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PubMed2003

Differential startle reactivity following central CCK-8S and systemic Boc CCK-4 administration in mice: antecedent stressor history and testing condition.

The influence of intraventricular cholecystokinin-8S (CCK-8S) and systemic N-t-Boc-Trp-Met-Asp-Phe-amide (Boc CCK-4) was evaluated in the acoustic and fear-potentiated startle paradigms in CD-1 mice. In the light + tone startle condition. CCK-8S increased startle 168 hr after administration, compared with saline. In the tone startle condition, CCK-8S decreased startle immediately and 24 hr after administration, compared with saline. Among nonshocked mice, CCK-8S increased startle at 48 and 168 hr, compared with saline. In the light + tone condition, 5 microg Boc-CCK-4 did not influence startle, whereas 15 microg Boc CCK-4 decreased startle immediately, 24 hr, and 48 hr following administration. Results demonstrate that antecedent environmental experiences interact with subsequent pharmacological challenges in provoking the temporal expression of alterations in startle magnitude.

Acoustic Stimulation↗
PubMed1992

Role of NMDA receptors in the compensation of ocular nystagmus induced by hemilabyrinthectomy in the guinea pig.

The possibility that N-methyl-D-aspartate (NMDA) receptor activation plays a role in inducing the vestibular compensation following hemilabyrinthectomy (HL) in guinea pigs, was verified by means of continuous intraventricular osmotic pumping of DL-2-Amino-5-phosphono-valeric acid (APV). Our results show that high doses (40 and 20 mM) of APV decrease both the combined OKR and VOR and the nystagmus following HL. Low doses of APV (2.5 mM), affect the time course of the ocular compensation by maintaining a higher level of nystagmus beat frequency and by delaying the nystagmus disappearance. On the contrary, the compensation time course is not affected by administering APV later on in the compensation period. Therefore, it appears that NMDA receptors are activated during the precocious phase of vestibular compensation, when a large vestibular imbalance is present. This finding is explained by the development of NMDA receptor hypersensitivity, in the functionally inactivated commissural system or by the occurrence of NMDA-mediated long-term potentiation.

2-Amino-5-phosphonovalerate↗
PubMed2003

Cognitive performance and magnetic resonance imaging findings after high-dose systemic and intraventricular chemotherapy for primary central nervous system lymphoma.

BACKGROUND: Long-term neurotoxicity is a frequent complication of combined radiotherapy and chemotherapy in patients with primary central nervous system lymphoma. Treatment protocols without radiotherapy have been implemented to avoid this; however, little detailed neuropsychologic and neuroradiologic data exist to assess the frequency of long-term treatment sequelae in this patient group. OBJECTIVE: To determine whether a polychemotherapy regimen based on high-dose methotrexate results in cognitive impairment and/or changes detectable by magnetic resonance imaging of the brain during long-term follow-up. PATIENTS AND METHODS: Twenty patients with histologically proven primary central nervous system lymphoma were treated with a novel chemotherapy protocol that included systemic and intraventricular administration of methotrexate and cytarabine (ara-C). Standardized neuropsychologic testing and magnetic resonance imaging investigations were performed prior to therapy and prospectively during a median follow-up period of 36 months (range, 21-69 months). RESULTS: Ten patients achieved durable remissions without relapse for more than 1 year after completion of chemotherapy. There was no gross cognitive decline in any of these patients during the follow-up period. In contrast, magnetic resonance imaging revealed therapy-induced white matter changes in 5 of these patients. CONCLUSIONS: We conclude that chemotherapy alone is associated with a low risk of long-term neurotoxicity in primary central nervous system lymphoma. Methotrexate-induced white matter lesions detectable on magnetic resonance imaging are not inevitably associated with significant cognitive decline.

Adult↗
PubMed1979

Studies on the behavioral and biochemical effects of hemicholinium in vivo.

Hemicholinium (HC-3) causes a behavioral reactivity in rats which is correlated with the depletion of brain acetylcholine (ACh). The decrease in ACh levels and behavioral effects caused by HC-3 are correlated in a dose-dependent manner, maximal effects being achieved at an intraventricular (i.vt.) dose of 1 microgram. The HC-3 concentration in the brain 2 hr after i.vt. injection does not increase further with doses greater than 10 microgram. HC-3 (i.vt.) does not affect the uptake of choline (Ch) into subcellular fractions prepared from treated animals. ACh depletion in the brain areas studied closely parallels the HC-3 distribution. HC-3 pretreatment results in greater effects on newly synthesized than on stored ACh. Utilizing a concentration equal to that found in brain after an in vivo dose, HC-3 does not inhibit the uptake of Ch in synaptosomal preparations in which the neuronal membrane was disrupted with ether. The commonly accepted mechanism of action of HC-3, i.e., an inhibition of high affinity Ch uptake at the cholinergic nerve terminal, appears to provide a satisfactory explanation of its effects in vivo.

