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PubMed1996

Loss of striatal DA innervation increases striatal trophic activity directed at DA neurons in culture.

Male rats received intraventricular infusions of the dopamine (DA) neurotoxin 6-hydroxydopamine (6-OHDA; 0, 75, 150, and 250 micrograms) in order to determine if DA neuron loss was associated with an increase in striatal trophic activity. After 4 weeks, the animals were sacrificed and perfused with normal saline, and the brains were removed, immediately frozen, and processed. Intraventricular infusions of 6-OHDA were associated with a dose-dependent reduction in striatal DA content and tyrosine hydroxylase-immunoreactive (THir) cell counts in the substantia nigra while striatal DA activity ([HVA]/[DA]) was increased. Extracts of the striatum from these animals increased the survival of E15 primary, dissociated rostral mesencphalic cultures growing at low cell density. This growth effect was positively correlated with the dose of 6-OHDA infused. THir cell counts present in high-cell-density mesencephalic cultures following 72 h of extract incubation were similarly correlated to 6-OHDA dose but inversely correlated with striatal DA content and THir cell counts in the substantia nigra. Trophic activity in the cerebellar extracts from these animals was significantly lower than that present in striatal extracts and was not influenced by 6-OHDA lesions. These data suggest that loss of DA innervation in the striatum is associated with an increase in striatal trophic activity directed at DA neurons. A compensatory response to the loss of DA neurons involving increased striatal trophic activity may result in increased DA terminal sprouting of remaining viable DA neurons that, in turn would serve to help reinstate normal DA tone.

Animals↗
PubMed1991

Intracerebral distribution of DL-2-amino-phosphonopentanoic acid (AP5) and the dissociation of different types of learning.

Chronic intraventricular infusion of the selective NMDA receptor antagonist AP5 appears to cause an impairment of spatial but not visual discrimination learning. However, Goddard (1986) has questioned whether this dissociation in task-selectivity reflects a difference in the underlying neural mechanisms or differential drug diffusion. Two experiments conducted to address this issue established (a) that chronic intraventricular infusion of AP5, at a dose sufficient to cause a spatial learning impairment, results in a relatively uniform distribution of the drug across the brain, and (b) that chronic bilateral intracortical infusion at sites very close to visual cortex also fails to impair visual discrimination learning. These findings argue against differential diffusion being a major cause of the sensitivity of spatial but not visual discrimination tasks to AP5, and raises the possibility that representational and procedural memory tasks may depend upon distinct cell-biological mechanisms of plasticity.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Cyclic nucleotides and ethanol tolerance and dependence.

Acute ethanol administration decreases cyclic AMP levels in brains of some animal strains. The ethanol-induced decrease of cyclic GMP levels cannot be blocked by intraventricular infusion of calcium but it can be prevented by pretreatment with pyrazole. Although cyclic AMP levels in the cerebral cortex change reciprocally after acute ethanol administration and during withdrawal, the increase observed during withdrawal is probably secondary to some withdrawal processes. Ethanol decreases cerebellar GABA levels only in rats which are stressed prior to sacrifice. Chronic intraventricular infusion of calcium increased the intensity of an acoustic startle response during ethanol withdrawal while EGTA infusion delayed the development of tolerance to the hypothermic effect of ethanol. The ratio of cyclic GMP to GABA levels is postulated to be important for expression of the withdrawal syndrome.

Animals↗
PubMed1996

Survival and proliferation of nonneural tissues, with obstruction of cerebral ventricles, in a parkinsonian patient treated with fetal allografts.

