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PubMed1978

Effect of central nervous system-acting drugs after selective destruction by neurotoxins of 5-hydroxytryptamine fibers in the brain.

Some behavioral effects of CNS-acting drugs have been studied in two animal species after functional impairment of central serotonergic activity. In rabbits, pretreatment with p-CPA or with 5,6-DHT counteracted the hyperthermia induced by d-amphetamine or apomorphine; the same pretreatments were ineffective in modifying pyrogen-induced fever. These data indicate a modulatory role of the 5-HT system in the hyperthermic response to dopaminergic agonists, such as d-amphetamine and apomorphine, and rule out 5-HT involvement in the hyperpyrexia induced by pyrogen. A previous intraventricular injection of 5,6-DHT significantly potentiated the increase in body temperature induced by 5-HTP in combination with a MAO inhibitor. Pretreatment with p-CPA, instead, strongly inhibited the hyperthermic response to 5-HTP. In unanesthetized fowl, at the time of the most dramatic degenerative signs of indoleaminergic neurons induced by 5,6-DHT, as documented by histofluorescence pictures, intraventricular infusion of 5-HT induced more intense behavioral, electrocortical, and body temperature modifications than in control animals. These results suggest the existence of receptor supersensitivity after 5-HT nerve ending degeneration but not after brain 5-HT depletion. The hyperthermic effect of a presynaptically acting drug, fenfluramine, was counteracted in rabbits and in fowl pretreated with either p-CPA or 5,6-DHT. Since identical behavioral, electrocortical, and body temperature effects have been observed after 5-HT or 5,6-DHT infusion into the third ventricle of fowl, it may be concluded that 5,6-DHT behaves also as a central 5-HT receptor agonist.

5-Hydroxytryptophan↗

PubMed1993

In vivo detection of neurotransmitter changes in Alzheimer's disease.

Alzheimer's disease (AD) is characterized by multiple deficits of neurotransmitters in brain. These observations are mainly based upon studies in postmortem brain material where the disease has reached a terminal state. In order to obtain further insight into the early disturbances of the neurotransmitter activities in AD, new imaging techniques such as positron emission tomography (PET) and single positron emission tomography (SPECT) can be applied in vivo for detection of neurotransmitter activity in normal as well as AD brains. Nicotinic receptors have been traced in AD patients by PET and 11C-nicotine at different stages of AD. A lower uptake of (R)(+)- compared to (S)(-)-11C-nicotine was observed in AD patients while the difference in uptake of the two enantiomers was less pronounced in normal individuals. A positive correlation has been observed between cognitive function (Mini-Mental-State-Examination) and uptake of (S)(-)-11C-nicotine in the temporal cortex of AD patients. 11C-benztropine has been used to measure muscarinic receptors in brain by PET. Oral tacrine treatment (80 mg daily) restore nicotinic receptors in AD patients as visualized by PET and 11C-nicotine. Kinetic analysis indicate increased binding of (S)(-)-11C-nicotine after 3 months of treatment with tacrine. The PET data are paralleled by improvement in neuropsychological testings. Intraventricular infusion of nerve growth factor (NGF) to an AD patients for 3 months resulted in an transient increase in uptake and binding of (S)(-)-11C-nicotine in the temporal and frontal cortex and a persistent increase in cortical blood flow.

Acetylcholine↗

PubMed1980

Osmoreceptors or sodium receptors: an investigation into ADH release in the rhesus monkey.

1. ADH secretion was studied in trained, preoperated conscious monkeys undergoing water diuresis after administration of isosmolar hypertonic solutions of different substances into any one of the following sites: (i) anterior third ventricle, (ii) the hypothalamus, just anterior to the third ventricle and (iii) common carotid artery. 2. Free water clearance was continuously monitored and the ADH released was measured by bio-assay on the same animals after administering graded doses of standard arginine vasopressin in a comparable manner. 3. Intraventricular infusions of hypertonic solutions of NaCl or Na acetate released significant amounts of ADH while sucrose or mannitol of comparable osmolality were ineffective. Graded increases in the concentration of NaCl infused into the c.s.f. resulted in secretion of ADH proportional to log Na concentration. 4. Infusion of the same hypertonic solutions into the anterior hypothalamus released ADH, though Na salts were more effective than the sugars. 5. Hypertonic solutions of NaCl, Na acetate, sucrose or mannitol were effective in releasing ADH when injected via the carotid artery, but hypertonic solutions of NaCl were significantly more effective than the other solutions. 6. These findings may be explained by the hypothesis that the 'osmoreceptors' of Verney are Na sensitive receptors composed of dendrites innervating the specialized ependyma of the anterior part of the third ventricle.

