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PubMed2006

[Central nervous system paracoccidioidomycosis: analysis of 13 cases].

Paracoccidioidomycosis (PCM) is a systemic granulomatous disease caused by Paracoccidioides brasiliensis, prevalent in Latin America, particularly in Brazil. Central nervous system (CNS) involvement occur in about 10% of cases. Thirteen patients with PCM involving CNS were studied considering clinical manifestation, neuroradiology and treatment modalities. Age ranged from 30 to 71 years-old (M=47.1+/-11.6 Me=46). There were eleven men and two women. The most frequent symptoms were motor deficits (53.8%), cognitive disturbance (53.8%), weight loss (46.1%), headaches (46.1%) and seizures (46.1%). The diagnosis was confirmed by the demonstration of P. brasiliensis. Granulomatous forms were present in all patients. Four (30.8%) of them had also meningeal involvement (mixed form). Computerized tomography (CT) scans were obtained in all cases and magnetic resonance imaging (MRI) was used in one case. Serology for HIV was done in ten patients (76.9%), and all the tests were negatives. Amphotericin B was used in twelve patients (92.3%), one of them by intraventricular infusion. In eight patients (61.5%), trimethopim and sulfamethoxazole were used, and, in two (15.4%), sulfadiazine and pirimetamine. Fluconazole, ketoconazole and itraconazole were each one used in a different patient as well. Six patients died (46.1%) and seven (53.9%) had satisfatory outcome. The follow-up period ranged from 2 to 74 (M=30.9) months. In conclusion, the CNS involvement in paracoccidioidomycosis is more frequent and more serious than thought before. The clinical manifestations, CT scans and MRI findings are not specific of paracoccidioidomycosis.

Adult↗

PubMed1985

Evidence for a stimulatory beta-adrenergic component in the release of the ovulatory LH surge in pro-oestrous rats.

The effect on ovulation of intraventricular infusions of noradrenaline, adrenaline and various pharmacological agents acting on the adrenergic receptor subtypes were investigated in cyclic female rats on the day of pro-oestrus. The inhibitory effects on ovulation of the different infusions were monitored by administering the drugs before 11.00 h (several hours before the critical period for the ovulatory LH surge). In experiments designed to show how the drugs under investigation might stimulate ovulation, pentobarbitone sodium (35 mg/kg) was given at 14.30 h; this anaesthetic inhibits ovulation and its effects can be overcome by substances that advance the preovulatory LH surge. Noradrenaline (an alpha-agonist) stimulated ovulation when administered on the morning of pro-oestrus to rats injected with pentobarbitone early in the afternoon of the same day. Phenoxybenzamine and phentolamine (non-selective alpha-antagonists) and clonidine (a selective alpha 2-agonist) all inhibited ovulation when infused on the morning of pro-oestrus. Yohimbine (a moderately selective alpha 2-antagonist) neither stimulated nor inhibited ovulation. Both isoprenaline (a non-selective beta-agonist) and fenoterol (a selective beta 2-agonist) stimulated ovulation in pentobarbitone-treated rats when administered on the morning of pro-oestrus and fenoterol was also able to overcome the pentobarbitone block when infused later in the afternoon. Propranolol (a non-selective beta-antagonist) and metoprolol (a selective beta 1-antagonist) were stimulatory only when administered in the afternoon. Adrenaline (both an alpha- and beta-agonist), prenalterol (a selective beta 1-agonist), atenolol (a selective beta 1-antagonist) and ICI 118,551 (a selective beta 2-antagonist) neither stimulated nor inhibited ovulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1987

The role of the hypothalamic beta-adrenergic system in controlling the LH rise in short-term castrated rats.

Intraventricular infusions of adrenaline and various pharmacological agents acting on beta-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 microliter) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed beta 1- and beta 2-agonist), fenoterol (a beta 2-agonist) and atenolol (a beta 1-antagonist). In contrast, prenalterol (a beta 1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)++ +butan-2-ol (ICI 118,551) (a selective beta 2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective beta 2-agonist), propranolol (a mixed beta-antagonist) and metoprolol (a beta 1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118,551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118,551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a beta 2-stimulatory component and the suppression of a beta 1-inhibitory component.