BACKGROUND: Since 1985, treatment of idiopathic Parkinson's disease (PD) by surgical transfer of adult or fetal chromaffin tissue or of fetal central neural tissue to the brains of afflicted patients has been attempted, with variable clinical results. Neuropathologic studies of the status of these transplants are few and show wide variation in degree of graft survival. METHODS: We report the case of a 52-year-old man, who, 23 months earlier, received both intrastriatal implantation and intraventricular infusion of tissues derived from fetuses of 15 to 16 weeks and 5 to 6 weeks gestational age. Clinical improvement, as measured by increased amounts of "on" time with reduced levodopa requirements, seemed to occur over the subsequent months. He died suddenly at home after a several-hours interval of progressive lethargy and breathing difficulties. RESULTS: At autopsy, the diagnosis of PD was confirmed. Intrastriatal graft sites were identified, but contained no viable neurons; astrogliosis, focal microgliosis, and mixed inflammatory response, suggesting allograft rejection, were present. Surprisingly, the intraventricular tissues survived and showed ectodermal and mesenchymal, but no neural, differentiation, as well as cellular response; the left lateral and fourth ventricles were filled completely by this proliferated tissue. CONCLUSIONS: By intraventricular infusion, tissues from early-gestation sources can engraft successfully, grow, and survive for at least 23 months in the brain of a PD patient. However, contamination by, or differentiation into, nonneural tissues can occur, can lead to proliferation of tissues within ventricular spaces, and may result in ventricular obstruction. Grafts, whether intraventricular or intraparenchymal, are capable of inciting host responses, which in turn may limit their long-term survival. Finally, post-transplant clinical improvement in symptoms of PD may be unrelated to survival of engrafted neurons.

Adult↗
PubMed1989

Effect of intraventricular nadolol infusion on shock-induced aggression in 6-hydroxydopamine-treated rats.

Increasingly, beta blockers are being utilized to treat patients with aggressive disorders secondary to brain lesions. To secure further data about the potential efficacy of beta blockers for this condition, a rat model was employed in which aggression was enhanced by 6-hydroxydopamine. Following lesioning of the brain, aggression in the rats increased from an average baseline of 10.9 +/- 2.1 to 42.7 +/- 2.0 fights per testing period. Thereafter, either pharmacologically inert, artificial CSF or nadolol was introduced through transcerebral, intraventricular perfusion with a significant reduction in aggression in the nadolol-treated animals when compared with those receiving artificial CSF.

Aggression↗
PubMed1997

Cathepsin B and middle cerebral artery occlusion in the rat.

Lysosomal proteases, although tightly regulated under physiological conditions, are known to contribute to cell injury after various forms of tissue ischemia have occurred. Because cathepsin B is a prominent lysosomal protease found in brain parenchyma, the authors hypothesized that it may contribute to neuronal cell death after focal cerebral ischemia. The authors measured the expression and spatial distribution of cathepsin B within the ischemic brain in 43 animals by means of immunohistochemical analysis in a rat model of transient middle cerebral artery (MCA) occlusion. Cathepsin B activity was also measured within specific ischemic brain regions by using an in vitro assay (22 animals). In addition, the authors tested the therapeutic effect of preischemic intraventricular administration of stefin A, a cysteine protease inhibitor, on the volume of cerebral infarction after transient MCA occlusion (15 animals). Increased cathepsin B immunoreactivity was detected exclusively within the ischemic neurons after 2 hours of reperfusion following a 2-hour MCA occlusion. Cathepsin B immunolocalization in the ischemic region decreased by 24 hours of reperfusion, but then increased by 48 hours of reperfusion because the infarct was infiltrated by inflammatory cells. Increased immunolocalization of cathepsin B in the inflammatory cells located in the necrotic infarct core continued through 7 days of reperfusion. Cathepsin B enzymatic activity was significantly increased in the ischemic tissue at 2, 8, and 48 hours, but not at 24 hours of reperfusion after 2 hours of MCA occlusion. Continuous intraventricular infusion of stefin A, before 2 hours of MCA occlusion (15 animals), significantly reduced infarct volume compared with control animals (12 animals): the percentage of hemispheric infarct volume was 20+/-3.9 compared with 33+/-3.5 (standard error of the mean; p = 0.025). These data indicate that neuronal cathepsin B undergoes increased expression and activation within 2 hours of reperfusion after a 2-hour MCA occlusion and may be a mechanism contributing to neuronal cell death. Intraventricular infusion of stefin A, an inhibitor of cathepsin B, significantly reduces cerebral infarct volume in rats.

