Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Injections, Intraventricular”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed1993

Stimulation of H3-histamine receptors increases the release of prolactin in male rats.

Histamine (HA) stimulates prolactin secretion via H1 and H2 receptors. In the present study, we examined the role of a third subtype of receptor recently described in brain, the H3-HA receptor, on prolactin secretion in male rats. R(-)alpha-methyl-HA (alpha-MHA), a selective H3 receptor agonist, was injected into the lateral ventricle of the brain in freely moving rats. alpha-MHA produced a dose-dependent (1-5 micrograms) and long-lasting increase in plasma prolactin levels. This increase was observed from 15 to 60 min after injection of alpha-MHA. Its stimulatory action was prevented by thioperamide (20 micrograms i.v.t), a selective H3 antagonist. This compound, injected intraventricularly, lacked effect by itself on basal plasma prolactin levels. Neither pyrilamine (H1 antagonist; 60 micrograms i.v.t.) nor ranitidine (H2 antagonist; 60 micrograms i.v.t.) affected alpha-MHA-induced prolactin release. The stimulatory effect was still present when brain HA was depleted by alpha-fluoromethylhistidine (30 mg/kg i.p.). Our findings suggest that alpha-MHA evokes prolactin release by activation of postsynaptic H3 receptors.

Animals↗
PubMed1975

Neurochemical regulation of feeding in the rat: facilitation by alpha-noradrenergic, but not dopaminergic, receptor stimulants.

Rats ate voraciously after intraventricular injections of the alpha-noradrenergic receptor stimulant clonidine. Intraventricular administration of l-norepinephrine also facilitated feeding, but similar injections of dopamine and apomorphine (a dopamine receptor stimulant) were ineffective and even tended to suppress feeding. Clonidine was 100 times more potent than norepinephrine and increased the intake of both the ordinary diet of powdered food and a highly palatable wet food. The anorexic action of amphetamine was reversed by centrally administered clonidine. These observations suggest "respondent" rather than "operant" regulation of feeding by noradrenergic systems. That is, in relation to noradrenergic mechanisms, feeding appears to be a respondent which is sensitized or disinhibited by activation of alpha-noradrenergic receptors, rather than an operant which is reinforced by the release of norepinephrine.

Adrenergic alpha-Agonists↗
PubMed1996

Effects of the metabotropic glutamate receptor antagonist MCPG on spatial and context-specific learning.

The effects of the metabotropic glutamate receptor antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG) on performance in a water maze and in context-specific associative learning were examined in rats previously implanted with cannulae. MCPG (20.8 micrograms) injected intraventricularly (i.c.v.) before testing impaired the performance of rats in the spatial version of the Morris water maze, but 1/10 of this dose did not. Memory retention, evaluated 24 hr post-training, was also affected by the high dose of MCPG. However, performance in a cued version of the water maze was not impaired by the high dose, excluding effects of the drug on perceptual faculties. The effects of the MCPG were further characterized on performance in another hippocampus-dependent spatial learning task, the context-dependent fear conditioning task. MCPG (20.8 micrograms, i.c.v.) did not interfere with conditioned freezing to context in this task. For comparison, a group of rats was injected with the NMDA receptor blocker MK801. MK801 at a dose that disrupted the performance in the spatial version of the Morris water maze (0.08 mg/kg), significantly reduced freezing compared to controls. These experiments indicate that MCPG-sensitive metabotropic receptors may be required for only a restricted subset of spatial learning tasks, while NMDA receptors may play an integral role in all spatial learning.

Animals↗
PubMed1977

Thyrotropin-releasing hormone: physiological concomitants of behavioral excitation.

Two doses (10 microng and 100 microng) of thyrotropin-releasing hormone (TRH) or saline were injected intraventricularly in rabbits pretreated with either saline, pentobarbital or phenobarbital. Behavior, EEG patterns, respiration rate and heart rate were monitored for 100 min posttreatment. TRH significantly altered all physiological indices except heart rate in both barbiturate- and saline-pretreated animals. The results support the contention that TRH modified central functioning by direct action. Results are discussed in terms of barbiturate antagonism and excitatory effects of TRH.

Animals↗
PubMed1991

Neurotensin selectively antagonizes apomorphine-induced stereotyped climbing.