Adrenergic beta-Agonists↗

PubMed1982

Angiotensin II-norepinephrine relationship in the central nervous system.

The effects of angiotensin II (AII) and bilateral nephrectomy on [3H] norepinephrine (NE) uptake in hypothalamus and medulla oblongata were studied in male rats. The endogenous NE content in hypothalamus increased 4, 24 and 48 h after nephrectomy with a simultaneous decreasing of plasma renin activity. Intraventricularly infused [3H] NE uptake increased in hypothalamus and medulla oblongata of nephrectomized animals in cytoplasmatic compartment as in granular stores, while it decreased in hypothalamus of AII-infused animals. [3H] NE metabolites radioactivity decreased in nephrectomized animals if they are compared with AII-infused ones. These changes were independent of systolic arterial pressure that was not modified in none of the groups. The study of the ratio granular/cytoplasmatic [3H] NE and metabolites radioactivity shows that AII probably acts on cellular membrane uptake of NE. The modification of metabolites/NE ratio in both stores would be due to AII action on MAO activity. The effects of AII and nephrectomy on [3H] NE uptake can explain the inverse relationship between circulating AII levels and NE content in the central nervous system (CNS).

Angiotensin II↗

PubMed1978

Experimental neurogenic pulmonary edema in cats.

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

Animals↗

PubMed1980

Systems analysis of intracranial pressure. Comparison with volume-pressure test and CSF-pulse amplitude analysis.

Systems analysis is explored as a method of evaluating intracranial pressure (ICP). The intracranial cavity is characterized by a transfer function that is evaluated by the blood pressure pulse acting as the system input and the ICP pulse acting as the output. A comparison is made of the ability of systems analysis, volume-pressure test (VPT), and cerebrospinal fluid-pulse amplitude analysis (CSFPAA) to distinguish between an epidural balloon inflation (EBI) and an intraventricular infusion (IVI) at various steady state levels of ICP. The VPT could not distinguish between EBI and IVI at any level of ICP, and above 30 mm Hg the volume-pressure response decreased. Spectral analysis was able to distinguish EBI from IVI above 30 mm Hg, and CSFPAA was demonstrated to be a simplified spectral analysis. Changes in ICP waveform generated during each cardiac cycle appear to be related to changes in vasomotor reactivity and may have value in the clinical monitoring of ICP.

Animals↗

PubMed1981

Experimental neurogenic pulmonary edema. Part 1: The role of systemic hypertension.

Neurogenic pulmonary edema (NPE) was produced consistently in normal cats by increasing intracranial pressure with an intraventricular infusion of mock cerebrospinal fluid. The usual elevation of systemic arterial pressure (SAP) that follows severe intracranial hypertension (the "Cushing response") was controlled by blood withdrawal at variable rates to achieve and maintain constant cerebral perfusion pressure (CPP) in three groups of cats of 50, 20, and 0 mm Hg, respectively, for 30 minutes. In this model, NPE occurs in the absence of increased SAP and in the presence of decreasing CPP. These results indicate that systemic arterial hypertension is not an essential stimulus for the development of NPE, and suggest that the lungs are directly affected by the intense sympathetic discharge evoked by severe intracranial hypertension.

Animals↗

PubMed1982

Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation.

Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.

Animals↗

PubMed1999

Reduction of calcineurin activity in brain by antisense oligonucleotides leads to persistent phosphorylation of tau protein at Thr181 and Thr231.

