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PubMed1982

Toxicity of pyrethroids to rats after direct injection into the central nervous system.

The administration of very small doses of two synthetic pyrethroids, cismethrin and deltamethrin, into the lateral ventricles of the brain or the subarachnoid space around the spinal cord, produced signs of toxicity in rats that were similar to those observed after iv injection of much larger doses. Intraventricular injection of the radiolabeled pyrethroids demonstrated that the onset of toxicity corresponded to the radiolabel reaching a threshold level in the brain stem, cerebellum or upper spinal cord. The injection of similarly labeled pyrethroid solutions into the lumbar region of the spine indicated that there was very little movement of the pyrethroid up the spinal cord to the brain. This corresponded to the signs of toxicity occurring only caudal to the site of injection. It was concluded that both pyrethroids produce their different syndromes of toxicity predominantly by their action on the spinal cord.

Animals↗

PubMed1979

Thyrotropin-releasing hormone stimulates release of arginine vasopressin and oxytocin in vivo.

The effects of TRH upon neurohypophyseal hormone release were studied in conscious rabbits. Intravenous infusion of 250 nm/kg TRH had no significant effect on either arginine vasopressin (AVP) or oxytocin (OT) release, but a 5-fold greater dose led to significant increases in plasma levels of both AVP and OT and behavioral arousal. Intraventricular injection of 3 nm TRH produced significant elevations of both plasma AVP and OT, with even greater effects on behavior than after iv infusion. The maximal hormone response to intraventricular injection was observed considerably earlier than that for iv injection and the response occurred after an almost 1000-fold lower dose of TRH. Neither artificial cerebrospinal fluid vehicle nor the inactive analogue D-tyrosine2 TRH (p-Glu-d-Tyr-Proamide) had any effect on neurohypophyseal hormone release or on behavior. MK-771 [L-N-(2-oxopiperidin-6-YL-carbonyl)-L-histidyl-L-thiazolidine-4-carboxamide], a TRH analog with enhanced central nervous system effects, had effects on AVP and OT release comparable to equimolar doses of TRH. TRH stimulates release of both AVP and OT after both intraventricular and iv injection, and these effects may be independent of behavioral activation.

Animals↗

PubMed1975

Effect of intracerebral serotonin administration on pituitary-thyroid function.

Thyroid function was investigated following intrahypothalamic implantation of cannulae containing 80 mug serotonin-creatine sulphate or after intraventricular injection of 100 mug of the same substance. Control animals received either needle implantations or intraventricular injections of creatine-sulphate. Thyroid/serum 131-I ratio, activity of the thyroid gland as evaluated histologically and thyrotrophic hormone (THS) content in the pituitary were significantly decreased in serotonin-treated animals. Thyrotrophic hormone releasing hormone (TRH) concentration of the hypothalamus was also significantly lowered in serotonin-treated animals when compared to intact controls. Creatine-sulphate injected rats showed a slight decrease of TSH content of the pituitary and of TRH concentration of the hypothalamus which is probably due to a stress effect caused by the intracranial intervention and/or by the intraventricular administration of a relatively large molecule, such as creatine sulphate. It is concluded that serotonin decreases the functional activity of the hypothalamo-pituitary-thyroid system by inhibiting the TRH-secretion of the hypothalamus.

Animals↗

PubMedDate not supplied

[The effect of calcium-regulating hormones on pain sensitivity in rats].

Analgesic effect of calcitonin administered in doses of 1, 3, and 5 U/100 g was studied in rats. Intrathecal administration of calcitonin (0.015 U) results in higher increase in analgesic effect compared to intraventricular injection. Intramuscular (1, 3, and 5 U/100 g) and intraventricular (0.1 U) injection of parathormone exert no analgesic effect, whereas intrathecal injection in a dose of 0.1 U resulted in statistically significant analgesia. High correlation was found for nociception and calcium level in blood. Nifedipine and isoptin (1, 5, and 10 mg/kg) were shown to reduce significantly the analgesic effect of calcitonin. On the membrane of the isolated neuron of mollusk calcitonin (10(-9) - 10(-7) M) increased and in a concentration of 10(-6) M decreased JCa. Inhibiting effect of isoptin on JCa was found for combined action of calcitonin and isoptin on the neuron membrane.