In order to better characterize the neuroleptic properties of neurotensin, the dose-related effects of the peptide on stereotyped climbing, sniffing and licking induced by 0.6 mg/kg apomorphine were examined. The following doses of the peptide were injected intraventricularly 30 min prior to apomorphine administration: 0.9, 3.75, 30.0 and 60 micrograms. Results indicate that, whereas oro-facial stereotypies remained unaffected by the peptide, stereotyped climbing was significantly decreased with the two largest doses of neurotensin. These findings indicate that the profile of neurotensin's neurobehavioral effects is more akin to that of atypical than typical neuroleptics.

Animals↗
PubMed1978

Stages of recovery from central norepinephrine lesions in enriched and impoverished environments: a behavioral and biochemical study.

Adult rats were injected intraventricularly with 6-OHDA and allowed to recover for varying time periods in either an enriched colony environment or in isolation cages. When tested behaviorally in a novel environment, isolated animals showed a cyclical recovery pattern, with behavioral changes at 14 days after lesioning which were different from those seen at 2 and 45 days after lesioning. In contrast, animals housed in a colony environment showed progressive improvement and better recovery than isolates. Biochemical studies of uptake of H3NE and histofluorescence indicated that colony housed animals had enrichment effects (higher cortical NE uptake), but they were also more susceptible to 6-OHDA and did not recover well from the lesions. Isolated animals showed somewhat better recovery of NE uptake following 6-OHDA injections, especially in cortex. Because behavioral recovery from 6-OHDA was dissociated from biochemical indicators of recovery in NE circuitry, these results imply that brain systems other than NE were primarily responsible for the enhanced behavioral recovery which occurs in enriched environments.

Animals↗
PubMed1988

Peripheral and central antinociceptive actions of ethylketocyclazocine in the formalin test.

The antinociceptive actions of ethylketocyclazocine and morphine were examined in rats in a thermal nociceptive test (tail-immersion) and a test involving minor tissue injury (formalin). In the formalin test, the antinociceptive effects of high doses of ethylketocyclazocine, but not morphine, were attenuated by the peripherally acting antagonist naloxone methylbromide. Naloxone methylbromide had no effect on antinociception produced by ethylketocyclazocine in the tail-immersion test. When ethylketocyclazocine was injected intraventricularly, only partial antinociception was observed in the formalin test. Conversely, naloxone given intraventricularly only partially attenuated the antinociception produced by ethylketocyclazocine given systemically. The data indicate that the antinociceptive effects of ethylketocyclazocine in the tissue injury-induced nociception are a result of summation of central and peripheral actions. Morphine antinociception reaches ceiling at doses that are devoid of such peripheral actions. The data imply that it may be possible to develop a new class of peripherally acting analgesics that are effective in acute inflammatory pain.

Analgesics↗
PubMed1985

Neuronal responses in subfornical organ and other regions to angiotensin II applied by various routes.

Effects of Angiotensin II (AII) and of signals of hydromineral deficiencies on neuronal firing in the subfornical organ (SFO) and the surrounding regions of the rat were examined. AII was applied in three ways: electrophoresis, intracarotid injection, or intracerebroventricular injection. Seventeen SFO neurons (52%) were facilitated by electrophoretic AII and one (3%) was inhibited (AII-responding neurons). Neurons in other regions (cerebral cortex, nucleus triangularis septi, hippocampus, nucleus periventricularis) were also facilitated (23%) or inhibited (14%). Prostaglandin (PG)F2, a universal vasoconstrictor, produced an effect similar to that by AII on neuronal activity of the SFO and surrounding regions, and this effect was antagonized by (NO2-), a vasoplegic agent. Intracarotid injection of AII caused biphasic facilitation of SFO activity. The second increase correlates with changes in blood pressure. Intraventricular injection of AII caused drastic and long lasting excitation of SFO activity. Simultaneous intraventricular application of NO2- blocked the AII effect on SFO neurons but not on blood pressure. Hypovolemia or cerebrospinal fluid withdrawal that might cause mechanical stimulation of circumventricular organs increased SFO neuronal activity. These results are compatible with the vasoconstriction hypothesis of an indirect effect of AII through change in diameter of the vasa that surround neurons.

Action Potentials↗
PubMed1988

Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment.