Acetylcholine↗
PubMed2000

Uptake of circulating insulin-like growth factor-I into the cerebrospinal fluid of normal and diabetic rats and normalization of IGF-II mRNA content in diabetic rat brain.

Brain injury has been prevented recently by systemic administration of human insulin-like growth factor-I (hIGF-I). It is widely believed that protein neurotrophic factors do not enter the brain from blood, and the mechanism by which circulating hIGF-I may be neuroprotective is uncertain. This investigation tested the hypothesis that hIGF-I is taken up into cerebrospinal fluid (CSF) from the circulation. (125)I-hIGF-I was injected subcutaneously into rats. The (125)I-IGF-I recovered from CSF and plasma were indistinguishable in size from authentic (125)I-hIGF-I on SDS-PAGE. An ELISA was used that detected immunoreactive hIGF-I, but not rat IGF-I, rat IGF-II, human IGF-II, or insulin. Osmotic minipumps were implanted for constant subcutaneous infusion of various hIGF-I doses. Uptake into CSF reached a plateau at plasma concentrations above approximately 150 ng/ml hIGF-I; the plateau was consistent with carrier-mediated uptake. The plasma, but not CSF, hIGF-I level was significantly reduced in streptozotocin diabetic vs. nondiabetic rats, and uptake of hIGF-I into CSF was nonlinear with respect to plasma hIGF-I concentrations. Nonlinear uptake excluded leakage or transmembrane diffusion of IGF-I from blood into CSF as a dominant route for entry, but the site and mechanism of uptake remain to be established. The IGF-II mRNA content per milligram brain (P < 0.02) as well as per poly(A)(+) RNA (P < 0.05) was significantly increased towards normal in diabetic rats treated by subcutaneous administration of hIGF-I vs. vehicle. This effect of circulating hIGF-I may have been due to regulation of IGF-II gene expression in the choroid plexus and leptomeninges, structures at least in part outside of the blood-central nervous system barrier. These data support the hypothesis that circulating IGF-I supports the brain indirectly through regulation of IGF-II gene expression as well as by uptake into the CSF.

Animals↗
PubMed1989

Neurosurgery in the treatment of cancer pain.

Patients with pain syndromes resulting from recurrent or metastatic cancer should be evaluated carefully to determine the cause of their pain and the need for appropriate antitumor treatment. Currently, opioid analgesics are the mainstay of pain control, but side effects limit their use in some patients. When pharmacologic pain control is inadequate or associated with intolerable side effects, neurosurgery should be considered. Currently the implantation of a pump for the intraspinal infusion of opioid analgesics is the most popular procedure, but its usefulness may be limited by the development of opioid tolerance. The most effective ablative pain control procedure at the current time is cordotomy, which is indicated in patients with unilateral pain. Although the place of neurostimulatory procedures in controlling cancer pain is not well established, they are attractive because of their nondestructive nature and potential usefulness in the treatment of bilateral pain syndromes. Specific antitumor surgical procedures should be considered in patients with certain spinal and plexopathy syndromes, because such intervention offers the prospect of both pain relief and tumor control. In this article, the neurosurgical procedures used in the management of cancer pain are reviewed.

Analgesics, Opioid↗
PubMed1987

Continuous intracerebroventricular infusion of dopamine and dopamine agonists through a totally implanted drug delivery system in animal models of Parkinson's disease.

We studied the effect of intracerebroventricular infusion of dopamine and dopamine agonists in rat and primate models of Parkinson's disease as an experimental approach to the treatment of levodopa-induced fluctuations. The infusion of dopamine, lisuride, and pergolide into the ventricle ipsilateral to the lesion, by 6-hydroxydopamine, of the nigrostriatal pathway induced a contralateral rotation which was maximal 24-48 h after infusion and whose intensity progressively decreased over the period of 1 week. [3H]Spiperone binding was decreased by the infusion of dopamine but the responses to subcutaneous apomomorphine were unchanged. The infusion of dopamine also restored the levels of monoamines in the rat brain. In chronic reserpized rats, the infusion of dopamine restored brain levels of dopamine but did not reverse akinesia unless monoamine oxidase inhibitors were simultaneously administered, either systemically or intracerebroventricularly. Lisuride and pergolide proved much weaker than dopamine in reversing the effects of reserpine. Intracerebroventricular infusion of dopamine plus deprenyl reversed MPTP induced akinesia in monkeys but the pump used for the delivery was not well tolerated, because of its size, by the animals.

