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PubMed2000

Preferential destruction of cerebellar Purkinje cells by OX7-saporin.

Saporin, a plant toxin derived from Saponaria officinalis, disrupts protein synthesis by inactivating the 60S portion of the ribosomal complex. OX7 is a mouse monoclonal antibody directed against the Thy-1.1 receptor that is differentially expressed on subpopulations of central nervous system neurons. Disulfide conjugation of OX7 to saporin permits delivery of saporin to target neurons. OX7-saporin was used to study the behavioral and morphological consequences of selective destruction of cerebellar Purkinje cells which abundantly express the Thy-1.1 antigen. Male Sprague-Dawley rats received bilateral intraventricular injections of 1- or 2 microg OX7-saporin or 8 microl artificial CSF. Rats were tested for behavioral changes 1 week before and 1, 2, and 8 weeks post-treatment. OX7-saporin treatment resulted in dose- and time-dependent changes in motor performance, activity, and negative geotaxis, but did not affect foot splay. Following behavioral testing, cerebellar sections were prepared for microscopic examination and the pattern of Purkinje cell loss was determined in anatomically matched sections. OX7-saporin induced dose-dependent death of Purkinje cells, particularly in the anterior and superior portions of cerebellar folia 1-6 and folium 9. Other brain regions appeared largely unaffected. Data suggest that intraventricular injection of rats with OX7-saporin is an effective model with which to examine the consequences of Purkinje cell destruction.

Animals↗
PubMed1986

Leukotriene C4 transport and metabolism in the central nervous system.

The transport and metabolism of radiolabeled leukotriene (LT) C4 in the CNS were investigated after intraventricular injection. Under thiopental (Pentothal) anesthesia, New Zealand white rabbits were injected intracerebroventricularly with 0.2 ml of artificial CSF containing 2.5 microCi of [3H]LTC4 (36 Ci/mmol), 0.3 microCi of [14C]mannitol, and, in some cases, 0.9 mg of probenecid, 1.8 mg of cysteine, 1.4 micrograms of unlabeled LTC4, or 2 mg of tolazoline HCl. After 2 h, the conscious rabbits were killed, and the quantity and nature of the 3H and 14C were determined in CSF, choroid plexus, and brain. The [3H]LTC4 recovered in CSF and brain was not extensively metabolized, as greater than 70% of the 3H remained [3H]LTC4, although some spontaneous conversion to 11-trans-[3H]LTC4 occurred. Oxidized forms of [3H]LTC4, [3H]LTD4, and [3H]LTE4 did not exceed 18% in CSF and brain. After intraventricular injection of [3H]LTC4, 3H was transferred from the CSF to blood by a probenecid-sensitive, but tolazoline-insensitive, transport system in the CNS much more rapidly than mannitol. Cysteine decreased the retention of [3H]LTC4 in brain. These results are consistent with previous in vitro observations that [3H]LTC4 is transferred from CSF into blood by an efficient transport system for LTC4 in choroid plexus.

Animals↗
PubMed1998

Selective in vivo fluorescence labelling of cholinergic neurons containing p75(NTR) in the rat basal forebrain.

The cholinergic system of the rat basal forebrain is used as a model for the homologous region in humans which is highly susceptible to neuropathological alterations as in Alzheimer's disease. Cholinergic cells in the basal forebrain express the low-affinity neurotrophin receptor p75NTR. This has been utilized for selective immunolesioning of cholinergic neurons after internalization of an immunotoxin composed of anti-p75NTR and the ribosome-inactivating toxin saporin. However, the goal of many studies may be not the lesion, but the identification of cholinergic cells after other experimentally induced alterations in the basal forebrain. Therefore, a novel cholinergic marker was prepared by conjugating the monoclonal antibody 192IgG directed against p75NTR with the bright red fluorochrome carbocyanine 3 (Cy3). Three days after intraventricular injection of Cy3-192IgG the fluorescence microscopic analysis revealed a pattern of Cy3-labelled cells matching the distribution of cholinergic neurons. Apparently the marker was internalized within complexes of p75NTR and Cy3-192IgG which were then retrogradely transported to the cholinergic perikarya of the basal forebrain. In addition to the even labelling of somata, a strong punctate-like Cy3-immunofluorescence was seen in structures resembling lysosomes. The specificity of the in vivo staining was proven by subsequent immunolabelling of choline acetyltransferase (ChAT) with green fluorescent Cy2-tagged secondary antibodies. In the medial septum, the diagonal band and the nucleus basalis only cholinergic neurons were marked by Cy3-192IgG. In parallel experiments, digoxigenylated 192IgG was not detectable within cholinergic basal forebrain neurons after intraventricular injection. Presumably, this modified antibody could not be internalized. On the other hand, digoxigenylated 192IgG was found to be an excellent immunocytochemical marker for p75NTR as shown by double labelling including highly sensitive mouse antibodies directed against ChAT. Based on the present findings, future applications of the apparently non-toxic Cy3-192IgG and other antibodies for fluorescent in vivo and in vitro labelling are discussed.

