid of the goat.

Melatonin profiles in the cerebrospinal fluid (CSF) of conscious goats were examined under long-day (16L:8D) and short-day (8L:16D) environments. CSF melatonin, collected from the lateral ventricle, showed distinct 24 h rhythms with high concentrations being restricted to the dark phase, which averaged 1,320.6 pg/ml under 16L:8D and 660.6 pg/ml under 8L:16D. On the contrary, the nocturnal rise in CSF melatonin was totally absent in the pineal sympathetically denervated animals. Night interruption by 1 h lighting (about 400 lux at the height of goat's head) resulted in an abrupt decline of CSF melatonin to the basal level within 30 min and immediate recovery to the previous high level after reestablishment of the dark phase. The CSF/plasma ratio was 10.8-18.4 during the dark phase and 1.7-1.8 during the light phase. CSF and plasma melatonin levels were also examined after exogenous melatonin given either peripherally or intraventricularly. Continuous subcutaneous infusion of melatonin (5 micrograms/h) maintained melatonin levels in the plasma about 3 times higher than that in the CSF during its application. On the other hand, an intraventricular injection of 2 micrograms melatonin elevated plasma melatonin by 100 pg/ml within 1 min. These results indicate that turnover of CSF melatonin is fairly rapid and favor a hypothesis for direct access of pineal melatonin to the brain ventricular system in the goat.

Animals↗
PubMed2004

Slight elevation of baseline intracranial pressure after fluid infusion into CSF space in patients with hydrocephalus.

OBJECTIVE: To investigate the elevation of resting cerebrospinal fluid (CSF) pressure recorded after a CSF infusion test in patients with hydrocephalus. MATERIAL AND METHODS: Fifty patients (30 men and 20 women, mean age 68 +/- 13 years) with ventriculomegaly and clinical symptoms of normal pressure hydrocephalus have been studied. Lumbar (56%) or intraventricular (44%) computerized infusion studies were performed to investigate the hydrodynamics of CSF. After infusion, the fall in ICP was recorded until a steady-state level was achieved and the difference between pre- and post-infusion resting ICP was calculated (DeltaICP). RESULTS: A positive difference (>2 mm Hg) between post- and pre-infusion resting ICP was identified in 31 infusion tests (62%). The mean value of the difference was 6.7 with an SD of 3.5 mm Hg. The patients who demonstrated this phenomenon had a greater elastance coefficient (p>0.05); DeltaICP was positively correlated with age (R=0.27; p=0.03), with the size of the brain's ventricles (R=0.63, p=0.03) and inversely with the severity of clinical impairment (Stein-Langfitt score R=-0.61, p=0.02; normal pressure hydrocephalus score: R=0.54; p<0.05). DeltaICP was independent of the site of infusion (lumbar or ventricular). CONCLUSION: In patients with a 'stiffer' brain, ICP returns to the resting level after the infusion test at a slightly higher level than before the test. The magnitude of this increase is greater when ventricles are more dilated and clinical symptoms are less severe.

Adult↗
PubMed1990

The effects of separate or combined infusions of corticotrophin-releasing factor and vasopressin either intraventricularly or into the amygdala on aggressive and investigative behaviour in the rat.

These experiments show that combined infusions of corticotrophin-releasing factor (CRF) and arginine vasopressin (AVP) into either the lateral ventricle or the amygdalae have synergistic effects on aggressive, investigative and other behaviours occurring during social interaction between male rats. They suggest, therefore, that the two peptides interact at intracerebral sites to control behaviour much as they do on the anterior pituitary to regulate ACTH release. CRF or AVP, alone or in combination, were infused into either the lateral ventricle (dose range: 10-250 pmol) or bilaterally into the amygdalae (dose range: 1-150 pmol) of male rats in two experiments. The rat was then paired with another, strange, male for 10 min. There was a U-shaped effect on aggressive behaviour after intra-amygdala infusions of CRF, lower doses increasing agonistic behaviour, higher ones decreasing it. This was not seen after icv infusions. AVP had no effect by either route; however, given together with CRF it potentiated the latter's effect on aggressive behaviour. Investigative behaviour was decreased by icv CRF but the effects of amygdala infusions were small. AVP had no consistent effect by either route. Combined infusions of both peptides given either icv or into the amygdala decreased investigative behaviour. Self-grooming increased, though in an irregular fashion, after incremental doses of either CRF or AVP given by either route. Both peptides given together showed additive effects on self-grooming. Climbing behaviour was lowered by CRF more prominently than by AVP and, again, the two peptides together profoundly reduced this behaviour. These experiments show that the behavioural effects of CRF and AVP on social interaction have different profiles, and that the effects of each peptide differ when it is given into the ventricles or directly into the amygdala. There is also clear evidence for synergistic effects of the two peptides on behavior after infusion by either route.

Aggression↗
PubMed1980

Effects of isoproterenol on abnormal intraventricular conduction.