Animals↗
PubMed1987

The effect of intracerebroventricular infusion of (+)-4-propyl-9-hydroxynapthoxacine (PHNO) through a totally implanted drug delivery system in rats with dopamine deficiency.

Rats with experimentally induced DA deficiency were treated with intracerebroventricular administration of (+)-4-propyl-9-hydroxynaphthoxacine (PHNO) through a totally implanted chronic delivery system which delivered PHNO, 0.9 microgram/h, continuously for up to 2 weeks. Rats with 6-OH-DA induced unilateral nigrostriatal lesion showed, after PHNO infusion, a potent and persistent contralateral turning behavior (8-11 turns/min) which was not present in vehicle-infused animals. The intensity of spontaneous and apomorphine-induced rotation did not decrease after 2 weeks of continuous infusion, suggesting that tolerance to PHNO or to other dopamine agonists did not develop. The magnitude of the spontaneous turning behavior in PHNO-infused animals correlated well with the baseline response to apomorphine (r = 0.505, p less than 0.025). Rats implanted with pumps delivering PHNO or vehicle were treated with reserpine, 0.5 mg/kg/day for 14 days. Vehicle-infused, reserpinized animals had a severe akinesia and weight loss during the experimental period (motor activity, measured in counts per minute was reduced to 5-10% of baseline levels, and body weight to 50% of baseline levels). PHNO-infusion partially restored activity to 60% of baseline counts and reduced the severity of weight loss. PHNO effects were observed for as long as the infusion was maintained. No side effects were observed. Intracerebroventricular infusion of PHNO may be an alternative experimental approach to untreatable motor fluctuations in Parkinson's disease.

Animals↗
PubMed1995

Aluminum impairs hippocampal long-term potentiation in rats in vitro and in vivo.

Although aluminum (Al) contributes to a variety of cognitive dysfunctions and mental diseases, the underlying mechanisms of Al interactions with the nervous system are still unknown. We have studied the action of Al on synaptic transmission and long-term potentiation (LTP) by performing electrophysiological recordings both in vivo, using freely moving animals, and in vitro, using hippocampal slices. In vivo recordings of the population spikes (PSs) of dentate gyrus granule cells in response to medial perforant path stimulation were performed on both acutely and chronically (Al each day for 5 days) intraventricularly injected animals. Acute Al-infusion (calculated brain concentrations of 0.27, 0.68, and 2.7 micrograms/ml) had no influence on baseline values. Al at 0.27 microgram/ml did not alter the induction and maintenance of LTP, but 0.68 and especially 2.7 micrograms/ml Al lead to a reduction in LTP, and the potentiation declined to baseline within 2 h. In chronic animals their neuronal responsiveness was reduced and in 30% of the rats the PS was completely lost. High-frequency tetanization failed to induce LTP. In slices, field potentials were evoked stimulating Schaffer collaterals and recording pyramidal cells of the CA1 region. Bath application of 0.68 microgram/ml Al increased the baseline amplitude of the PS slightly, whereas 2.7 micrograms/ml decreased the amplitude and concentrations > 5.4 micrograms/ml blocked the PS completely. Induction of LTP in the presence of 0.68 microgram/ml Al led to a smaller increase of the PS amplitude compared to controls, but the duration of LTP was not affected. In the presence of 2.7 micrograms/ml Al LTP was further reduced and declined to baseline levels within 60 min. Given that LTP is a form of synaptic plasticity underlying some forms of learning, our data suggest that both preparations are suitable models for investigating actions of Al-induced neurotoxicity.

Aluminum↗
PubMed1989

Central angiotensin II stimulates arteriolar vasomotion in conscious hamsters.

The effects of intracerebroventricular (icv) injections of 10 ng angiotensin II (ANG II) on mean arteriolar diameter and spontaneous arteriolar vasomotion were studied in subcutaneous tissue of conscious, restrained hamsters, using the skin fold window chamber preparation. Angiotensin II caused a significant decrease in mean arteriolar diameter which was associated with a significant elevation in the amplitude of vasomotion. The frequency of vasomotion did not change significantly. The central ANG II-induced effects on arteriolar vasomotion were not significantly altered by continuous intravenous (iv) infusion of hexamethonium (1 mg.kg-1.min-1). In contrast, iv bolus injection of the vascular vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10 micrograms.kg-1) 5 min prior to icv injection of ANG II significantly attenuated the effects of the neuropeptide on mean arteriolar diameter and the amplitude of vasomotion. These data indicate that central ANG II stimulation enhances arteriolar vasomotion in peripheral subcutaneous tissue of conscious hamsters and that this effect may be mediated by release of vasopressin.