Phosphorylation of tau protein promotes stability of the axonal cytoskeleton; aberrant tau phosphorylation is implicated in the biogenesis of paired helical filaments (PHF) seen in Alzheimer's disease. Protein kinases and phosphatases that modulate tau phosphorylation have been identified using in vitro techniques; however, the role of these enzymes in vivo has not been determined. We used intraventricular infusions of antisense oligodeoxynucleotides (ODNs) directed against the major brain isoforms of the Ca2+/calmodulin-dependent phosphatase calcineurin to determine how reduced activity of this enzyme would affect tau dephosphorylation. Five-day infusions of antisense ODNs (5 and 10 nmol/day) in rats decreased immunoreactive levels and activity of calcineurin throughout the brain; sense ODNs, scrambled ODNs, and infusion vehicle alone had no effect. When neocortical slices were prepared from antisense ODN-treated rats and incubated for 1 to 2 h in vitro, tau protein remained phosphorylated as determined by using the phosphorylation-sensitive monoclonal antibodies AT-180 (Thr231) and AT-270 (Thr181). In contrast, AT-180 and AT-270 sites were completely dephosphorylated during incubation of neocortical slices from vehicle-infused controls and sense ODN-treated rats. Neocortical slices from antisense-treated rats were incubated with the phosphatase inhibitors okadaic acid (100 nM; 10 microM) and FK-520 (5 microM); these preparations showed enhanced tau phosphorylation, consistent with a significant loss of calcineurin activity. Thus, we conclude that phosphorylation of at least two sites on tau protein, namely, Thr181 and Thr231, is regulated by calcineurin.

Animals↗

PubMed2000

Does senile impairment of cholinergic system in rats concern only disturbances in cholinergic phenotype or the progressive degeneration of neuronal cell bodies?

The trophic effect of continuous intraventricular infusion of nerve growth factor (NGF) on morphology of the basal forebrain (BF) cholinergic neurons was tested in 4- and 28-month-old male Wistar rats. All studies were conducted using behaviorally uncharacterized animals from the same breeding colony. Immunohistochemical procedure for choline acetyltransferase (ChAT) and p75NTR receptor has been applied to identify cholinergic cells in the structures of basal forebrain (BF). Using a quantitative image analyzer, morphometric and densitometric parameters of ChAT- and p75NTR-positive cells were measured immediately after cessation of NGF infusion. In 28-month-old non-treated rats the number of intensively ChAT-positive cells in all forebrain structures was reduced by 50-70% as compared with young animals. The remaining ChAT-positive cells appeared shrunken and the neuropil staining was NTR markedly reduced. In contrast, the same neurons when stained for p75 were numerous and distinctly visible with perfect morphology. Analysis of Nissl stained sections also showed that 28-month-old rats did not display significant losses of neuronal cell bodies. NGF restored the number of intensely stained ChAT-positive cells to about 90% of that for young controls and caused a significant increase in size of those cells in 28-month-old rats as compared with the control, age-matched group. NGF did not influence the morphology of p75NTR-positive neurons, which were well labeled, irrespective of treatment and age of the rats. In 4-month-old rats, NGF infusion decreased the intensity of both ChAT and p75NTR immunostaining. These data provide some evidence for preservation of BF cholinergic neurons from atrophy during aging and indicate that senile impairment of the cholinergic system in rats concerns decrease in ChAT-protein expression rather than an acute degeneration of neuronal cell bodies. Treatment with NGF resulted in restoration of cholinergic phenotype in the BF neurons of aged rats. However, the present study also rises issue of possible detrimental effects of NGF in young normal animals.

Aging↗

PubMed2003

Matrix metalloproteinase inhibition alters functional and structural correlates of deafferentation-induced sprouting in the dentate gyrus.

Molecules comprising the extracellular matrix (ECM), and the family of matrix metalloproteinases (MMPs) that regulate them, perform essential functions during neuroplasticity in both developing and adult nervous systems, including substrate guidance during neuritogenesis and the establishment of boundaries for axonal terminal fields. MMP proteolysis of ECM molecules may perform a permissive or inductive role in fiber remodeling and synaptogenesis initiated by deafferentation. This study examined functional and structural effects of MMP inhibition during the early phases of deafferentation-induced sprouting, characterizing components of the degeneration/proliferation cycle that may be dependent on MMP activity. Adult rats received unilateral lesions of the entorhinal cortex to induce collateral sprouting of the crossed temporodentate fiber pathway. This was followed by intraventricular infusion of the MMP inhibitor FN-439 (2.9 mg/kg) or saline vehicle. After 7 d postlesion, rats underwent in vivo electrophysiological recording or histological processing for electron microscopic analysis. Lesioned rats receiving vehicle exhibited normal sprouting and synaptogenesis, with the emergence of the capacity for long-term potentiation (LTP) within the sprouting pathway, and the successful clearance of degenerating terminals with subsequent synaptic proliferation. In contrast, lesioned rats receiving the MMP inhibitor failed to develop the capacity for LTP and showed persistent cellular debris. Current source density analysis also revealed an FN-439-induced disruption of the current sink, normally localized to the middle region of the granule cell dendrites, corresponding to the terminal field of the crossed temporodentate fibers. These results establish a role for MMP-dependent processes in the deafferentation/sprouting cycle.