Animals↗
PubMed1996

Effects of unilateral or bilateral lesions within the anteroventral third ventricular region on c-fos expression induced by dehydration or angiotensin II in the supraoptic and paraventricular nuclei of the hypothalamus.

This paper reports the effects of AV3V lesions on the pattern of c-fos induced by 24 h dehydration. As expected, bilateral electrolytic lesions within the AV3V region (the ventral median preoptic nucleus) suppressed water intake following 24 h water deprivation. C-fos expression was also suppressed in the supraoptic (SON) and (less completely) in the paraventricular (PVN) nuclei, but not in the subfornical organ (SFO). Unilateral lesions of the AV3V region suppressed c-fos expression in the ipsilateral SON, but this selective ipsilateral effect was less in the PVN. The SFO was again unaffected. Unilateral lesions also suppressed c-fos expression in the ipsilateral SON and PVN (to a lesser degree) following intraventricular infusions of angiotensin II (250 pmol). These results suggest that the cellular response of supraoptic neurons to osmotic stimuli require inputs from the AV3V region, but that this is less absolute for the PVN; that the projection from the ventral AV3V area to the SON is ipsilateral, but that to the PVN may be less lateralised. Activation of the SFO by dehydration is not dependent upon the integrity of the ventral AV3V region. These results are closely comparable to the effects of similar lesions on c-fos expression following intraventricular infusions of angiotensin II, and suggest that the effect of dehydration on forebrain c-fos expression may be related to the central actions of angiotensin II.

Angiotensin II↗
PubMed1984

Reduction of food intake and body weight by chronic intraventricular insulin infusion.

This study examined the effect of chronic infusions of insulin in one of three doses (5, 7.5 or 10 mU/day) into the third ventricle, on food and water intake and body weight in the rat. Solutions were infused via osmotic minipumps at a rate of 1 microliter/hour for seven days. The two highest doses of insulin produced a dose-related suppression of food intake and weight loss, which was greater than the effect produced by 5 mU/day or a control infusion of Ringers solution. The effect of 5 mU/day on food and water intake and body weight was similar to the effect of the control infusion. All groups treated with insulin decreased food intake during the day and night, although only differences in nighttime food intake were statistically significant. Ten mU/day also produced a significantly greater reduction in water intake than each of the other solutions. Weight loss in the animals infused with insulin could not be explained by a decrease in caloric intake alone. Food intake returned to normal in all groups by the end of a seven day post-infusion period, with recovery being slowest among the animals receiving the highest doses of insulin. All animals recovered body weight at approximately the same rate. These results provide further evidence for the view that brain insulin plays a role in the regulation of food intake and body weight.

Animals↗
PubMed2000

Transforming growth factor-beta1 induces transforming growth factor-beta1 and transforming growth factor-beta receptor messenger RNAs and reduces complement C1qB messenger RNA in rat brain microglia.

Transforming growth factor-beta1 is a multifunctional peptide with increased expression during Alzheimer's disease and other neurodegenerative conditions which involve inflammatory mechanisms. We examined the autoregulation of transforming growth factor-beta1 and transforming growth factor-beta receptors and the effects of transforming growth factor-beta1 on complement C1q in brains of adult Fischer 344 male rats and in primary glial cultures. Perforant path transection by entorhinal cortex lesioning was used as a model for the hippocampal deafferentation of Alzheimer's disease. In the hippocampus ipsilateral to the lesion, transforming growth factor-beta1 peptide was increased >100-fold; the messenger RNAs encoding transforming growth factor-beta1, transforming growth factor-beta type I and type II receptors were also increased, but to a smaller degree. In this acute lesion paradigm, microglia are the main cell type containing transforming growth factor-beta1, transforming growth factor-beta type I and II receptor messenger RNAs, shown by immunocytochemistry in combination with in situ hybridization. Autoregulation of the transforming growth factor-beta1 system was examined by intraventricular infusion of transforming growth factor-beta1 peptide, which increased hippocampal transforming growth factor-beta1 messenger RNA levels in a dose-dependent fashion. Similarly, transforming growth factor-beta1 increased levels of transforming growth factor-beta1 messenger RNA and transforming growth factor-beta type II receptor messenger RNA (IC(50), 5pM) and increased release of transforming growth factor-beta1 peptide from primary microglia cultures. Interactions of transforming growth factor-beta1 with complement system gene expression are also indicated, because transforming growth factor-beta1 decreased C1qB messenger RNA in the cortex and hippocampus, after intraventricular infusion, and in cultured glia. These indications of autocrine regulation of transforming growth factor-beta1 in the rodent brain support a major role of microglia in neural activities of transforming growth factor-beta1 and give a new link between transforming growth factor-beta1 and the complement system. The auto-induction of the transforming growth factor-beta1 system has implications for transgenic mice that overexpress transforming growth factor-beta1 in brain cells and for its potential role in amyloidogenesis.

