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PubMed1982

Biosynthesis of biopterin by rat brain.

A method for the determination of [14C]biopterin biosynthesis from [14C]guanosine-5'-triphosphate by a desalted preparation from rat striatum, based on sequential reverse-phase and cation-exchange high performance liquid chromatography, is described. Synthesis of reduced forms of biopterin by this striatal extract was found to be dependent on enzymatic activity, guanosine-5'-triphosphate, magnesium ions, and a reduced pyridine nucleotide. As demonstrated by the technique of isotope dilution, isotope trapping, 6-lactyl-7,8-dihydropterin (sepiapterin) was found to be an intermediate in biopterin biosynthesis that is catalyzed by the striatal extract. Rat brain was also shown to synthesize biopterin in vivo from intraventricularly administered [14C]guanosine or sepiapterin. Intraventricular injection of sepiapterin increased dihydro- and 5,6,7,8-tetrahydrobiopterin levels in rat brain by more than eightfold. The temporal relationship between the appearance of dihydro- and 5,6,7,8-tetrahydrobiopterin following intraventricular injection of sepiapterin suggests that dihydrobiopterin is the immediate product of sepiapterin reduction which is then reduced further to the functional cofactor 5,6,7,8-tetrahydrobiopterin. Therefore, in contrast to previous reports, the biosynthesis of biopterin by rat brain does not appear to differ from that occurring in other, nonneural tissues.

Animals↗
PubMed1978

Increased sensitivity to 5-hydroxytryptamine due to intraventricular administration of 5,6-dihydroxytryptamine.

The possibility that intraventricular administration of 5,6-dihydroxytryptamine (5,6-DHT) can cause a development of denervation hypersensitivity to central 5-hydroxytryptamine (5-HT) was examined in rats with special reference to the pituitary-adrenocortical functions. Pretreatment with intraventricular injection of 5,6-DHT itself did not affect the basal concentrations or stress-induced increases of plasma B. The same pre-treatment, however, elicited augmented responses to subcutaneous injection of 5-HTP, i.e. there was a significant rise in the concentrations of plasma B as compared with those in the controls. These results suggest a development of denervation hypersensitivity to 5-HT following intraventricular injection of 5,6-DHT.

5,6-Dihydroxytryptamine↗
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↗
PubMed1990

Physiological significance of the negative short-loop feedback of prolactin.

The aim of the present study was to evaluate the physiological significance of the rapid, short-loop, negative feedback of prolactin by passive immunization with antiserum to rat prolactin injected into the third cerebral ventricle (3V) of conscious, freely moving intact or castrated male rats. Blood samples for measurement of plasma prolactin concentrations were removed through implanted external jugular catheters. After injection of 3 microliters of undiluted antiserum, plasma levels of prolactin decreased rapidly (within 5 min) to values undetectable by RIA. Further study revealed that this dose of antiprolactin serum had combined with circulating prolactin, thus rendering it undetectable by RIA. To overcome this problem, we repeated the experiment injecting 2 microliters of diluted antiserum (dilution factors 20, 100, 200, 2,000) into the 3V. When compared to values of plasma prolactin in control rats injected with 2 microliters of normal rabbit serum, none of the dilutions of antiserum induced a significant change in prolactin concentrations for as long as 4 h after injection. Since there was no effect of intraventricularly injected antiprolactin serum on basal prolactin secretion, in the next experiment, intact as well as castrated male rats were subjected to ether stress 30 min after intraventricular injection of antiserum (dilution factor 100). The elevation of plasma prolactin which followed ether stress was significantly higher in male rats pretreated with antiprolactin serum than that which occurred in control rats. A similar enhancement of the increase in plasma prolactin following ether stress, but of longer duration, was obtained in castrated rats injected with antiprolactin serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Biogenic amines and the photomyoclonic syndrome in the baboon, Papio papio.