Animals↗
PubMed1982

The effects of neurotensin on anterior pituitary hormone secretion.

The present experiments were conducted to determine the effects of neurotensin on secretion of a variety of anterior pituitary hormones. Conscious rats with indwelling cannulae in the third ventricle and external jugular vein were used and the effects on plasma hormone levels measured by radioimmunoassay. Neurotensin was found to decrease plasma prolactin levels in ovariectomized females, normal males, and males in which prolactin levels had been elevated by ether or by a combination of fluoxetine and 5-hydroxytryptaphane. The prolactin-lowering effect was blocked by alpha-methyl-tyrosine to inhibit catecholamine synthesis and by the specific dopamine receptor blocker, spiroperidol. In ovariectomized females, neurotensin was also capable of suppressing LH and elevating growth hormone following its intraventricular injection. Intravenous injection of the peptide elevated prolactin but had no effect on the release of the other pituitary hormones. When hemipituitaries of ovariectomized rats were incubated in vitro, neurotensin elevated prolactin and TSH release into the medium. The minimal effective dose to elevate prolactin and TSH release was 50 ng/ml. Release of gonadotropins and growth hormone was unaffected. It is concluded that neurotensin inhibits prolactin release by a CNS, presumably hypothalamic action, to stimulate the tuberoinfundibular dopaminergic neurons. The dopamine released then inhibits prolactin release either by a direct action on the pituitary or by release of another prolactin-inhibiting factor. In addition, the peptide has a direct prolactin-releasing action on the pituitary. Neurotensin can inhibit LH and stimulate growth hormone presumably by a hypothalamic action since there was no effect on the release of these pituitary hormones by glands incubated in vitro. Although the peptide had no effect on TSH release following its intraventricular injection, it stimulated prolactin release by pituitaries incubated in vitro. The physiological significance of these results is not yet established; however, the presence of the peptide in regions concerned with pituitary control suggests that it may play a physiological role.

5-Hydroxytryptophan↗
PubMed1981

Magnitude and duration of hyperactivity following neonatal 6-hydroxydopamine is related to the extent of brain dopamine depletion.

This experiment examined the relationship between the extent of brain dopamine (DA) neuron destruction in the neonatal rat and locomotor hyperactivity during subsequent development. Brain DA neurons were destroyed selectively in neonatal rats by intraventricular injections of 6-hydroxydopamine (6-OHDA) following desmethylimipramine (DMI) pretreatment of both days 3 and 6 of life. Groups of rats received total doses of 50, 70, 100 or 200 microgram of 6HDA or the vehicle solution. Each group of rats given 6-OHDA displayed 3- to 5-fold increases in locomotor activity relative to vehicle control rats on days 16 and 18 of life. Rats given 50 or 70 microgram of 6-OHDA displayed hyperactivity that diminished during days 18-32 of life, approaching the level of activity seen in vehicle-treated rats. It contrast, rats given 100 or 200 microgram of 6-OHDA displayed consistently high levels of locomotion during days 18-32 of life. When tested as adults (days 55-66 of life) only those rats given 200 micrograms of 6-OHDA as neonates continued to display locomotor hyperactivity. The extent of 6-OHDA-induced depletion of DA was proportional to the magnitude of locomotor hyperactivity seen during neonatal life. Brain DA was depleted to the greatest extent in rats which displayed permanent hyperactivity. Regardless of the extent of depletion of brain DA, adult rats given intraventricular injections of 125, 200 or 275 micrograms of 6-OHDA at 48 days of age (following pargyline and DMI pretreatment) displayed no significant change in locomotor activity. These results indicate that the magnitude and duration of locomotor hyperactivity seen following neonatal 6-OHDA injections are correlated with the extent of loss of central DA neurons and suggest that brain DA projections exert important influences on the ontogeny of normal locomotion.