Animals↗

PubMed1987

Delayed transneuronal death of substantia nigra neurons prevented by gamma-aminobutyric acid agonist.

In an investigation of the mechanism by which brain lesions result in delayed degeneration of neurons remote from the site of injury, neurons within the caudate nucleus of rats were destroyed by local injection of the excitotoxin ibotenic acid. Treatment resulted in the rapid degeneration of the striatonigral pathway including projections containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and delayed transneuronal death of neurons in the substantia nigra pars reticulata. The distribution of nigral cell loss corresponded to the loss of GABAergic terminals. Neuronal death was prevented by long-term intraventricular infusion of the GABA agonist muscimol. Delayed transneuronal degeneration may be produced by neuronal disinhibition consequent to loss of inhibitory inputs. Replacement of inhibitory transmitters by suitable drugs may prevent some forms of delayed neuronal death.

Animals↗

PubMed1992

Low dose intraventricular fibrinolytic treatment to prevent posthaemorrhagic hydrocephalus.

Posthaemorrhagic ventricular dilatation (PHVD) is thought to be due to clots from intraventricular haemorrhage obstructing cerebrospinal fluid pathways involved in reabsorption. Over 60% of infants with progressive PHVD have gone on to require surgical shunt placement. Previous treatments all have major problems. The object of this pilot study was to achieve enough fibrinolysis to restore pathways of cerebrospinal fluid reabsorption and so avoid shunt surgery. Nine preterm infants with progressive PHVD were treated with intraventricular infusion of streptokinase for 12-72 hours. All the infants survived and surgical shunting was required in only one case. A 200% increase in fibrinolytic activity was demonstrated in both ventricular and spinal fluid during streptokinase treatment. There were no cases of infection. Minor rebleeding occurred in one case and was not a serious problem. This represents the first direct therapeutic approach to the pathology of PHVD.

Cerebral Hemorrhage↗

PubMed1977

Can hepatic coma be caused by a reduction of brain noradrenaline or dopamine?

Intraventricular infusions of octopamine which raised brain octopamine concentrations more than 20 000-fold resulted in reductions in brain noradrenaline and dopamine by as much as 90% without affecting the alertness or activity of normal rats. As this reduction of brain catecholamines is much greater than any reported in hepatic coma, we do not believe that values observed in experimental hepatic failure have aetiological significance for the encephalopathy that ensues.

Animals↗

PubMed1979

Reversal of ammonia coma in rats by L-dopa: a peripheral effect.

Ammonia coma was produced in rats within 10 to 15 minutes of an intraperitonealinjection of 1.7 mmol NH4CL. This coma was prevented with 1.68 mmol L-dopa given by gastric intubation 15 minutes before the ammonium salt injection. The effect of L-dopa was correlated with a decrease in blood and brain ammonia, an increase in brain dopamine, and an increase in renal excretion of ammonia and urea. Intraventricular infusion of dopamine sufficient to raise the brain dopamine to the same extent did not prevent the ammonia coma nor affect the blood and brain ammonia concentrations. Bilateral nephrectomy eliminated the beneficial effect of L-dopa on blood and brain ammonia and the ammonia coma was not prevented. Thus, the reduction in blood and brain ammonia and the prevention of ammonia coma after L-dopa, can be accounted for by the peripheral effect of dopamine on renal function rather than its central action. These results provide a reasonable explanation for the beneficial effects observed in some encephalopathic patients receiving L-dopa.