Analgesics↗

PubMedDate not supplied

Behavioral effects of dibutyryl cyclic 3'5'AMP and biogenic amines in rats.

White male Wistar rats were injected intraventricularly with 200 mug of dibutyryl cyclic 3'5'AMP (DAMP. 30 min later part of animals was injected intraventricularly with 10 mug of dopamine (DA), 10 mug of 5-hydroxytryptamine (5-HT) or 50 mug of acetylcholine (Ach). Immediately after injection of the amines the time of walking, convulsions, immobility and number of jumps during 10 min periods of observation was measured. DAMP induced excitation of animals expressed by convulsions, jumping and short period of immobility. All studied biogenic amines inhibited convulsions and caused periodically stereotypical behavior. 5-HT and Ach increased the time of immobility in animals injected with DAMP. DA increased the number of jumping. These results indicate the interaction between DAMP and DA, 5-HT and Ach on behavioral phenomena in rats.

Acetylcholine↗

PubMed1996

Epileptogenic activity induced by combined treatment with antiinflammatory drugs and enoxacin and its inhibition by a calcium antagonist, nicardipine.

Epileptogenic activity induced by combined treatment with antiinflammatory drugs and enoxacin was investigated in chronic electrode-implanted rats. Ferubinac ethyl and aspirin DL-lysine showed a spike and wave complex in EEG without showing remarkable behavioral changes when they were injected intraventricularly, although a relatively high dose was needed. Enoxacin, on the other hand, elicited potent epileptogenic activity characterized by uninterrupted high voltage spike and wave complex at doses of 50 and 100 micrograms. At the same time, rats showed hyperactivity, jumping and violent convulsion. Combined treatment with enoxacin (p.o.) and ferubinac ethyl (i.v.) caused potent epileptogenic activity characterized by uninterrupted burst of high voltage spike and wave complex. Behaviorally, animals showed forelimb clonus, head nodding and generalized convulsion. High voltage spike and wave complex was also observed after combined treatment with enoxacin (i. vent.) and ferubinac ethyl (i.v. or i. vent.) in association with hyperactivity and jumping and violent convulsion. Nicardipine remarkably inhibited epileptic seizures induced by combined treatment with enoxacin (p.o.) and ferubinac ethyl (i.v.). It is concluded that simultaneous treatment with enoxacin and ferubinac ethyl produced epileptogenic activity when injected intraventricularly, and nicardipine inhibited convulsions induced by combined use of enoxacin (p.o.) and ferubinac ethyl (i.v.).

Animals↗

PubMed1973

Cellular localization of the uptake of 5-hydroxytryptamine in the area postrema of the rabbit after injection into a lateral ventricle.

1. The cellular localization of 5-hydroxytryptamine (5-HT) was investigated in the area postrema of the rabbit after intraventricular injection under different experimental conditions.2. 5-HT was found to be accumulated in different parts in and near to the area postrema, e.g. in glial cells, dorsal surface of the area postrema and ependyma of the central canal.3. The concentrations of 5-HT and 5-hydroxy indol-3-yl acetic acid (5-HIAA) were measured in different parts of the brain and CSF in control and in 5-HT treated animals with and without pargyline pretreatment. Intraventricular injection of 5-HT increased the concentration of 5-HT and 5-HIAA in the brain and in the CSF; pretreatment with pargyline further increased the concentrations of 5-HT but decreased the concentration of 5-HIAA.

Animals↗

PubMed2006

Only through the brain nuclei, arginine vasopressin regulates antinociception in the rat.