The role of biogenic amines in the proclivity of the baboon, Papio papio, to exhibit an epileptoid response to flashing light was studied. Intraventricular injections of epinephrine and norepinephrine reduced or blocked the photomyoclonic syndrome without modifying ongoing behavior. Epinephrine was effective at doses of 100 mg and more, and norepinephrine was effective at doses of 250 mg and more. Neither intraventricular injections of as much as 1.5 mg of dopamine and 1.0 mg of serotonin nor chronic systemic administration of L-dopa and L-tryptophan affected the syndrome, but reserpine, administered chronically at doses of 0.5 and 1.0 mg/kg/day, induced photosensitivity in previously nonphotosensitive animals. Seizure testing of usually photosensitive animals 12 hours after reserpine, 0.5 mg/kg, showed that the drug prevented totally or reduced the intensity of seizures in these animals. Studies of the spontaneous electroencephalogram and of visually evoked potentials of the reserpine-treated animals revealed changes in power spectra and in the averaged evoked response from the occipital area which paralleled the induction of photosensitivity. The probability that epinephrine and norepinephrine brain concentrations are essential for inhibitory modulation and control of seizures in this species is discussed.

Animals↗
PubMed1981

Comparison of behavioral changes in cats treated with intracerebroventricular 6-hydroxydopamine and reserpine.

In singly- and group-housed cats, an intraventricular injection of 6-hydroxydopamine (6-OHDA) in doses up to 1.0 mg, after a latent period of 1 to 3 days, evoked motor responses including tremor, ataxia, rigidity, weakness with adynamia and clonic-tonic convulsions. However, the intraventricular administration of 6-OHDA in a dose of 2.0 mg in group-housed cats, also after a latent period of 1 to 3 days, caused aggression, a restlessness, irritability, rage, fear, threat, attack, fighting and flight. These responses were accompanied by autonomic signs of mydriasis and dyspnoea and motor changes including tremor, ataxia, rigidity, weakness with adynamia and clinic-tonic convulsions. In the singly-housed cat only the latter motor phenomena were observed after the higher dose. Intraventricular injection of reserpine (0.5-1.0 mg) in both singly- and group-housed cats produced catalepsy, sedation, miosis, ptosis, defecation and micturition as well as motor responses of tremor, rigidity and akinesia. It is concluded that although 6-OHDA and reserpine evoke different behavioral effects, the motor changes are similar.

Affect↗
PubMed1998

Increased immunogold labelling of neural cell adhesion molecule isoforms in synaptic active zones of the chick striatum 5-6 hours after one-trial passive avoidance training.

An area of the chick striatum, the lobus parolfactorius plays an important role in one-trial passive avoidance learning tasks. In the present study we report evidence that 5-6 h post-training, a significantly higher proportion of synaptic active zones in this area contain labelled epitopes of the neural cell adhesion molecule, with the greatest occurrence of labels at the edges of active zone profiles (in both control and trained groups). This suggests that there is a period after training when expression of the neural cell adhesion molecule in synaptic membranes almost doubles, and that events at active zone edges may play a specific role in mechanisms of synaptic adhesion. Cellular mechanisms of long-term memory formation are believed to include alterations in neural circuitry at the synaptic level. The involvement of the neural cell adhesion molecule (NCAM) in functional synaptic modifications has been demonstrated using a number of physiological models. Performance of rats in the Morris water maze, a spatial learning paradigm which requires the hippocampus, is impaired by either intraventricular injection of NCAM antibodies, or injection into the hippocampus of an enzyme which increases homophilic adhesion of the molecule, due to the removal of polysialic acid residuals from extracellular NCAM domains. In addition, intraventricular injections of anti-NCAM antibodies 6-8 h post-training were shown to impair memory for a one-trial passive avoidance task in the rat. An avoidance training model in the one-day-old chick indicates a similar time window, 5-6 h post-training during which memory for the task can be impaired by intraventricular injection of NCAM antibodies. In the hyperstriatum ventrale, a chick forebrain area involved in the passive avoidance task. subtle changes in the distribution pattern, but not density of NCAM molecules in synaptic membranes were revealed 5-6 h post-training. However, on the basis of studies of synaptic morphometry, a region of striatum, the lobus parolfactorius (LPO), appears to play a more important role in longer term memory storage for the task.

Animals↗
PubMed1998

Central pressor effect of parathyroid hormone-related protein in conscious rats.

Although the parathyroid hormone-related protein gene is widely expressed in the central nervous system, the role of this protein in blood pressure is unknown. This article examines whether parathyroid hormone-related protein is involved in the central regulation of blood pressure. An intraventricularly injected solution of parathyroid hormone-related protein elicited a dose-dependent increase of mean arterial pressure accompanied by a decrease of heart rate in conscious Sprague-Dawley rats. An anti-parathyroid hormone-related protein monoclonal antibody, given in an intraventricularly injected solution, blocked the pressor effect of parathyroid hormone-related protein. Furthermore, this pressor effect of parathyroid hormone-related protein was also abolished after pretreatment by intravenous administration of either hexamethonium bromide or doxazosin mesylate. These results suggest that central parathyroid hormone-related protein is implicated in the regulation of blood pressure, and that this effect may be mediated through sympathetic activation.