Ammonia↗

PubMed1980

Sleep-promoting material from human urine and its relation to factor S from brain.

A sleep-promoting factor was extracted from human urine. Intraventricular infusion of the purified material induced excess slow-wave sleep in rats and rabbits for 5--10 h after the infusion. Chemical properties of the urinary factor were similar to those of factor S derived from whole brains of sleep-deprived goats, sheep, and rabbits. The behavior of the urinary factor in two ion exchange chromatographic steps, high voltage electrophoresis, gel-filtration, and ultrafiltration was similar to that of factor S. Effects of the purified urinary factor on slow-wave sleep of rats and rabbits were similar in time-course and duration to those of factor S from brain. However, the factor obtained from human urine did not increase the amplitude of cortical slow waves to the same extent as did factor S from brains of sleep-deprived animals.

Animals↗

PubMed1989

Cerebral blood flow and evoked potentials during Cushing response in sheep.

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

Animals↗

PubMed1991

Influence of brain renin-angiotensin system on renal sympathetic and cardiac baroreflexes in conscious rabbits.

The role of the brain renin-angiotensin system (RAS) in the baroreflex regulation of renal sympathetic nerve activity (RSNA) and heart rate (HR) was studied in conscious rabbits. RSNA and HR were recorded during slow ramp changes in mean arterial pressure (MAP) before and after intraventricular infusion of 1) angiotensin II (ANG II), 2) ANG II receptor antagonist, [Sar1,Ile8]ANG II, or 3) converting enzyme inhibitor (CEI, enalaprilat). Central ANG II increased resting MAP and RSNA by 10.6 +/- 0.9 mmHg and 21 +/- 7%, respectively, but did not alter HR. There was a marked increase of 107 +/- 15% in the maximum RSNA evoked by slowly lowering MAP. In contrast, maximum reflex tachycardia was only modestly elevated, and baroreflex inhibition of RSNA and HR during MAP rises was unaffected. Central [Sar1,Ile8]ANG II had no effect on RSNA or HR, either at rest or during baroreflex responses, while CEI slightly enhanced maximal reflex responses. Thus exogenous ANG II causes a powerful excitation of renal sympathetic motoneurons, the magnitude of which is revealed when tonic baroreceptor inhibition is removed during transient pressure falls. However, in quietly resting conscious rabbits, we found no evidence for a tonic influence of endogenous ANG II on these neurons, and the physiological stimuli required for their activation by the brain RAS remain to be found.

Angiotensin II↗

PubMed1986

Brain temperature changes coupled to sleep states persist during interleukin 1-enhanced sleep.

The effects of human interleukin 1 (IL 1) on the architecture of rabbit sleep-wake cycles and brain temperature (Tbr) changes coupled to states of vigilance were examined. Cerebral intraventricular infusion of IL 1 induced increased slow-wave sleep (SWS), increased electroencephalographic slow-wave (0.5-4 Hz) amplitudes, and fever. Heat-inactivated IL 1 failed to elicit these responses. IL 1 also significantly inhibited rapid-eye-movement (REM) sleep; however, inactivated IL 1 also reduced REM sleep; thus some of the IL 1-induced REM reduction may be related to the infusion process. The duration and number of sleep cycles (REM-to-REM interval) were unaffected by IL 1. Similarly, Tbr changes that normally occur during the transition from one arousal state to another remained unchanged after IL 1 infusion, even though rabbits were simultaneously febrile. We conclude that IL 1 selectively enhances SWS while leaving sleep cycles and Tbr changes coupled to states of vigilance undisturbed.

Animals↗

PubMed1975

Extraction of sleep-promoting factor S from cerebrospinal fluid and from brains of sleep-deprived animals.