The effect of arginine vasopressin (AVP) on rat antinociception was investigated. Intraventricular injection of 50 or 100 ng AVP dose-dependently increased the pain threshold; in contrast, intraventricular injection of 10 microl anti-AVP serum decreased the pain threshold; both intrathecal injection of 200 ng AVP or 10 microl anti-AVP serum and intravenous injection of 5 microg AVP or 200 microl anti-AVP serum did not influence the pain threshold. Pain stimulation reduced AVP concentration in hypothalamic paraventricular nucleus (PVN), and elevated AVP concentration in hypothalamic supraoptical nucleus (SON) and periaqueductal gray (PAG), but no change in AVP concentration was detected in pituitary, spinal cord and serum. The results indicated that AVP regulation of antinociception was limited to the brain nuclei.

Animals↗

PubMed2005

Agonist and hypertonic saline-induced trafficking of the NK3-receptors on vasopressin neurons within the paraventricular nucleus of the hypothalamus.

The neurokinin 3 receptor (NK3R) is colocalized with vasopressinergic neurons within the hypothalamic paraventricular nucleus (PVN) and intraventricular injections of NK3R agonists stimulate vasopressin (VP) release. Our objectives were to test the hypotheses that intraventricular injections of the selective NK3R agonist, succinyl-[Asp6, N-Me-Phe8] substance P (senktide), activate NK3R expressed by vasopressinergic neurons within the PVN, and see whether NK3R expressed by vasopressinergic neurons in the PVN are activated by hyperosmolarity. NK3R internalization was used as a marker of receptor activation. Immunohistochemistry revealed that NK3Rs were membrane-bound on VP immunoreactive neurons in control rats. Following senktide injection, there was a significant increase in the appearance of NK3R immunoreactivity within the cytoplasm and a morphological rearrangement of the dendrites, indicating receptor internalization, which was reversible. Furthermore, pretreatment with a selective NK3R antagonist, SB-222200, blocked the senktide-induced VP release and internalization of the NK3R in the PVN. These results show that the trafficking of the NK3R is due to ligand binding the NK3R. In a subsequent experiment, rats were administered intragastric loads of 2 or 0.15 M NaCl, and NK3R immunohistochemistry was used to track activation of the receptor. In contrast to control rats, 2 M NaCl significantly increased plasma VP levels and caused the internalization of the NK3R on VP neurons. Also, NK3R immunoreactivity was located in the nuclei of vasopressinergic neurons after senktide and 2 M NaCl treatment. These results show that hyperosmolarity stimulates the local release of an endogenous ligand in the PVN to bind to and activate NK3R on vasopressinergic neurons.

Animals↗

PubMed1982

Chlorpromazine methiodide-induced barrel rotation: an antimuscarinic effect.

Barrel rotation is a motor response observed in rats in which the animal twists about its long axis and rolls laterally. This response was first described following intracerebroventricular injection of somatostatin. The pharmacologic specificity of the response has been questioned, and its physiologic basis is unknown. Recently, barrel rotation following intraventricular injection of quaternary chlorpromazine, chlorpromazine methiodide (CPZMI), has been reported. We have studied the specificity and pharmacologic basis of CPZMI-induced barrel rotation. The response was not induced by 26 compounds injected as controls, and was induced by 6 anti-muscarinic compounds. Dose-response relationships for onset, duration and magnitude of CPZMI-induced barrel rotation response were studied; number of rotations increased linearly with CPZMI dose up to 20 micrograms, after which number of rotations decreased and toxic effects (sedation, seizures) occurred. CPZMI barrel rotation was inhibited by intraventricular injection of the muscarinic agonist carbachol and enhanced by intraventricular or systemic atropine. Muscarinic and dopamine receptor studies indicated that CPZMI has high affinity for the muscarinic cholinergic receptor and low affinity for the spiperone binding site. Modified Scatchard analysis of CPZMI displacement of [3H]QNB at the muscarinic receptor is consistent with muscarinic antagonist properties. We conclude that CPZMI-induced barrel rotation has a specific pharmacologic basis, that of muscarinic cholinergic antagonism.

Animals↗

PubMed1989

Complement-derived polypeptide C3adesArg as a mediator of inflammation at the blood-brain barrier in a new experimental cat model.