Angiotensin II↗
PubMed1994

Central and renal I1 imidazoline preferring receptors: two unique sites mediating natriuresis in the rat.

Based on previous studies we postulated that, whereas the natriuresis observed following intracerebroventricular (i.c.v.) moxonidine was mediated by a decrease in renal sympathetic nerve activity, the natriuresis observed following intrarenal (i.r.) infusion of moxonidine was mediated by a direct stimulation of renal I1-imidazoline preferring receptors. Sprague-Dawley rats were unilaterally nephrectomized and i.c.v. cannulated 7 to 10 days and 3 days prior to the day of the experiment, respectively. On the day of the experiment, rats were anesthetized (pentobarbital) and the renal function was isolated. Administration of i.c.v. as well as i.r. moxonidine produced an increase in sodium excretion and urine flow fate. Pretreatment with intravenous prazosin (0.15 mg/kg) completely attenuated the response to i.c.v. moxonidine (1 nmol/5 microliters) but only slightly altered the response to i.r. moxonidine (3 nmol/kg/min). Conversely, intravenous pretreatment with the imidazoline preferring receptor antagonist idazoxan (0.3 mg/kg) completely blocked the response to i.r. moxonidine (3 nmol/kg/min) without altering the response to i.c.v. moxonidine (0.3 nmol/kg). These results would be consistent with the natriuresis observed following i.c.v. moxonidine as being mediated by imidazoline preferring receptors located centrally, whereas that following i.r. moxonidine was mediated directly by renal imidazoline-preferring receptors, with a small component of this response conceivably due to activation of central imidazoline preferring receptors. In summary, the antihypertensive effect of imidazoline preferring receptor agonists may be associated with a natriuresis that is due to stimulation of these receptors, found both peripherally (renal) and centrally.

Adrenergic alpha-Antagonists↗
PubMed1992

Effect of intracisternal and intravenous calcitonin gene-related peptide on experimental cerebral vasospasm in rabbits.

We investigated the vasodilatory effect of intracisternal (i.c.) and intravenous (i.v.) administration of calcitonin gene-related peptide (CGRP) on arterial narrowing after experimental subarachnoid hemorrhage (SAH). Forty-one rabbits were divided into five groups: control (normal animals); SAH plus i.c. infusion of vehicle; SAH plus i.c. infusion of CGRP; SAH plus i.v. infusion of vehicle; SAH plus i.v. infusion of CGRP. In all but the control group, either CGRP (100 ng/kg/min) or vehicle solution was infused for two hours immediately prior to sacrifice by perfusion-fixation. A morphometric technique was employed to measure the luminal diameter of rabbit basilar arteries two days after SAH. The diameter of the basilar arteries in either the i.c. or i.v. CGRP groups was significantly greater than that of the respective vehicle group (i.c., p < 0.001; i.v., p < 0.01). Although there was no significant difference in systemic arterial blood pressure after infusion between the i.c. vehicle and i.c. CGRP groups, i.v. CGRP caused significant hypotension. Our results suggest that exogenous CGRP has some therapeutic potential for arterial narrowing after SAH not only by intrathecal application, but also by systemic use.

Animals↗
PubMed1988

Treatment of esthesioneuroblastoma with chemotherapy: a report of two cases.

Esthesioneuroblastoma is an uncommon tumor arising from the olfactory epithelium within the nasopharynx. Conventional treatment consists of surgical resection and irradiation. The use of chemotherapy in limited responses has been reported using cyclophosphamide, thio-TEPA, nitrogen mustard, vincristine, doxorubicin, and chlorambucil as single drugs or in various combinations. Two cases are presented in which neurologic involvement prompted the application of intraventricular methotrexate by an implantable constant infusion drug delivery system in one patient and intra-arterial cis-platinum in combination with intravenous 5-fluorocytosine in a second patient. The tumor of the first patient responded to irradiation followed by methotrexate for four years. The second patient experienced a brief response to the combined chemotherapy following surgery for a recurrent esthesioneuroblastoma. A brief review of the literature regarding chemotherapy and the aggressive form of esthesioneuroblastoma is presented.

Adult↗
PubMed2002

Effects of corticotropin-releasing factor on prepulse inhibition of the acoustic startle response in two rat strains.