Alzheimer Disease↗
PubMed1981

Cerebrospinal fluid pulse wave form analysis during hypercapnia and hypoxia.

Systems analysis of cerebrospinal fluid pulse wave forms (CSFPWs) was carried out in 19 cats during the inhalation of 5% CO2 + 95% O2. 10% CO2 + 90% O2 and 10% O2 + 90% N2. The results were compared to CSFPWs obtained during the inhalation of 100% O2 and during an intraventricular infusion to the same level of cerebrospinal fluid (CSF) pressure (CSFP) as produced by the test gas. The systemic arterial pressure pulse was utilized as the system input, and the CSFP pulse was used as the output. The harmonic amplitudes of the two pulses and the amplitude transfer function (XFRa) between the pulses were calculated. Hypercapnia and and hypoxia produced an increase in CSF pulse pressure (delta Pcsf), an increase in primarily the XFRa of the fundamental frequency, and as a result, an increase in amplitude of the fundamental frequency of the CSFPW with rounding of the pulse wave. The changes are greater than those noted during an intraventricular infusion (IVI) to the same level of CSFP. In addition, the volume-pressure test was performed on the hypercapnic animals. The volume-pressure response was less during hypercapnia than during the IVI at the same mean level of CSFP. The result suggest that the increase in deltaP csf is related to cerebral arteriolar vasodilation and not to a steepening of the volume-pressure curve and that rounding of the CSFPW is related to a decrease in cerebrovascular tone.

Animals↗
PubMed1989

Intraventricular NGF infusion in the mature rat brain enhances sympathetic innervation of cerebrovascular targets but fails to elicit sympathetic ingrowth.

The ability of peripheral axons to regenerate long distances in the peripheral nervous system (PNS) is well documented; however, examples of axonal elongation within the adult mammalian central nervous system (CNS) are rare. One example of axonal growth in the mature brain is the sprouting of sympathetic axons into the hippocampal formation following disruption of the septohippocampal pathway. A current hypothesis is that elevated hippocampal NGF levels, secondary to loss of retrograde transport by septal neurons, elicits sympathetic ingrowth, In this study, we sought to determine whether elevation of hippocampal NGF activity without septal denervation is sufficient to elicit sympathetic sprouting. Forty-one female rats were infused for two weeks with NGF or cytochrome C in the right lateral ventricle through cannulae connected to an osmotic minipump. In some animals the brains were sectioned and stained for acetylcholinesterase (AChE) activity and norepinephrine histofluorescence; in others, CNS tissue was assayed for nerve growth factor (NGF) content with a two-site ELISA. A Farrand microspectrophotometer was used to measure the intensity of catecholamine fluorescence around the internal carotid artery. The average fluorescence intensity of the sympathetic innervation of the internal carotid artery in the NGF-injected animals was over twice that of vehicle-injected rats indicating that the infused NGF was both accessible to the sympathetic axons and biologically active. However, in none of the cases with elevated hippocampal NGF levels were sympathetic axons observed within the hippocampal formation or any other brain region. These results suggest that simple elevation of brain NGF, while perhaps necessary, is insufficient to permit the growth of sympathetic axons into the mature mammalian CNS.

Adrenergic Fibers↗
PubMed1989

Synergism of intraventricular NaCl infusion and subpressor angiotensins in rats.