An isoproterenol infusion (1.0-4.0 microgram/min) was administered to 15 patients with intermittent bundle branch block (BBB) and two patients with apparently fixed BBB. Three main effects were documented: (1) In all patients with phase 3, or tachycardia-dependent, BBB, isoproterenol caused a pronounced shortening of refractoriness in the affected fascicle. (2) In patients showing phase 4, or bradycardia-dependent, BBB, isoproterenol prolonged the phase 4 block range, probably because of enhanced diastolic depolarization. In one patient (four studies) in whom phase 4 block was not present, isoproterenol caused the appearance of a phase 4 block range. (3) In the two patients with fixed BBB, isoproterenol restored conduction, probably as a result of a hyperpolarizing effect. This study shows that isoproterenol tends to restore or improve conduction related to tachycardia-dependent block, but may impair conduction related to bradycardia-dependent block.

Bundle-Branch Block↗
PubMed2006

Intrathecally infused antibodies against Nogo-A penetrate the CNS and downregulate the endogenous neurite growth inhibitor Nogo-A.

Neutralizing antibodies against the neurite growth inhibitory protein Nogo-A are known to induce regeneration, enhance compensatory growth, and enhance functional recovery. In intact adult rats and monkeys or spinal cord injured adult rats, antibodies reached the entire spinal cord and brain through the CSF circulation from intraventricular or intrathecal infusion sites. In the tissue, anti-Nogo antibodies were found inside Nogo-A expressing oligodendrocytes and neurons. Intracellularly, anti-Nogo-A antibodies were colocalized with endogenous Nogo-A in large organels, some of which containing the lysosomal marker cathepsin-D. This suggests antibody-induced internalization of cell surface Nogo-A. Total Nogo-A tissue levels in spinal cord were decreased in intact adult rats following 7 days of antibody infusion. This mechanism was confirmed in vitro; cultured oligodendrocytes and neurons had lower Nogo-A contents in the presence of anti-Nogo-A antibodies. These results demonstrate that antibodies against a CNS cell surface protein reach their antigen through the CSF and can induce its downregulation.

Animals↗
PubMed2005

Ruptured saccular aneurysm of distal vertebral artery fenestration managed with Guglielmi detachable coils and intraventricular tissue plasminogen activator.

BACKGROUND: Aneurysms associated with vertebrobasilar fenestrations are uncommon. We report on an unusual presentation of such aneurysm with a dedicated arterial pedicle, manifesting with significant intraventricular hemorrhage. Equally important, the aneurysm was managed in a multidisciplinary fashion, which, we think, greatly contributed to a good outcome. CASE DESCRIPTION: A 55-year-old man presented in good condition after subarachnoid and massive intraventricular hemorrhage. The aneurysm location and the extent of intraventricular hemorrhage both presented concerns regarding treatment approach. The aneurysm was first treated with transarterial coil obliteration, and intraventricular tissue plasminogen activator (tPA) infusion was given, with rapid resolution of evolving hydrocephalus. The patient had an excellent outcome. CONCLUSION: To our knowledge, this is the first report of a vertebrobasilar fenestration saccular aneurysm with a dedicated pedicle projecting toward the foramen of Magendie with significant intraventricular hemorrhage. In addition, this patient was successfully managed with endovascular obliteration and intraventricular tPA infusion.

Aneurysm, Ruptured↗
PubMed1985

Hemodynamic effects of intravenous bepridil in patients with normal left ventricular function.

Calcium-channel blockers are known to have depressant effects on atrioventricular (AV) nodal conduction and myocardial contractility. Because of these known depressant effects, bepridil hydrochloride, a new, long-acting, antianginal and antiarrhythmic calcium-channel blocker, was administered intravenously to patients without heart failure to determine acute hemodynamic effects. The patients studied had normal ventricular function, were without electrocardiographic conduction disturbances and were taking no drug except sublingual nitroglycerin for at least 24 hours before bepridil infusion. The study protocol included right- and left-sided cardiac catheterization with infusion of bepridil at 2 mg/kg for 15 minutes followed by 1 mg/kg for 15 minutes in 10 patients, and infusion of bepridil at 3 mg/kg for 15 minutes followed by 1 mg/kg for 15 minutes in 8 patients. Pressures, Fick cardiac output, resistances, left ventricular (LV) dP/dt, LV stroke work index and rate-pressure product of the left ventricle were monitored. There were no significant changes during bepridil infusion at either dose for cardiac output, systemic vascular and pulmonary vascular resistances, LV stroke work index, heart rate, arterial blood pressure and rate-pressure product. There was mild depression of LV dP/dt during bepridil infusion. Further, LV end-diastolic pressure, pulmonary capillary wedge pressure and pulmonary arterial pressures were significantly increased during bepridil infusion. There were no apparent changes in AV nodal or intraventricular conduction during bepridil infusion. We conclude that bepridil appears to be a safe drug for intravenous administration despite mild depression of myocardial function in patients with normal baseline hemodynamic function who are not receiving concomitant beta-blocker therapy.

Adult↗
PubMed1989

Degeneration of neuronal processes in rats induced by a protease inhibitor, leupeptin.

Severe degeneration of neuronal processes, including axons and dendrites, as well as accumulation of lipofuscin-like dense bodies have been induced in rats by continuous intraventricular administration by infusion of a protase inhibitor, leupeptin. The aggregation of degenerated processes in neuropils mingled with glial cells and their processes resembled the aggregation of degenerated neurites that are important constituents of the senile plaque of Alzheimer's disease. The present findings provide morphological evidence supporting the hypothesis that protease inhibitors participate in the process of senile plaque formation.

Animals↗