Sleep-promoting factor (factor S) was extracted, partially purified, and concentrated from cerebrospinal fluid and from acid-acetone extracts of brain stem anc cortex of sleep-deprived goats and sheep. 2. Solutes greater than 500 daltons were largely removed by serial ultrafiltrations through molecular sieves (Amicon membranes UM10 and UM05); solutes less than 350 daltons were largely eliminated by gel filtration through Sephadex G10 columns. Sleep-promoting activity was found in a fraction eluted prior to [14C] sucrose marker. 3. Concentrated fraction were infused intraventricularly in rats (0.1 ml in 30 min just prior to 12-h dark cycle) and in rabbits (0.3 ml in 90 min in morning). Sleep-promoting activity was assayed by decrease in nocturnal locomotor activity of rats and by duration and amplitude of slow-wave cortical EEG in rabbits.

Animals↗

PubMed1983

Site of action of sleep-inducing muramyl peptide isolated from human urine: microinjection studies in rabbit brains.

1. Sleep-promoting muramyl peptide purified from human urine (SPU) was injected through chronically implanted guide tubes into defined regions of the basal forebrain and brain stem of unanesthetized rabbits. Electroencephalogram (EEG) and body movements were recorded subsequent to each injection. 2. Of 52 injection sites, there were 8 in which microinjection of SPU induced significant increases of slow-wave sleep (SWS) for 5 or more hours. Each active site was tested twice with SPU and once with vehicle control. 3. Seven of the active sites were located in a region extending from the basal forebrain at the level of the optic chiasm to the mesodiencephalic junction. No active sites were found in the lower brain stem. 4. The behavioral and EEG characteristics of the excess SWS induced by microinjection of SPU appeared normal and similar to the excess sleep that follows intraventricular infusions of sleep factor. However, the responses occurred sooner after injections into an active site than after infusion into a lateral ventricle.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed2002

Regulation of prolactin secretion by dopamine at the level of the hypothalamus in the turkey.

Avian prolactin (PRL) secretion is regulated by vasoactive intestinal peptide (VIP) neurons residing in the infundibular nuclear complex (INF) of the hypothalamus. This VIPergic activity is modulated by stimulatory dopaminergic inputs. Dynorphin, serotonin (5-HT), dopamine (DA) and VIP all appear to stimulate PRL secretion along a hypothalamic pathway, expressing kappa opioid, serotonergic, dopaminergic and VIPergic receptors in succession, with the VIPergic system as the final mediator. Electrical stimulation (ES) within the turkey hypothalamus at the level of the medial preoptic area (POA), the ventromedial hypothalamic nucleus (VMN), the INF or the median eminence (ME) results in the release of PRL. When the selective D(1) DA receptor antagonist SCH-23390 HCl was infused intraventricularly at the rate of 10 nmol/min, ES in the POA or VMN was unable to increase PRL levels, while ES in the INF and ME did increase PRL to the same level as that of controls. These results were interpreted to suggest that the D(1) DA receptors involved in PRL release lie caudally to the VMN and dorsally to the INF. Bilateral microinjections (50 ng) of the D(1) DA receptor agonist SKF-38393 HCl into the POA or VMN failed to produce any increase in PRL, while similar microinjections in the INF increased PRL significantly within 15 min. Bilateral microinjections of the D(1) DA antagonist (50 ng) into the INF blocked the rise in PRL associated with ES in the POA. Bilateral microinjections of a D(2) DA antagonist (50 ng) into the INF failed to block PRL secretion induced by ES in the POA. Tract tracing, using double-label immunocytochemistry, revealed the presence of a monosynaptic dopaminergic pathway projecting from the POA to the INF. These data imply that the only hypothalamic D(1) DA receptors involved in the regulation of avian PRL secretion are those residing within the INF in the same region as the VIP neurons known to be involved in PRL secretion.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMedDate not supplied

Etiology of ventriculomegaly in choroid plexus papilloma.

In order to test the hypothesis that overproduction of cerebrospinal fluid can cause the hydrocephalus seen in choroid plexus papillomas, adult mongrel dogs with and without hydrocephalus were subjected to high pressure intraventricular infusions of artificial cerebrospinal fluid (CSF). Pre- and postinfusion volumes were calculated, using a new method for on-line measurement of ventricular volume involving linear measurements from Conray ventriculograms. Ventricular volumes increased an average of 8% in 36 h. The dogs previously made hydrocephalic by the intracisternal injection of kaolin had a significant volume increase (34% in 36 h). Overproduction of CSF alone can produce hydrocephalus, but the presence of hydrocephalus in choroid plexus papillomas is more likely to be a result of the complex interaction of CSF overproduction and partial restriction of CSF flow.