Animals↗
PubMed1997

Transmyocardial laser revascularization induces cerebral microembolization.

BACKGROUND: Transmyocardial laser revascularization may vaporize fluid in the left heart, allowing bubbles to form. This study aimed to determine whether the laser pulse resulted in cerebral emboli and to examine changes in middle cerebral artery flow velocity and jugular bulb oxygen saturation (SjO2) during transmyocardial laser revascularization. METHODS: Twelve patients (American Society of Anesthesiologists physical status III) were studied after the authors received institutional review board approval and the patients' informed consent. Monitored variables included mean arterial blood pressure (measured in millimeters of mercury), heart rate (measured as beats/min), and partial pressure of carbon dioxide (measured in millimeters of mercury). A 5-MHz transesophageal-sonography system was used to record intraventricular events after laser injection. Mean blood flow velocity (Vmean; measured in centimeters per second) was monitored in the middle cerebral artery using transcranial Doppler sonography, and SjO2 (expressed as a percentage) was measured using a fiberoptic thermodilution catheter placed in the right jugular bulb. Data were recorded before, during, and for 4 min after laser injection. RESULTS: After laser injection, intraventricular echogenic contrast was seen in transesophageal-sonography, and 2-4 s later high-intensity signals (microemboli) appeared in the transcranial Doppler sonography spectra. As long as mean arterial pressure remained stable during the observation period, Vmean and SjO2 did not change. CONCLUSIONS: These data show that microemboli can be detected after laser injection in the middle cerebral artery, although they do not effect Vmean and SjO2. The results suggest that these microemboli do not induce a global oxygen imbalance.

Aged↗
PubMed1984

Neurophysiological effects of capsaicin.

Data obtained from neonatally treated rats are fairly consistent. However, there is disagreement as to whether mechanical and thermal nociceptive thresholds are elevated or unchanged in this group. There are at least two major areas of disagreement in adult animal capsaicin research. Behavioral data are extremely variable. The thermal nociceptive threshold after systemic capsaicin has been reported to be both raised and lowered. After intrathecal capsaicin injection, the thermal nociceptive threshold was reported raised, but onset and duration of responses varied and some animals exhibited no changes. Capsaicin application to peripheral nerve, however, drastically increased thermal threshold. Mechanical pain threshold has been reported both increased and unchanged after systemic capsaicin treatment and unchanged after intrathecal injection. Obviously, capsaicin's effects upon pain perception are not fully understood. Although lower on the phylogenetic scale than many mammals, rodents exhibit complex individualistic behavior. Lower vertebrates may eventually provide more simple behavioral models for pain tolerance. Investigators also disagree as to whether C fibres can conduct action potentials after local capsaicin application. C fibre conduction was reported unaffected by capsaicin in an acute preparation and for 13-21 days after treatment. On the other hand, C fibre compound action potentials have been reported diminished for up to 2 h after capsaicin application. Additional conduction impairment studies will be useful in comparing peripheral and intrathecal capsaicin application. There is general agreement that, allowing for variation in dosages and route of administration, capsaicin causes central and peripheral C fibre damage, though never as extensive in adults as in neonates. Neonatal capsaicin treatment (always s.c.) results in destruction of C and some A delta fibres and their central terminals. Capsaicin causes degeneration of C terminals in the adult CNS only when applied centrally. In both neonates and adults, s.c. capsaicin depletes the putative 'pain' peptide neurotransmitter, SP, from peripheral and sensory neurons and the tissues they innervate but not from the gut. Capsaicin-induced SP depletion in neonates is permanent. Systemic administration to adult depleted SP from much the same areas as observed in neonates, but all areas but the medulla exhibited a slow, regional recovery. Intraventricular injection of capsaicin depleted SP in the adult medulla only, while other SP-containing areas affected by systemic injection remained intact.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

Effect of intracerebroventricular bradykinin and related peptides on rabbit operant behavior.