Afferent Pathways↗

PubMed1991

[Participation of central and peripheral mu- and delta opiate receptors in anti-arrhythmia action of enkephalins].

It was found, that injection of delta-receptors agonist dalargin before the occlusion of left anterior coronary artery in rats prevented the decrease of ventricular fibrillation threshold (VFT). An injection of naloxone in dose 0.5 mg/kg (for the blockade of mu-receptors only) had no influence on the VFT. Naloxone in dose 1 mg/kg (for the blockade peripheric mu- and delta-receptors) decreased VFT. An intraventricular infusion of dalargin (10 mkg) induced bradycardia and an increase of VFT. It was assumed that anti-arrhythmic effects of enkephalins in acute myocardial ischemia could be realized by an activation of peripheric delta-receptors and central mu-receptors.

Animals↗

PubMed1989

Synaptic plasticity and learning: selective impairment of learning rats and blockade of long-term potentiation in vivo by the N-methyl-D-aspartate receptor antagonist AP5.

This paper reports a series of 5 experiments concerned with a possible role for N-methyl-D-aspartate (NMDA) receptors in certain types of learning. The results show that chronic intraventricular infusion of the NMDA receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (D,L-AP5) caused an impairment of spatial but not of visual discrimination learning in rats. Such selectivity of the learning impairment occurred despite widespread distribution of the drug throughout the CNS. AP5 sometimes caused a disturbance of sensorimotor function during learning, but one experiment addressing whether this disturbance could be responsible for the spatial learning impairment established that it was statistically independent. Another experiment showed that AP5 did not affect the retention of previously acquired spatial information. These behavioral effects were all obtained with a concentration of AP5 that, in a final study, was found to be sufficient to block hippocampal long-term potentiation (LTP) in vivo without affecting normal synaptic transmission. Taken together, these observations (1) implicate NMDA receptors in certain types of learning, and (2) extend recent work showing that saturation of LTP causes an anterograde spatial amnesia (McNaughton et al., 1986). A preliminary report of parts of this work has been published (Morris et al., 1986a).

Animals↗

PubMed1989

[Ventricular subarachnoidal hydrocephalus of arachnoid villi origin].

In 102 infants (0.5 to 22 months), the C.T. scan performed for various neurological symptoms, was systematically reviewed with analysis of ventricular size, pericerebral space and interhemispheric fissure. In 70% of the cases, an increase of the intracranial volume of C.S.F. was noted, with a good correlation between the ventricular and pericerebral volume. The authors discuss the pathophysiological mechanism of this condition an evoke the possibility of an idiopathic disturbance of the C.S.F. reabsorption. In two cases, suffering from severe axial hypotonus, this fact was explored by four methods: continuous monitoring of intracranial pressure, intraventricular infusion test, isotopic cisternography through ventricular injection and venous phase of angiography. From these investigations showing no venous anomaly, and because of the lack of any pathological event able to induce a C.S.F. obstruction, we suggest a delay in the maturation of arachnoïd villi (normally ended at 18 months) to explain this condition.

Arachnoid↗

PubMedDate not supplied

Activity of noradrenergic neurons of medial-basal hypothalamus of female rabbits in some stages of reproduction.

Activity of noradrenergic neurons of medial-basal hypothalamus of female rabbits in some stages of reproduction. Acta Physiol. Pol., 1978, 29 (2): 111--115. The differences were found in the activity of noradrenergic neurons of medial-basal hypothalmus (MBH) estimated by the analysis of metabolism of intraventricularly infused 3H-noradrenaline (3H-NA) in various stages of reproduction in female rabbits. The gonadal hormones and especially 17beta-estradiol seem to be involved in this activity. The rapid disappearance of 3H-NA from MBH, found immediately after mating, implicates an involvement of noradrenaline in the process of Gn-RHs release form the rabbit hypothalamus.