The effect of selective salt infusion to the central nervous system on the blood pressure (BP) regulation was examined in male Wistar rats. Hypertonic NaCl (0.8 M, 1 microliter/h) was infused into the lateral ventricle concomitantly with intravenous infusion of a subpressor dose (5.4 pmol.kg-1.min-1) of angiotensin II (ANG II) or its analogues for 7 days using osmotic minipumps. The BP was not increased by intracerebroventricular infusion of NaCl alone at this dose but was significantly and consistently increased by concomitant intravenous infusion of ANG II or its analogues. The increases in the BP over the base-line values on day 7 in groups on infusions of ANG II, ANG III, and pentasarcosyl-ANG II [(Sar)5ANG II] were 29 +/- 5 mmHg (n = 9, P less than 0.05), 8 +/- 2 mmHg (n = 8, P less than 0.05), and 19 +/- 3 mmHg (n = 6, P less than 0.05), respectively. The responses to hexamethonium, prazosin, and antagonists of arginine vasopressin and ANG II were examined in separate sets of conscious and unrestrained animals that had received intracerebroventricular infusion of NaCl and intravenous infusion of ANG II for the preceding 6 days. These animals showed significantly greater depressor responses only to hexamethonium and prazosin than control. These results indicate that the pressor effect of continuous and concomitant administration of intracerebroventricular NaCl and intravenous ANG II is mainly due to activation of the sympathetic nerve function. Synergism of the effects of selective central sodium administration and a subpressor dose of ANG II in the central nervous system is suggested.

Angiotensins↗
PubMed1977

Search for a natriuretic mechanism sensitive to sodium in the brain of the monkey.

1. The effects of hypertonic saline infusion into the third ventricle were investigated in ten monkeys which were pre-operated, trained, and used in the conscious state under controlled conditions. 2. In non-hydrated monkeys, intraventricular infusion of NaCl 1.0 M, 0.01 ml./min for 30 min did not affect urine volume or Na output but produced a small increase in urine osmolality. Comparable infusion of NaCl 0.15 M had no effect on any parameter. 3. In monkeys undergoing water diuresis (with i.v. infusion of 5% dextrose), intraventricular hypertonic saline produced large reciprocal changes in urine volume and osmolality while urine Na showed no significant change. The effects on urine volume and osmolality were greater than those of lysine-vasopressin 30 m-u./kg i.v. 4. The absence of natriuresis after intraventricular hypertonic saline infusion in the monkey was in notable contrast to the results reported in lower species. However, the data suggested that the infusion probably released ADH as in other species.

Animals↗
PubMed2002

The effects of melatonin and Ginkgo biloba extract on memory loss and choline acetyltransferase activities in the brain of rats infused intracerebroventricularly with beta-amyloid 1-40.

Intraventricular infusion of rats with beta-amyloid for 14 days resulted in memory deficit in the water maze as well as decreases in choline acetyltransferase activities and somatostatin levels in the cerebral cortex and hippocampus. These changes were not altered by daily intraperitoneal injection of 20 mg/Kg melatonin. Orally administered Ginkgo biloba extract, however, partially reversed the memory deficit and the decrease in choline actyltransferase activities in the hippocampus. The latter treatment failed to reverse the decrease in somatostatin levels. The results indicate that orally administered Ginkgo biloba extract can protect the brain against beta-amyloid from changes leading to memory deficit through its effect on the cholinergic system.

Administration, Oral↗
PubMed1991

Effects of intracerebroventricular administration of d-fenfluramine and d-norfenfluramine, as a single injection or 2-hr infusion, on serotonin in brain: relationship to concentrations of drugs in brain.