RATIONALE: Prepulse inhibition (PPI) of the acoustic startle response is altered by manipulations that affect brain monoamine neurotransmission. Corticotropin-releasing factor (CRF), a neurotransmitter that is released during stress, and CRF receptors are expressed in areas of the brain which contribute to PPI, and central administration of CRF changes extracellular concentrations of the monoamines. Therefore, CRF is in a position to alter PPI, either by causing the release of other neurotransmitters, or by direct effects at CRF receptors. OBJECTIVES: The present experiments were conducted to test the hypothesis that intracerebroventricular (ICV) administration of CRF would decrease PPI in rats. Additionally, these experiments were used to examine whether CRF results in differential changes in PPI in rat strains that show high and low basal PPI, and whether CRF-induced grooming behavior and increased startle amplitude are also strain-dependent. METHODS: Male Wistar-Kyoto (WKY) rats inbred in our colony in La Jolla, WKY rats obtained from Charles River, and Brown Norway (BN) rats from Harlan, Sprague-Dawley were tested for grooming behavior, PPI and startle amplitude following ICV infusion of either CRF (1.0-3.0 microg) or saline. RESULTS: CRF significantly decreased PPI in both BN rats, which show relatively little PPI in the basal condition and, in WKY rats. The amplitude of the acoustic startle response was increased in WKY rats only and, only by the 3.0 microg dose of CRF. CRF increased grooming behavior in the La Jolla colony WKY and BN rats. However, within the time frame during which the rats were being observed, CRF failed to significantly increase grooming in Charles River WKY rats. CONCLUSIONS: CRF diminished PPI of the acoustic startle response in rats that show high (WKY) and low (BN) basal PPI. This effect does not appear to be dependant on CRF-induced changes in startle amplitude. The results suggest the possibility that stress-induced exacerbation of symptoms in schizophrenia, which is characterized by deficient PPI, may be CRF-dependent.

Acoustic Stimulation↗
PubMed2005

Elimination kinetics of L-alanyl-L-glutamine in ICU patients.

A randomised, double blind, placebo-controlled study was performed giving 0.5 g x kg(-1) x day(-1) of undiluted alanyl-glutamine (20%) or saline in a peripheral vein during 4 hours in ICU patients (n = 20). During the infusion period a steady state in plasma concentration was reached for alanyl-glutamine, but not for alanine, glutamine or glutamate. On the other hand there was no accumulation of any of the amino acids, as the pre-infusion concentrations were reached within 8 hours after the end of infusion. The half-life of the dipeptide was 0.26 hours (range, 0.15-0.63 h). The distribution volume of alanyl-glutamine was larger than the extracellular water volume, indicating a rapid hydrolysis of the dipeptide. There was no detectable alanyl-glutamine in the urine of any of the patients. All patients had excretion of small amounts of amino acids in urine, but the renal clearance of alanine, glutamine and glutamate were not different between the two groups.

Adult↗
PubMed1980

The site of the dipsogenic action of angiotensin II in the North American opossum.

Adult North American opossums (Didelphis virginiana), predominantly nocturnal water drinkers, were found to respond by drinking to water deprivation, cellular dehydration produced by intravenous infusion of hypertonic saline, and to both intravenous and intracerebroventricular administration of angiotensin II (AII). By taking advantage of the absence of the corpus callosum, an anatomical characteristic of the marsupial, we removed the subfornical organ and implanted a cannula into the anterior third ventricle under direct visual guidance. In these animals: (1) spontaneous drinking, and responses to water deprivation and cellular dehydration were unaffected; (2) after a postoperative period of unresponlsiveness, attenuated and unreliable responses only to high doses of intracerebroventricular AII could be elicited; and (3) the dipsogenic effect of intravenous AII was abolished. We conclude that the subfornical organ is necessary for the physiologically appropriate effect of AII on drinking but that, in the absence of the subfornical organ, the brain can mediate the dipsogenic effect of intracranially administered AII, although the physiological significance of the latter phenomenon is unclear.

Angiotensin II↗
PubMed1980

Stimulation of LH and FSH secretion following intraventicular injection of cysteic acid but not taurine.

Taurine and related neurally active metabolites, were tested for their ability to influence basal secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH). The animal model used was the unanesthetized, unrestrained adult rat with an indwelling catheter in the jugular vein and a cannula implanted in the right lateral cerebroventricle or anterior pituitary. The proposed inhibitory neurotransmitter traurine, and its metabolic precursor, hypotaurine, did not affect the secretion of LH or FSH following infusion of 0.2 or 2.0 mumol intraventricularly or into the pituitary. In contrast, intraventricular injection of cysteic acid, a neurally excitant amino acid, in doses of 2.0 and 0.2 mumol promoted pituitary secretion of LH in both male and female rats. FSH secretion was also increased slightly by cysteic acid (2.0 mumol). These studies provide additional evidence that excitatory amino acids have a stimulatory role in the release of pituitary gonadotropins.

Amino Acids, Sulfur↗