We earlier reported that chronic intraventricular injections of NGF into adult rats with partial transection of the fimbria prevent the lesion-induced disappearance of cholinergic neurons in the medial septal nucleus and the diagonal band of Broca (Hefti, 1986). The present study assessed the specificity and treatment requirements of this effect of NGF. Immunohistochemical visualization of NGF receptors (NGF-R) revealed that these molecules are selectively located in forebrain cholinergic neurons of unlesioned brains. Fimbrial transection resulted in transient accumulation of NGF-R in proximal stumps of lesioned axons but failed to induce the expression of NGF-R by other cells in the septal area or near the lesion. Two to three weeks after lesioning, the number of septal neurons expressing NGF-R was reduced by approximately 50% in parallel with the reduction of the number of neurons expressing cholinergic marker enzymes. Repeated intraventricular NGF injections during 4 weeks prevented the disappearance of these cells. Fimbrial transections also reduced the number of septal GABAergic neurons visualized by glutamate decarboxylase immunohistochemistry. The loss of GABAergic neurons was not prevented by NGF. These findings suggest that NGF prevents the lesion-induced degeneration of cholinergic neurons by directly acting on NGF-R expressed by cholinergic cells and that NGF does not affect any neuron with an axonal lesion. Delayed start of the NGF treatment failed to prevent the disappearance of lesioned cholinergic neurons, providing evidence that NGF treatment indeed promotes the survival of these cells rather than simply upregulating the expression of transmitter-specific enzymes. A single injection of NGF at the time of the lesion was not sufficient to prevent the lesion-induced degeneration of cholinergic neurons. Furthermore, termination of chronic NGF treatment after 4 weeks was followed by loss of septal cholinergic neurons after an additional 4 weeks. These findings suggest that the continuous presence of NGF during more than 4 weeks is required to prevent the degeneration of cholinergic cells. The data are discussed in the context of a possible physiological role of NGF in the function of adult forebrain cholinergic neurons.

Acetylcholinesterase↗
PubMedDate not supplied

Immunocytochemical evidence for calcitonin gene-related peptide-like neurons in the dorsal horn and lateral spinal nucleus of the rat cervical spinal cord.

Calcitonin gene-related peptide (CGRP) in the dorsal horn of the rat spinal cord was assumed until now to be principally of primary afferent origin. It is shown here, on the basis of both light and electron microscopic immunocytochemical evidence, that some cell bodies of the dorsal horn and lateral spinal nucleus (LSn) of the rat cervical spinal cord contain a CGRP-like immunoreactivity. At the light microscopic level, immunoreactive cell bodies were observed in animals pretreated with colchicine injected intraventricularly, CGRP-like cell bodies were morphologically heterogeneous and distributed in the three superficial layers of the dorsal horn. They were very rare in lamina I and more numerous in laminae II and III. A group of immunoreactive cell bodies was also observed in the LSn. Using electron microscopic techniques, a few immunoreactive cell bodies were observed even in control animals. In addition, relatively numerous immunoreactive dendrites were observed in lamina II. The specificity of the reaction and the physiological implications of the results are discussed.

Animals↗
PubMed1979

The effect of metal complex of thyrotropin-releasing hormone on locomotor activity of neonatal chicken.

Neonatal chickens were injected intraventricularly with Ni(II), Pd(II), Cu(II) or Zn(II) complex of TRH and the potencies of stimulating locomotor activity were compared with that of TRH, Ni(II)-TRH was more potent than the ligand while Pd(II)-TRH was inert. Cu(II)- and Zn(II)-TRH induced the response to the same extent of the ligand. These results indicate that the action of TRH in the CNS resulting in the locomotor hyperactivity is dependent on the tertiary conformation of molecule which is modified by chelate formation.

Animals↗
PubMed1975

Vasopressin release by nicotine: the site of action.

1. In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood. 2. Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur. 3. Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system. 4. Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without ocytocin. The amount of nicotine placed in each ring was usually 80 mug, but a release was obtained with 10 mug and in one experiment with as little as 5 mug. 5. The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies. 6. The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects. 7. It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra-optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution.

Administration, Topical↗
PubMed1984

Uptake and transport of lectins from the cerebrospinal fluid by cells of the immature mouse brain.