Animals↗

PubMed1980

Dose-response relation of CSF sodium and renal sodium excretion, and its absence in homozygous Brattleboro rats.

Constant intraventricular infusion (3.3--6.6 microliters/min) of artificial cerebrospinal fluid with sodium concentrations of 100, 150, 200, 250, 300, and 350 mM produced a linear dose-related change in renal sodium excretion in conscious, unrestrained Sprague-Dawley rats. The periventricular receptors stimulated were able to evoke substantial changes in body sodium balance; the 350 mM Na CSF produced an estimated 14% deficit in the content of Na in the extracellular fluid over a 5-hour infusion period. This is the first demonstration of such a dose-response relation over a wide range of CSF Na concentration (above and below normal) in conscious animals. Both the dose-response relation, and the magnitude of the effects, suggests an important physiologic role for this control mechanism. The natriuresis in response to 300 mM sodium infusion was identical in Long-Evans Brattleboro rats heterozygous for diabetes insipidus (DI), and in Sprague-Dawley rats, but was completely absent in homozygous animals. Although the experimental methods (conscious unrestrained rats) precluded simultaneous evaluation of efferent pathways other than antidiuretic hormone (ADH), the evidence from the DI rats suggests that ADH may be the efferent pathway for the response.

Animals↗

PubMed1980

Stimulation of prolactin secretion by taurine, a neurally depressant amino acid.

The neurally depressant amino acid taurine and related metabolites were tested for their ability to alter prolactin (PRL) secretion in conscious, unrestrained male rats. The intraventricular infusion of taurine (0.2 and 2.0 mumol) elicited a significant increase in PRL secretion. Hypotaurine (0.2 and 2.0 mumol), cysteic acid (2.0 mumol), mannitol (2.0 mumol) and 0.9% saline were ineffective in altering PRL secretion. When infused directly into the pituitary of conscious, unrestrained male rats none of the substances tested stimulated PRL secretion. Taurine (50.0 mumol) was similarly ineffective in stimulating PRL secretion when an in vitro pituitary preparation was used. These studies indicate that taurine is capable of stimulating PRL secretion in the male rat. This effect appears to be mediated centrally, presumably at the hypothalamus.

Animals↗

PubMed1981

Immunohistochemical demonstration of LHRH neurons and their pathways in the rat hypothalamus.

LRHR neurons and fiber tracts have been studied immunohistochemically in rats. After the intraventricular infusion of colchicine, a number of immunoreactive LHRH neurons were consistently evident in the preoptico-septal area and in the diagonal band of Broca. The immunoreactive fiber tracts originating in those areas were classified into two groups: preoptico-terminal and preoptico-infundibular tracts. The former terminated in the OVLT. The latter was further divided into the mediobasal and laterobasal tracts; both were found to terminate in the median eminence. The mediobasal tract ran posteriorly through the ventral portion of the lateral periventricular area. The laterobasal tract ran posteriorly in the medial forebrain bundle and was accompanied by several immunoreactive neurons. The immunoreactive cell bodies were further scattered in the base of the tuberal hypothalamic area. An anterior bilateral Halász cut in the retrochiasmatic region was followed by a great reduction of the immunoreactive materials in the median eminence and by the appearance of the immunoreactive perikarya and in the preoptico-septal area and in the diagonal band of Broca. A horizontal hypothalamic cut, on the other hand, which disconnected the tubero-infundibular tract between the median eminence and the arcuate nuclei, caused neither reduction of the immunoreactive materials in the median eminence nor appearance of the immunoreactive perikarya in the arcuate nuclei. Those results indicate that the bulk of the immunoreactive LHRH is synthesized in the anterior hypothalamic area and transported by the preoptico-terminal and -infundibular tracts but a minor part is produced in the cell bodies located in the basal tuberal hypothalamus and transported to the median eminence.

Afferent Pathways↗