The dose-effect relationships of intraventricularly injected bradykinin, Gly-Arg-Met-Lys-bradykinin (GAML-bradykinin), synthetic substance P and angiotensin II on lever-lifting behavior of rabbits in a variable-interval (VI) 72-second schedule of sweetened water presentation were determined. All peptides used caused dose-dependent decreases in overall rates of VI responding during the experimental session in the following order of potency: angiotensin II greater than bradykinin = substance P greater than GAML-bradykinin. The angiotensin II dose-effect curve was less steep than those of the other peptides. The administration of nearly equimolar doses of the bradykinin potentiating peptides, BPP5a and BPP9a, slightly decreased overall VI response rates and caused a 10- to 20-fold potentiation of the rate-decreasing effect of bradykinin on VI responding. Both angiotensin II and bradykinin caused pauses in responding of dose-dependent duration at the beginning of the experimental session that were followed by normal VI responding. The effect of GAML-bradykinin on VI performance was similar to that of bradykinin and angiotensin II but had a delay of onset of 3 to 6 minutes. In contrast, substance P caused actual decreases in response output and pauses of variable duration interspersed between periods of regular VI responding. At the doses used, both bradykinin-potentiating peptides caused uniform decreases in VI responding throughout the experimental session. Gross behavioral changes caused by the peptides were also observed. After the intraventricular injection of bradykinin or GAML-bradykinin, rabbits showed decreased motility, ptosis, miosis and lowered ears; after angiotensin II, animals remained motionless but with wide open eyes, fully raised ears and no miosis. In turn, substance P caused restlessness and increased locomotion. These results together with reported evidence on other powerful central actions of bradykinin, angiotensin and substance P and on the existence of components of their releasing and destroying enzymatic systems in the brain suggest that linear peptides may play a role in the functioning of the central nervous system.

Angiotensin II↗
PubMed1976

Influence of uridine-5-monophosphate on 3H-leucine incorporation into hippocampal neurons during learning.

The influence of UMP (injected intraventricularly) on the incorporation of 3H-leucine (injected intraperitoneally) was studied in rats using the microautoradiographic technique. Under the conditions of a brightness discrimination, the incorporation of labeled leucine into hippocampal neurons was significantly increased by UMP pretreatment, whereas under control conditions UMP caused only a tendency of increase without any statistical significance. It is suggested, that under learning conditions UMP substitution increases RNA synthesis, which would yield an enhanced protein synthesis.

Animals↗
PubMed1996

Electrographic patterns of postprandial sleep after food deprivation or intraventricular adrenaline injections in pigeons.

Intense postprandial sleep-like behavior was previously reported to occur, in a similar fashion, either after feeding evoked by intracerebroventricular adrenaline injections or after interruption of prolonged (96 h) fasting in conscious pigeons. These behavioral similarities were taken as indication of a physiological role for central adrenergic circuits in avian food intake regulation. In the present study we compared sleep-related electrographic signs (EEG, EMG, and EOG) that develop following both food intake-inducing situations to further examine these correspondences and their corollaries. Our data indicate that postprandial behaviors in the pigeon include dramatic increases in the incidence of slow-wave (SWS) and rapid eye movement sleep (REMS). The temporal distribution, total amount, and mean bout duration of these sleep states, as well as the latency for the first SWS episode, were statistically similar in both feeding behavior-inducing situations. Besides confirming early behavioral data, indicative of an engagement of adrenergic central components in food intake control, our results suggest that postprandial SWS could represent an important element of the feeding-related metabolic changes in pigeons, in a similar fashion to the observed in mammalian forms.

Animals↗
PubMed1984

Right ventricular imaging with digital subtraction angiocardiography using intraventricular contrast injection.