Animals↗

PubMed1986

Muramyl peptide enhancement of slow-wave sleep.

Sleep-promoting Factor S, derived from brain or urine, has been characterized as a muramyl peptide. In rabbits, one pmol of Factor S induced excess slow-wave sleep (SWS) for several hours following cerebral intraventricular infusion. Factor S also induced increases in EEG slow-wave (1/2-4 Hz) amplitudes similar to those observed during the deep sleep that follows sleep deprivation. Sleep following Factor S treatment remained normal in that it was episodic and waking behaviours such as eating, drinking and grooming persisted. The structure of Factor S is similar to those of naturally occurring monomers of bacterial cell wall peptidoglycans. Other muramyl peptides such as muramyl dipeptide (MDP) were also found to be somnogenic. Structure-activity studies of various MDP derivatives indicated that somnogenic activity is dependent on precise structural requirements. Muramyl peptides also are immunomodulators and pyrogens. These activities could be separated from somnogenic activity by using various MDP derivatives or by pharmacologic intervention. Muramyl peptides may induce their somnogenic effects through the release of the cytokine interleukin-1; interleukin-1 also has the capacity to induce excess SWS. Although muramyl peptides have many biological activities in mammals, the role(s) they may play in mammalian physiology remains unknown. It is possible that mammalian tissue may store and/or modify muramyl peptides in conjunction with their use as modulators of sleep, temperature and immune responses.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1985

Influence of prostacyclin on coronary thrombosis and myocardial ischemia in conscious canine experiments.

The effects of intraventricular infusion of prostacyclin (PGI2; 50, 100 ng/kg/min) on hemodynamics, the ECG, coronary thrombosis and myocardial ischemia were studied in chronically equipped, resting conscious dogs and compared to those of intracardiac administration of Tris-HCl as vehicle. Coronary thrombosis was induced by electrical stimulation of an artery over an implanted wire for 6 hr. PGI2 infusion at 100 ng/kg/min decreased blood pressure by 24 +/- 3% (p less than 0.01) for 5 hr, increased heart rate at 1 hr by 28 +/- 4% (p less than 0.05) followed by a decrement, and elevated cardiac output by 41 +/- 3% (p less than 0.05). Filling pressure and dP/dtmax did not change. Treatment with PGI2 prevented ischemic S-T segment alterations in the ECG and arrhythmias observed in controls. The prostanoid infusion reduced coronary thrombus weight from 64 +/- 7.8 mg (mean +/- S.D.) in controls to 10.7 +/- 6.3 mg and 5.2 +/- 7.1 mg (both p less than 0.001) after 50 and 100 ng/kg/min, respectively. It also reduced myocardial ischemia following occlusive coronary thrombosis from 48 +/- 12% of the left ventricle in controls to 8.8 +/- 8.7% (p less than 0.01) and 2.4 +/- 5.2% (p less than 0.001) in the hearts treated with 50 or 100 ng/kg/min PGI2. The results suggest that PGI2 infusion exerts beneficial effects on heart performance by long-lasting blood pressure reduction and elevation of cardiac output caused by dilation of arterial vessels. PGI2 infusion prevents occlusive coronary artery thrombosis in response to intimal damage by anti-thrombotic properties and vasodilation of coronary arteries. This protects the heart from ischemia observed in controls.

Animals↗

PubMed1979

"Nature's soft nurse": a sleep-promoting factor isolated from brain.

A sleep promoting factor has been extracted and purified from cerebrospinal fluid of sleep-deprived goats, from whole brains of sleep-deprived rabbits and from brainstems of slaughterhouse cattle. Intraventricular infusion of the purified material into rats, cats, rabbits or squirrel monkeys induces excess slow-wave sleep in the recipients for several hours following the infusion. The excess sleep appears similar to the deep slow-wave sleep which normally follows sleep deprivation; it is characterized by EEG slow waves of greater than normal amplitude and an increase in both the number and duration of sleep episodes. The sleep factor appears to be a small peptide of molecular weight 350--500 daltons and the effective dose is of the order of a few picomols per gram brain. A similar, perhaps identical, factor is present in human urine.

Animals↗