Analysis of Variance↗
PubMed1968

Effect on temperature of 5-hydroxytryptamine injected into the cerebral ventricles of cats.

1. In unanaesthetized cats the effect on rectal temperature was examined of 5-HT injected through a Collison cannula chronically implanted into the left lateral ventricle. The response depended on the amount of 5-HT injected and on the solvent employed.2. An intraventricular injection of 200 mug 5-HT creatinine sulphate dissolved in 0.9% NaCl solution resulted in a long-lasting rise often interrupted initially by a transient fall in temperature.3. This fall became more prominent with larger doses of 5-HT; even more when the 5-HT was dissolved in distilled water, and then the hyperthermic effect was attenuated.4. It is concluded that intraventricular 5-HT raises rectal temperature in cats when the amount is not too large, and that a hypothermic effect when it occurs results from paralysis of cells in the anterior hypothalamus which are excited by small doses. This would be similar to the actions of acetylcholine in the perfused superior cervical ganglion of the cat, where small doses excite but large doses paralyse the ganglion cells.5. An intraventricular injection of distilled water produced a steady rise in temperature which is attributed to release of 5-HT.

Animals↗
PubMed1986

The colliculus superior modulates ACTH-induced excessive grooming.

In previous studies the involvement of nigrostriatal dopaminergic activity in ACTH(1-24)-induced grooming has been established. It was suggested that the dopaminergic modulation of ACTH(1-24)-induced excessive grooming is exerted through the striato-nigro-collicular pathway. To obtain further evidence it was investigated, whether local application of GABAergic agents into the colliculus superior modulates excessive grooming occurring after an intraventricular injection with ACTH(1-24). It appeared that intra-collicular picrotoxin (a GABAergic antagonist) suppressed ACTH-induced grooming, whereas muscimol (a GABAergic agonist) enhanced the grooming response. The picrotoxin-induced R(unning) F(it) B(ehavior), elicited from the colliculus superior was also seen after intraventricular administration of picrotoxin. A detailed comparison of this behavioral response seen after both routes of administration of picrotoxin suggests that intraventricularly injected picrotoxin may well induce the RFB via a direct effect on the colliculus superior. Lesions placed in the colliculus superior completely abolished picrotoxin-induced RFB, exploration and orientation behavior. Yet, these lesions did not reduce excessive grooming suggesting that although this region may be involved in the modulation of ACTH-induced grooming it is not the primary site of peptide action.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[The effect of cholecystokinin octapeptide on ethanol-induced changes in motor activity and in dopamine metabolism in the nucleus accumbens of the rat brain].

The effect of intraventricular injection of cholecystokinin-octapeptide (CCK-8) in doses of 0.1875; 0.375; 0.75 and 1.5 micrograms/rat on the extracellular level of dopamine (DA) and its metabolites (DOPAC and HVA) after intraperitoneal injection of 1.5 g/kg ethanol was studied by microdialysis in n. accumbens of the brain of freely moving rats. CCK in a dose of 0.75 mg had no effect on the DA level, but significantly reduced the ethanol-induced increased DOPAC and HVA level. The effect of intraventricular injection of 0.75 microgram/rat CCK-8 on the motor activity of rats after intraperitoneal injection of ethanol (1.5 g/kg) was studied by the open field method. CCK-8 blocked the ethanol-induced inhibition of rat motor activity.

Alcohol Deterrents↗
PubMed1996

The reduction of antinociceptive effect of morphine administered intraventricularly is correlated with the decrease of serotonin release from the spinal cord in streptozotocin-induced diabetic rats.

1. The antinociceptive effect of morphine (25 micrograms) administered into the 3rd ventricle was significantly attenuated in streptozotocin-induced diabetic rats as measured by the tail-flick assay. 2. The release of serotonin (5-HT; 5-hydroxytryptamine) from the spinal cord caused by intraventricular injection of morphine (25 micrograms) was significantly reduced in streptozotocin-induced diabetic rats. 3. No differences of 5-HT contents of the spinal cord (lumbar cord) between streptozotocin-induced diabetic- and vehicle-treated rats were found. 4. It is concluded that the reduction of antinociception produced by intraventricular injection of morphine in streptozotocin-induced diabetic rats might be, at least partly, due to the decrease of 5-HT release from the spinal cord.