The effect of the complement-derived polypeptide C3adesArg as a mediator of inflammation in the central nervous system was examined. Twenty-five anesthetized cats received 4 mg of this polypeptide by intraventricular injection, 20 cats who served as controls received saline. Cerebrospinal fluid (CSF) was sampled 3 h after intraventricular injection and the brains were removed. For assessment of the permeability of the blood-brain barrier the CSF penetration of four antibiotics, which were given intravenously was measured. Five control animals were employed for each antibiotic (tobramycin, ampicillin, imipenem, fosfomycin), whereas six C3adesArg-treated animals were used for each antibiotic and seven for tobramycin. Besides CSF levels of glucose, the prostanoids 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 were measured. The morphological examinations in the CSF sediments and histological brain sections in the C3adesArg-treated animals disclosed a distinct inflammation with leptomeningeal and perivascular infiltration of polymorphonuclear granulocytes compared to normal findings in the controls. The CSF/serum ratios of all of the antibiotics were markedly elevated compared to controls, indicating a blood-brain barrier disruption. The levels of all prostanoids were significantly higher in the treatment group than in the control group, whereas the glucose levels were lower. These findings are in accordance with a granulocytic meningitis as seen in some infections at the acute stage. It is concluded that C3adesArg acts as a mediator of inflammation in the central nervous system.

6-Ketoprostaglandin F1 alpha↗

PubMed1980

Effect of noradrenaline and 5-hydroxytryptamine depletion on locomotion in the cat.

It has recently been hypothesized that stimulation of the mesencephalic locomotor region (MLR) can give rise to locomotion in mesencephalic cats due to activation of descending monoaminergic pathways to the spinal cord. This notion is based on the findings that monoamine agonists and precursors can induce hindlimb stepping in acute low spinal animals, and on the similarities between the effects of the noradrenaline (NA) precursor, L-DOPA, and stimulation of the MLR. The hypothesis that the descending monoamine systems comprise the only pathways which control the initiation of locomotion has been tested in the present study. NA was depleted from the CNS using intraspinal and intraventricular injections of 6-hydroxydopamine and i.v. injections of the NA synthesis inhibitor, alpha-methyltyrosine. Depletion of 5-hydroxytryptamine (5-HT) was achieved using intraventricular injections of 5,6-dihydroxytryptamine and i.p. p-chlorophenylalanine. These treatments did not abolish evoked locomotion in spite of substantial depletion of NA and 5-HT in the spinal cord and brain stem (maximal depletions of NA up to 14% of control in lumbar cord and 16% of control in pons; maximal depletions of 5-HT up to 19% of control in sacral cord and 25% of control in medulla). Combined depletion of NA and 5-HT did not abolish evoked locomotion in mesencephalic cats, although the treated animals displayed pronounced ataxia prior to decerebration. Depletion of NA or 5-HT alone did not alter locomotion in otherwise intact animals. A previous report that phenoxybenzamine antagonizes the effects of MLR stimulation was not confirmed. The results therefore do not support the hypothesis that descending pathways containing monoamines are essential for locomotion evoked by brain stem stimulation.

5,7-Dihydroxytryptamine↗

PubMed1999

Brain tachykinins and the regulation of salt intake.

The regulation of salt intake is achieved through the coordination of behavioral and physiological responses. Brain neuropeptides, such as the tachykinins, play an important role in orchestrating both of these responses. Intraventricular injections of NK3 receptor agonists, such as senktide, are potent in suppressing salt intake. Experimental results show that intraventricular injections of senktide that suppress salt intake have no effect on the ingestion of other tastes, such as sucrose. The means by which senktide suppresses salt intake was investigated in a series of experiments. Taste reactivity and lick rate analyses suggest that the activation of NK3 receptors reduces salt intake by modulating the oral-stimulating property of salt taste.

Animals↗

PubMed1968

Temperature effects of reserpine injected into the cerebral ventricles of rabbits and cats.

1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.2. In rabbits the reserpine (0.5-0.6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.3. In cats the reserpine (0.5-0.75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic fibres ending at these cells. When these fibres are depleted of their noradrenaline by one or two injections of reserpine, these effects are not obtained because noradrenaline is no longer available to be released in sufficient amounts to raise temperature in rabbits and to lower it in cats.