Angiocardiography is of considerable value in the dimensional analysis of the right ventricular (RV) cavity, but conventional angiocardiography requires large amounts of contrast medium. In this study digital subtraction angiocardiography was applied to biplane RV projections of 25 children with congenital heart disease after direct injection of a small dose of contrast medium. Volume measurements were compared with those obtained by conventional angiocardiography. The amount of contrast medium required was reduced to 30%, flow rate to 57% and ventricular ectopic activity to 60% of that used in conventional angiocardiography, and the degree of radiation exposure was reduced considerably. There was a good correlation for end-diastolic (r = 0.996) and end-systolic volume (r = 0.990) determined with both techniques. Digital subtraction angiography after selective RV injection allows accurate volume measurements of the right ventricle in children with congenital heart disease. The main benefits of this method are reduction of the amount of contrast medium, flow rate during injection, radiation and ventricular ectopic activity.

Adolescent↗
PubMed2003

HVJ-envelope vector for gene transfer into central nervous system.

To overcome some problems of virus vectors, we developed a novel non-viral vector system, the HVJ-envelope vector (HVJ-E). In this study, we investigated the feasibility of gene transfer into the CNS using the HVJ-E both in vitro and in vivo. Using the Venus reporter gene, fluorescence could be detected in cultured rat cerebral cortex neurons and glial cells. In vivo, the reporter gene (Venus) was successfully transfected into the rat brain by direct injection into the thalamus, intraventricular injection, or intrathecal injection, without inducing immunological change. When the vector was injected after transient occlusion of the middle cerebral artery, fluorescence due to EGFP gene or luciferase activity could be detected only in the injured hemisphere. Finally, luciferase activity was markedly enhanced by the addition of 50 U/ml heparin (P<0.01). Development of efficient HVJ-E for gene transfer into the CNS will be useful for research and clinical gene therapy.

Animals↗
PubMed1975

Effects of benzodiazepines on central serotonergic mechanisms.

If the rat conflict test were a valid animal model of anxiety neurosis, evidence which implicates serotonin systems in the anxiety-reducing actions of benzodiazepine tranquilizers could be summarized as follows: (1) The punishment-lessening effects of benzodiazepines in the conflict test are mimicked by serotonin antagonists (methysergide, cinanserin, bromolysergic acid), serotonin synthesis inhibition (PCPA), and serotonin nerve terminal damage (5,6-dihydroxytryptamine). (2) Punishment effects may be intensified by the serotonin precursor, 5-hydroxytryptophan (in combination with a monoamine oxidase inhibitor), serotonin agonists (alpha-methyltryptamine), or intraventricular injections of serotonin itself. Intraventricularly administered serotonin also antagonizes the punishment-lessening effects of benzodiazepines. (3) Stimulation of the serotonergic cell bodies in the dorsal raphe nucleus by local application of crystalline carbachol causes intense suppression of behavior. The suppressive effects of raphe stimulation are antagonized by systemic administration of benzodiazepines. (4) In biochemical experiments, the decrease in norepinephrine turnover induced by oxazepam rapidly undergoes tolerance, whereas the decrease induced in serotonin turnover is maintained over repeated doses. These results parallel findings in the conflict test which indicate that the depressant action of oxazepam rapidly undergoes tolerance, whereas the anxiety-reducing action is maintained over repeated doses. Although central serotonin neurons are thus implicated in the therapeutic actions of benzodiazepine tranquilizers, it is quite possible that the drugs actually act indirectly to reduce serotonin activity. The concept that benzodiazepines may exert a primary action on GABA-containing neurons, which in turn regulate serotonergic transmission, was supported by preliminary psychopharmacological evidence. The GABA-antagonist picrotoxin, at doses that do not disrupt unpunished behavior, fully antagonizes the punishment-lessening effects of benzodiazepines in the conflict test.

Animals↗
PubMed1985

"Epileptic" brain damage is replicated qualitatively in the rat hippocampus by central injection of glutamate or aspartate but not by GABA or acetylcholine.