Analgesics, Opioid↗
PubMed1983

Intravenous vs. left ventricular injection of ionic contrast material: hemodynamic implications for digital subtraction angiography.

Because of the increased use of intravenous injection of contrast material for the evaluation of cardiac structure and function by digital subtraction techniques, a study was done to assess the hemodynamic effects of contrast material when used in this fashion in man. In 10 patients, with each serving as his own control, the effects of intravenous and intraventricular injections of sodium meglumine diatrizoate (Renografin 76) in the same dose were compared. There was no difference between these two methods with respect to changes in pulmonary wedge pressures, systemic pressures, and pulmonary vascular resistance. The elevation of mean pulmonary artery and right atrial pressure was greater after the intraventricular injection (p less than 0.05). The elevated cardiac output and systemic vascular resistance returned to control values somewhat more quickly after the intravenous injection (p less than 0.001 and p less than 0.05, respectively); and the increase in cardiac output was greater after the intravenous injection at 1 min (p less than 0.05), but less than after the intraventricular injection at 2 min (p less than 0.05). Despite the detection of these statistically significant differences, the magnitude and timing of these differences are too small to justify the notion that imaging by intravenous injections of standard ionic contrast media provides any substantial hemodynamic benefits or decreased risk to the patient.

Aged↗
PubMed1995

Cholinergic lesions by 192 IgG-saporin and short-term recognition memory: role of the septohippocampal projection.

Two experiments examined the effects of cholinergic basal forebrain lesions by intraventricular and intrahippocampal infusions of the immunotoxin 192 IgG-saporin on recognition memory in an operant delayed-non-matching-to-position task in rats. Intraventricular infusions produced extensive reductions in cortical and hippocampal choline acetyltransferase activity in the first experiment. Behaviourally, a mixed delay-dependent/independent accuracy deficit and increased biased responding was observed post-lesioning. Thus, both mnemonic as well as non-mnemonic processes were affected by the lesion. This performance deficit was indistinguishable from the impairment induced by acute intraventricular injections of the choline uptake inhibitor hemicholinium-3, which suggests that cholinergic damage induced by 192 IgG-saporin disrupted performance. In the second experiment more discrete intrahippocampal 192 IgG-saporin lesions were made, which reduced hippocampal choline acetyltransferase activity about 57%, although this reduction was not as extensive as following intraventricular injections. Although intrahippocampal lesions also impaired non-matching accuracy, this effect failed to reach significance during most stages of the experiment. Scopolamine just failed to significantly impair (P = 0.053) performance in hippocampal lesioned rats more than in controls. The nicotinic antagonist mecamylamine did not affect the lesion-induced changes in performance. These results suggest that the cholinergic basal forebrain, including the septohippocampal system, is important for the mediation of recognition memory, and muscarinic receptor-mediated mechanisms may be of greater importance than alterations of nicotinic receptor-mediated processes in the septohippocampal system.

Acetylcholinesterase↗
PubMed1987

Effects of N-(2-ethylhexyl)-3-hydroxybutyramide hydrogen succinate on the metabolisms of monoamines in the rat brain.

N-(2-Ethylhexyl)-3-hydroxybutyramide hydrogen succinate (M-2H) has been reported to increase REM sleep. The effects of M-2H on the metabolisms of monoamines which have been implicated in the regulation of the sleep-wakefulness cycle were studied in rats. M-2H (500 mg/kg p.o.) increased the levels of 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid and 3-methoxy-4-hydroxyphenylethyleneglycol sulfate in various regions of the rat brain. However, no appreciable changes occurred in levels of serotonin (5-HT), norepinephrine, dopamine, or 3,4-dihydroxyphenylacetic acid. The effect of M-2H (500 mg/kg p.o.) on 5-HT metabolism was investigated with intraventricularly-injected [14C]-5-HT. Although [14C]-5-HT level was not significantly changed, [14C]-5-HIAA level was above control level in four brain regions such as the hypothalamus, hippocampus, midbrain and pons-medulla at 3 h after the administration of M-2H. M-2H retarded the efflux of intraventricularly-injected [14C]-5-HIAA in all brain regions except the cortex. These results suggest that M-2H preferentially impaired the transport system for acid metabolites of monoamines, resulting in increase of monoamine metabolite levels in the brain.