Animals↗

PubMed1972

Benzodiazepines: anxiety-reducing activity by reduction of serotonin turnover in the brain.

The anxiety-reducing effects of minor tranquilizers in the rat conflict test were mimicked by serotonin antagonists and by p-chlorophenylalanine, an inhibitor of serotonin synthesis; the depressant effects of the minor tranquilizers were mimicked by norepinephrine antagonists. Intraventricular injections of serotonin led to a suppression of behavior, and also antagonized the anxiety-reducing action of benzodiazeprines. Intraventricular injections of norepinephrine led to a release of punished behavior from suppression, and also antagonized the depressant action of benzodiazepines. The anxiety-reducing activity, and the decrease in serotonin turnover induced by benzodiazepines, were maintained over repeated doses, whereas depressant activity, and the decrease induced in norepinephrine turnover, both rapidly underwent tolerance. Tranquilizers may exert their anxiety-reducing effects by a reduction of serotonin activity in a behaviorally suppressive punishment system, and they may exert their depressant effects by a reduction of norepinephrine activity in a behaviorally facilitatory reward system.

Animals↗

PubMed1986

Release of immunoreactive met-enkephalin by intraventricular beta-endorphin in anesthetized rats.

The release of immunoreactive met-enkephalin and leu-enkephalin from the spinal cord by intraventricular injection of different doses of beta-endorphin was studied using the intrathecal perfusion technique. The intraventricular beta-endorphin elicited the release of immunoreactive met-enkephalin from the spinal cord in a dose dependent manner. Immunoreactive leu-enkephalin in the spinal perfusate was not increased after intraventricular beta-endorphin injection. Both immunoreactive met-enkephalin and leu-enkephalin in the spinal cord were not changed by low doses (2-6 micrograms) of beta-endorphin but were increased markedly by 60-70% after high doses of beta-endorphin (32-64 micrograms). It is likely that the biosynthesis of enkephalins was also increased after intraventricular beta-endorphin injection. Intraventricular naloxone, 30 micrograms did not induce any release of immunoreactive met-enkephalin from the spinal cord and did not block the release of immunoreactive met-enkephalin induced by intraventricular beta-endorphin, 15 micrograms.

Animals↗

PubMed1983

Uptake of elemental mercury by brain in relation to concentration of glutathione and activity of glutathione peroxidase.

Uptake of mercury by brain after i.v. injection of elemental mercury was investigated in the rat, after depletion of glutathione or inhibition of glutathione peroxidase in brain tissue. When glutathione in brain was depleted 76% by an intraventricular injection of diethylmaleate, a 13% increase in mercury uptake by brain was observed. After an intraventricular injection of iodoacetate, activity of glutathione peroxidase in brain was inhibited 19% and the content of reduced glutathione was decreased 20%. In these animals mercury uptake by brain increased 66% relative to controls.

Animals↗

PubMed1981

Role of the dopaminergic system in luteinizing hormone release and ovulation in the hen.

Two experiments were conducted to examine further the role of the dopaminergic system in the ovulatory cycle of the hen. In experiment 1, dopamine (DA; 8 microgram) was injected intraventricularly 14 hr prior to the C1 ovulation (to determine the efficacy of DA in causing premature ovulation) and the DA-receptor blocker, pimozide, implanted intraventricularly for the previous 24 hr was used to assess the specificity of the response. The luteinizing hormone (LH) radioimmunoassays from serial blood samples subsequent to the injection, indicated no effect of the DA treatment on either the time or the magnitude of the preovulatory LH surge. In Experiment 2, an intraventricular injection of DA (10 microgram) was made 8 hr prior to the C1 ovulation (to examine the effect of DA on the normal preovulatory LH surgery) and assay results from blood samples at short intervals immediately after the injection showed no effect of the treatment on plasma LH levels. These results, in addition to the finding that the pimozide implant caused no disruption of the ovulatory cycle, suggest that the dopaminergic system is not essential to the ovulatory process in the hen.

Animals↗