Repeated intraventricular injection of the excitatory amino acids glutamate and aspartate for one hour produced morphologic changes in the hippocampus that were qualitatively identical to the acute and chronic changes seen in the brains of human epileptics and in experimental animals in which hippocampal seizure activity was induced by kainic acid or electrical stimulation of the perforant path. Light and electron microscopy revealed acute effects of glutamate and aspartate consisting of glial and dendritic swelling and neuronal soma necrosis ("dark cell degeneration"). Electron microscopy showed the focal dendritic swelling induced by glutamate or aspartate to be of the axon-sparing type with presynaptic terminals relatively unaffected. Four weeks after injection, irreversible neuron loss and reactive gliosis had occurred. The inhibitory amino acid gamma-aminobutyric acid caused acute glial swelling similar to that caused by glutamate and aspartate but did not produce neurotoxic effects, indicating that glial swelling may not be causally related to neuronal death but may be the result of amino acid uptake. The excitatory non-amino acid acetylcholine produced no direct, periventricular hippocampal damage or glial swelling but did produce dendritic swelling in the CA3 region innervated by the perforant path, presumably as a result of acetylcholine-induced seizure activity in this pathway. Glutamate and aspartate also caused glial and neuronal changes in other periventricular structures, e.g., septum, hypothalamus, caudate and habenula, as well as in the most dorsal portion of the cerebellum. Dendritic swelling induced by glutamate and aspartate in the cerebellar molecular layer was accompanied by acute necrosis of Purkinje cell somata. These results suggest that seizure-associated brain damage is initiated by excessive endogenous excitatory amino acid receptor activation.

Acetylcholine↗
PubMed1981

Biochemical consequences of kainic acid injection into the lateral brain ventricle in rat.

Effects of a single intraventricular injection of kainic acid (KA) in a dose of 0.1 microgram per rat on the activity of different brain neurotransmitter systems were investigated. A decreased level of norepinephrine at 3 and 24 h and acceleration of its utilization at 3 h after application of KA were observed. These changes were also accompanied by a decreased level of dopamine at 24 h, increased utilization of dopamine at 3 h, increased levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid at 3 and 24 h, as well as by shortened time of the turnover of 5-hydroxytryptamine. No disturbances in the function of the aminergic systems were noted at 120 h after injection of KA. Lowered activity of glutamic acid decarboxylase in the striatum, hippocampus, hypothalamus and cerebellum was observed at 24 h after administration of KA. At 480 h following application of KA, this lowering persisted in the hippocampus only. The most prominent changes in the level of gamma-aminobutyric were observed at 120 h in the striatum, hippocampus and cerebellum. A decreased level of gamma-aminobutyric acid was found in the striatum and cerebellum at 480 h following injection of KA. The observed changes in the dynamic equilibrium between various neurotransmitter systems may be a consequence of the direct or indirect influence of KA.

Animals↗
PubMed1986

Effect of dexamethasone, indomethacin, ibuprofen, and probenecid on carrageenan-induced brain inflammation.

A model of brain inflammation has recently been developed in mice using intraventricular injection of carrageenan (CAR). This model is characterized by increased brain water and vascular permeability, by neutrophil extravasation, and by evidence of increased pro-inflammatory arachidonic acid metabolites. The purpose of the current experiments was to determine the mechanism(s) by which CAR induces brain inflammation and to determine the utility of the CAR model in testing systemically administered therapeutic agents for their capacity to inhibit brain inflammation. Dexamethasone inhibited the increased brain water but not the increased vascular permeability produced by CAR. Indomethacin, an inhibitor of prostaglandin formation, suppressed peripheral inflammation produced by local injection of CAR but not brain inflammation produced by intraventricular CAR injection. Subsequent studies with carbon-14-labeled indomethacin showed that indomethacin penetrates peripheral tissues but is excluded from normal brain or brains inflamed by injection of CAR. Ibuprofen, another prostaglandin synthesis inhibitor, also had no effect on brain inflammation. Probenecid, an organic acid transport inhibitor, completely inhibited CAR-induced brain inflammation and also slowed brain elimination of intraventricularly administered prostaglandins. These experiments suggest, but do not conclusively prove, that increased prostaglandin formation contributes to brain inflammation. Also, the results with indomethacin and CAR-induced brain inflammation indicate that CAR-induced inflammation may be a useful model for screening for the ability of anti-inflammatory agents to cross the blood-brain barrier and exert their effect on brain inflammation.

Animals↗