Amides↗
PubMed1972

Changes in body temperature produced by cholinomimetic substances injected into the cerebral ventricles of unanaesthetized cats.

1. The effects on body temperature of a number of substances injected into a lateral cerebral ventricle were examined in the unanaesthetized cat.2. Nicotine (50 and 100 mug) caused a fall in body temperature ranging from 0.95-2.1 degrees C associated with skin vasodilatation, tachypnoea and panting. These responses were prevented by the intraventricular injection of hexamethonium or mecamylamine, but not of atropine or phentolamine.3. Carbachol (5 mug) caused a rise in temperature associated with skin vasoconstriction, piloerection and severe shivering. These effects were prevented by the intraventricular injection of atropine, but not of hexamethonium or mecamylamine.4. An acetylcholine/eserine mixture (10 mug of each) had no reproducible effect on body temperature. Because of the variability in the response, interaction studies with antagonist drugs were not performed.5. Hexamethonium (100 mug) or mecamylamine (100 mug) caused a prolonged rise in temperature, together with skin vasoconstriction, piloerection and intense shivering. Atropine (200 mug) was without effect on body temperature.6. Noradrenaline (100 mug) caused a fall in temperature with skin vasodilatation. The fall was converted to a rise with skin vasoconstriction, piloerection and vigorous shivering following an intraventricular injection of phentolamine (100 mug).7. These observations suggest the existence of cholinergic heat loss and heat gain mechanisms in the hypothalamic thermoregulatory pathways of the cat and the interaction studies with hexamethonium, mecamylamine and atropine, support the involvement of ;nicotinic' and ;muscarinic' receptors within the cholinergic thermoregulatory system.

Acetylcholine↗
PubMed1989

[Immunohistochemical studies of insulin receptors in the liver].

The indirect peroxidase-labeled antibody method was used to localize Insulin Receptors (IR) in rat livers. For experiments the rabbit antisera against synthetic peptides correspond to the deduced amino acid sequence of alpha- and beta-subunits of human placenta insulin receptors were used as the first sera. Our results have shown that 30 min after intraperitoneal and intraventricular injections of I U insulin in controls and MSG-treated animals the staining of DAB reaction products in livers became stronger as compared to those injected with saline solution. After intraperitoneal and intraventricular injections of insulin the electron-microscopic investigations of rat livers have found the internalization of IR in hepatocytes by interaction of receptors with exo- and endogenous insulin.

Animals↗
PubMed1991

Carrier-mediated transport of labeled oxytocin from brain to blood.

The transport of 125I-oxytocin from brain to blood was investigated in mice after intraventricular injection of radioactively labeled oxytocin with or without unlabeled candidate inhibitors. Residual radioactivity in the brain detected after decapitation was the principal determinant of transport activity. The half-time disappearance from the central nervous system of labeled oxytocin was 19.1 min. Inhibition by 10 nmol/mouse of oxytocin showed a saturable component to transport. A 10-nmol dose of tyrosine-melanocyte-stimulating hormone release inhibiting factor (Tyr-MIF-1) and pressinamide also significantly inhibited transport of labeled oxytocin (p less than 0.05). There was no inhibition of the system by a 10-nmol dose of tyrosine, iodotyrosine, MIF-1, or arginine vasopressin. Studies performed with 125I-oxytocin injected simultaneously with 131I-Tyr-MIF-1 with or without unlabeled oxytocin or Tyr-MIF-1 were consistent with both peptides being transported by the previously described peptide transport system-1 (PTS-1). Pretreatment with aluminum (100 mg/kg of elemental aluminum given 60-90 min before intraventricular injection), previously shown to inhibit PTS-1 and some other transport systems, inhibited the transport of labeled oxytocin. Radioactivity collected from the blood after intraventricular injection of 125I-oxytocin eluted on HPLC at the same position as the labeled oxytocin standard and differently from tyrosine, Tyr-MIF-1, MIF-1 and tocinamide. It is concluded that a saturable system exists for the transport of intact oxytocin from brain to blood which appears to be the previously described PTS-1.

Aluminum↗