The effects of d-fenfluramine (DF) and d-norfenfluramine (DNF), administered intracerebroventricularly (i.c.v.) on levels of serotonin (5-HT) in the brain, was assessed in relation to levels of drugs in brain. d-Fenfluramine, as a single injection (500 micrograms/20 microliters), caused no significant changes in 5-HT in whole brain from 15 to 480 min after injection. When infused intraventricularly for 2 hr, DF and DNF at 500 but not at 125 250 micrograms/hr, markedly reduced concentrations of 5-HT in brain 4 hr after the end of the infusion. At this time levels of DNF in brain were similar (between 4 and 5 micrograms/g) with both compounds, whereas levels of DNF after single intraventricular injections of DF were below 2 micrograms/g at all times after injection. Infusion of 500 micrograms/hr of DNF for 2-hr reduced concentrations of 5-HT in various regions of the brain, with the exception of the brainstem, whereas 250 micrograms/hr of DNF significantly lowered levels of 5-HT only in the cortex. The effect of infusion of 500 micrograms/hr of DNF was specific for 5-HT (no effect on dopamine and norepinephrine) and lasted for at least 168 hr. The results suggest that the effect on 5-HT in brain of intraventricular infusion of DF, but not a single injection, was due to the fact that, only in the former condition were adequate levels of DNF, the active metabolite of DF, reached in the brain. These results are relevant to the interpretation of studies in which biochemical changes in the brain after intraventricular administration, are reported without any measurement of the drug or its active metabolites, in plasma and brain.

Animals↗
PubMed1975

Prostaglandin E2-induced release of LHRH into hypophysial portal blood(1).

Prostaglandin E2 (PGE2) was infused into a lateral ventricle of adult male rats or infused into a hypophysial portal vessel. Intraventricularly administered PGE2 stimulated the release of LH, FSH, and prolactin but not TSH. Intraventricular infusion of the control solution did not alter the basal release of any of these hormones. PGE2 was found to be a potent stimulator of LH release, but larger quantities were needed to stimulate the release of FSH or prolactin. In addition, lateral ventricle infusion of 5 mug or 20 mug of PGE2 stimulated a 2- to 3-fold increase in the concentration of LHRH in hypophysial portal plasma but did not affect LHRH levels in arterial plasma. PGE2 infused into a hypophysial portal vessel at a rate of 0.167 mug/min for 30 min, or infusion of the control solution, resulted in similar changes in the concentration of FSH, LH, and prolactin in arterial plasma. The results of this investigation suggest that PGE2 stimulates the release of gonadotropins in vivo by enhancing the release of LHRH. The portal vessel infusion studies do not support a direct stimulatory effect of PGE2 on the pituitary gonadotrophs.

Animals↗
PubMed1994

Cerebral subarachnoid sampling of cerebrospinal fluid in the rhesus monkey.

A previously described rhesus monkey model with two intraventricular catheter systems was expanded to provide a means of studying drug concentrations of chemotherapeutic agents such as methotrexate (MTX) in the cerebral subarachnoid cerebrospinal fluid (CSF) following intrathecal drug injection. A continuous intraventricular infusion of MTX was started through the lateral ventricular catheter 44 h before surgical placement of the cerebral subarachnoid catheter to allow for steady-state concentrations to be attained throughout the subarachnoid space. Monkeys were anesthetized intramuscularly with ketamine hydrochloride (7 mg/kg) and xylazine (6 mg/kg) to allow placement of a temporary lumbar catheter for sampling of lumbar CSF Sodium thiopental (2.5%) was given intravenously if needed for intubation and anesthesia was maintained with isoflurane (0.5 to 1.5%) and oxygen during the surgical placement and sampling of the cerebral subarachnoid catheter. A midline incision was made over the frontal bone and a 3/8-inch trephine was used to expose the dura adjacent to the lateral midline. Following puncture of the dura with an 18-gauge spinal needle, the cerebral subarachnoid catheter (0.025-inch [i.d.] x 0.047-inch [o.d.] Silastic tube) was passed into the subarachnoid space for approximately 10 to 17 mm. The CSF from the cerebral subarachnoid catheter was collected by gravity flow Ventricular, lumbar subarachnoid, and cerebral subarachnoid CSF were collected concurrently at 44, 46, and 48 h after the start of MTX infusion. Mean ventricular, lumbar subarachnoid, and cerebral subarachnoid CSF methotrexate concentrations at steady state were 5.8, 1.0, and 1.5 mumol/L, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