40 mice (C57BL/6J) 2, 3, 6, and 10 d old were injected intraventricularly with 2% wheat germ agglutinin (WGA) or soybean agglutinin (SBA). The transport of lectins from the ventricular cerebrospinal fluid (CSF) into brain parenchyma was studied by an unlabelled antibody technique ( BORGES and SIDMAN 1982). The granule product of the immunohistochemical reaction was found in the cytoplasm of ventricular ependymal cells, the choroid plexus and meninges in all age groups studied. Penetration of lectins into brain parenchyma was higher in younger animals and at more immature-cell-surrounded parts of lateral and the IVth ventricle. The stain product was dispersed throughout the neuropil excepting cell nuclei. Higher concentration of lectins appeared in nerve cell cytoplasm of some regions of the brain of younger animals (P2 to P3); in 10 d old mice granules of stain appeared in the cytoplasm of PURKINJE cells and pyramidal neurons of the hippocampus. A fiber-like staining, apparent especially in large commissures adjacent to brain ventricles (corpus callosum, fornix hippocampi) in all age groups, suggests that lectins are transported within axons, even at the earliest postnatal ages. Unlike WGA, densely stained glial cells appeared in parenchyma of SBA injected animals, especially of the younger age group (P3 to P6). The results of this study confirm earlier findings that macromolecules within the ventricular CSF can penetrate into brain parenchyma but suggest that the penetration is higher in less mature animals and at the ventricle regions surrounded by less differentiated parenchyma.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

The influence of alpha-fluoromethylhistidine and histamine receptor antagonists on the beta-endorphin-induced corticosterone response.

Involvement of a central histaminergic mechanism in the stimulating effect of beta-endorphin (beta-End) on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, was investigated in conscious rats. The rise in serum corticosterone levels, induced by beta-End injected intraventricularly (icv) was considerably impaired by pretreatment with naltrexone, an opioid receptor antagonist. The stimulating effect of beta-End was almost totally suppressed by a prior icv administration of mepyramine, a histamine H1-receptor antagonist, and also considerably reduced by pretreatment with cimetidine, an H2-receptor antagonist. The strongest suppression, by 83%; of the beta-End-induced corticosterone response was evoked by a prior administration of alpha-fluoromethylhistidine, an inhibitor of neuronal histamine synthesis in the brain. These results indicate that both the brain neuronal histamine and central histamine H1- and H2-receptors are considerably involved in the beta-endorphin-induced stimulation of the pituitary-adrenocortical activity.

Animals↗
PubMed1992

Effects of lesion of the cholinergic basal forebrain nuclei on the activity of glutamatergic and GABAergic systems in the rat frontal cortex and hippocampus.

The effects of cholinergic basal forebrain lesions on the activity of the glutamatergic and GABAergic systems were investigated in the rat frontal cortex and hippocampus. Bilateral quisqualic acid injections in the nucleus basalis magnocellularis (NBM) at the origin of the main cholinergic innervation to the neocortex induced a cholinergic deficit in the cerebral cortex 15 days later, as shown by the marked selective decrease in cortical choline acetyltransferase (CAT) activity observed. Concurrent alterations in the kinetic parameters of high affinity glutamate uptake consisting mainly of a decrease in the Vmax were observed in the cerebral cortex. These changes presumably reflect a decreased glutamatergic transmission and provide support for the hypothesis that cortical glutamatergic neurons may undergo the influence of cholinergic projections from the NBM. Surprisingly, similar alterations in the glutamate uptake process were found to occur at hippocampal level in the absence of any significant change in the hippocampal cholinergic activity. These data indicate that the NBM may contribute to regulating hippocampal glutamatergic function without interfering with the hippocampal cholinergic innervation that mainly originates in the medial septal area-diagonal band (MSA-DB) complex. No change in parameters of GABAergic activity, namely the glutamic acid decarboxylase (GAD) activity and high affinity GABA uptake, were observed in any of the structures examined. In a second series of experiments involving bilateral intraventricular injections of AF64A, marked survival time-dependent decreases in CAT and high affinity choline uptake activities but no significant change in the high affinity glutamate uptake rate were observed in the hippocampus. No significant change in either parameters of cholinergic activity or in the glutamate uptake was concurrently observed in the cerebral cortex. The GABAergic activity was again unaffected whatever the survival time and the structure considered. Taken as a whole, these data suggest that basal forebrain projections originating in the NBM may play a major role in regulating glutamatergic but not GABAergic function in both the cerebral cortex and the hippocampus; whereas the glutamatergic and GABAergic activities in these two structures may not be primarily under the influence of the cholinergic projections from the MSA-DB complex.

Animals↗
PubMed2001

Estrogen receptor-alpha antisense decreases brain estrogen receptor levels and affects ventilation in male and female rats.

We hypothesized that administration of an antisense oligodeoxynucleotide (ODN) to estrogen receptor (ER)-alpha mRNA decreases the ER protein in the neonatal rat brain, alters the sex-specific ventilatory responses to aspartic acid in rats, and counteracts the effects of testosterone proportionate (TP) in females. One-day-old rat pups were injected intraventricularly with vehicle, antisense ER ODN, or scrambled ODN control. Additional groups of females received TP or vehicle and one of the three treatments. Brain ER protein levels were decreased by 65% at 6 h and 35% at 24 h after antisense ODN. Aspartic acid decreased ventilation in all groups of weanling males and females except ER ODN-treated females and TP-vehicle-treated females. Aspartic acid decreased ventilation in all groups of adult females except those given TP and in males. Weanling ER ODN-treated rats were shorter and weighed less than controls. Only adult ER ODN-treated males exhibited these traits. Thus neonatal ER affects aspartic acid modulation of breathing and body growth in a sex-specific and developmental manner.

Animals↗
PubMed1986

Nerve growth factor promotes survival of septal cholinergic neurons after fimbrial transections.

Several findings obtained in recent years suggest that NGF, aside from its well-established function as a neurotrophic factor for peripheral sympathetic and sensory neurons, also has trophic influence on the cholinergic neurons of the basal forebrain. The present study assessed whether NGF was able to affect survival of central cholinergic neurons after axonal transections in adult rats. The septo-hippocampal pathway was transected unilaterally by cutting the fimbria, and animals were implanted with a cannula through which NGF or control solutions were injected intraventricularly over 4 weeks. The lesions reduced the number of large cell bodies, as visualized by Nissl staining in the medial septal nucleus and in the vertical limb of the diagonal band of Broca. Furthermore, in the same nuclei, they reduced the number of cell bodies positively stained for AChE after pretreatment with diisopropylfluorophosphate (a method known to result in reliable identification of cholinergic neurons in the septal area). On lesioned sides, the number of cholinergic cells in medial septal nucleus and the vertical limb of the diagonal band was reduced by 50 +/- 4%, as compared to the number on contralateral sides. On lesioned sides of animals chronically treated with NGF, the number of AChE-positive cells in these areas was reduced only by 12 +/- 6%, as compared to control levels. These findings suggest that fimbrial transections resulted in retrograde degeneration of cholinergic septo-hippocampal neurons and that NGF treatment strongly attenuated this lesion-induced degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Acceleration of desipramine-induced changes on the dopamine receptor-coupled adenylate cyclase system by pertussis toxin.

The response of adenylate cyclase to GTP and to dopamine (DA) was investigated in striatal membranes from desipramine (DMI)-treated rats (10 mg/kg, b.i.d., for 5 days). GPT exerted the same biphasic effect on basal and DA-stimulated enzyme activity in membranes from DMI-treated rats as on saline-treated rats. Rats were injected intraventricularly once with islet activating protein (IAP), pertussis toxin, and given extended treatment with DMI in order to study the effects on the inhibitory GTP-binding protein (Gi). Gi loses its function as a signal transducer on being ADP-ribosylated selectively by the IAP. D2 inhibition of adenylate cyclase by DA was attenuated by the IAP treatment in both DMI-and saline-treated rats; peak levels of DA plus GTP stimulation shifted from 1 microM to 100 microM GTP. D1 stimulation of adenylate cyclase by DA was also attenuated by the IAP in the DMI-treated rats. Since long-term treatment with DMI (15 mg/kg, once a day, for 3 weeks) resulted in suppression of D1 stimulation similar to that seen in the present findings, uncoupling between D2 receptors and Gi due to IAP treatment might accelerate DMI-induced adaptive changes of dual control of adenylate cyclase system by DA.

Adenosine Diphosphate Ribose↗