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PubMed1985

The modulation of cortical acetylcholine release by GABA, GABA-like drugs and benzodiazepines in freely moving guinea-pigs.

In order to define the modulatory role played by gamma-aminobutyric acid (GABA) in corticopetal cholinergic projections, the effect of this amino acid and related drugs on gross behaviour, the EEG and the release of acetylcholine (ACh) from the cerebral cortex in freely moving guinea-pigs was studied. gamma Aminobutyric acid, injected intracerebroventricularly (20-50 mumol) induced a three-phase picture: first (5-15 min) behavioural activation and increased release of ACh, then (30-90 min) depression, EEG synchronization and reduced release of ACh, and finally "rebound" stimulation. Ethanolamine-O-sulphate (EOS) injected intraventricularly (28 mumol/kg) or intraperitoneally (14 mmol/kg) reproduced the first two phases of the effects of GABA (i.e. stimulation followed by inhibition), while diazepam (0.7 and 3.5 mumol/kg, i.p.) and flurazepam (32 mumol/kg, i.p.) caused, at first, only depression. Muscimol and 4,5,6,7-tetrahydroisoxazolo(4,5-c)pyridine-3-ol (THIP) injected intraventricularly (in the nmol range) or intraperitoneally (in the mumol range) produced behavioural activation and increased release of ACh; the depressant signs appeared only after very large, toxic doses. Picrotoxin and bicuculline, at sub-convulsive doses, reduced the symptomatology caused by GABA and antagonized the sedation produced by diazepam. Methysergide (8-16 mumol/kg, i.p.) prevented the behavioural activation and the increased release of ACh by GABA, unmasked the depression due to subthreshold doses of diazepam (i.c.v., 7-70 nmol) and reversed the stimulation induced by muscimol into sedation and reduced the outflow of ACh. Pretreatment with 5,7-HT also dampened and shortened the stimulation by muscimol.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1979

Accuracy of ventricular volume estimation.

Sources of error in the estimation of ventricular volume from CAT scans are discussed and the accuracy of the measurement assessed. Two methods of calculating ventricular volume from an intraventricular injection of radioisotope are described and compared. Finally, the CAT scan and isotope methods are compared and contrasted. The error associated with a single measurement of volume by any of these techniques is between 20% and 30%. In patients with no ventricular catheter there is no choice other than to use CAT scanning, but if intraventricular injection is possible this method offers a potentially more accurate volume determination because of his higher signal-to-noise ratio.

Cerebral Ventricles↗
PubMed1977

Brain catecholamine metabolism and avoidance conditioning in rats.

Male albino rats were trained in a shuttle-box by presentation of 50 trials and were grouped according to the performance level. The disappearance of labelled catecholamine pool was studied after intraventricular injection of tritiated noradrenaline in the neocortex, brain stem, hypothalamus and hippocampus. Rats with a high performance level showed a greater disappearance rate of the labelled catecholamine pool than low or medium performers. In another experimental series the animals were grouped on the basis of their performance level which was tested 2 days before the intraventricular injection of the tracer. There was no significant difference in disappearance rates between the good and poor performances. It is assumed that integration of the goal-directed motor pattern is mediated through catecholaminergic (noradrenergic) neuronal mechanisms.

Animals↗
PubMed1978

Brief communication. Generalization of [DAla2]-enkephalinamide but not of substance P to the morphine cue.

Rats were trained to discriminate morphine (7.5 mg/kg, IP) from saline in a two bar positively reinforced lever pressing paradigm on a FR4 schedule. Morphine (IP) showed a naloxone reversible dose-related generalization to the training dose. [DAla2]-Methionine enkephalinamide (DAE) at 1 mg/kg and Substance P (SP) at 0.1 and 0.25 mg/kg showed vehicle appropriate responding after IP injection. DAE (5 mg/kg) disrupted responding completely; SP (0.5 and 0.1 mg/kg) disrupted responding in 50% of the rats. The disruption caused by IP injection of DAE was not naloxone reversible. Intraventricular injection of morphine (5 microgram/rat) and DAE (5 microgram/rat) produced generalization to the opiate cue. The effect of DAE was reversed by naloxone (1 mg/kg, SC). SP (500 and 750 ng/rat, IVT) produced saline-like responding; 1 microgram/rat disrupted responding completely. These data demonstrate that morphine and enkephalin, but not Substance P, share similar discriminative properties.

Animals↗
PubMed1959

Central effects produced by injection of 48/80 into the cerebral ventricles of mice.

Injections of 20 to 30 mug. of 48/80 into the cerebral ventricular spaces of mice produced a condition of motor excitement termed "delirium ambulatorium." This condition was aggravated by previous intraperitoneal injection of tranquillizers, atropine, and promethazine, not affected by previous injection of mepyramine and abolished by a previous injection of pentobarbitone. When an intraperitoneal injection of strychnine was followed by an intraventricular injection of 48/80, the strychnine convulsions became more violent, but the pattern of delirium ambulatorium was not produced.

Animals↗
PubMed1981

Effect of cytidine diphosphate choline (CDP-choline) on ischemia-induced alterations of brain lipid in the gerbil.

Brain ischemia was produced in gerbils (Meriones unguiculatus) by the bilateral ligation of the carotid arteries. Definite changes in the energy status of brain demonstrated that carotid occlusion was effective. Five minutes before ligation, an intraventricular injection of either saline or cytidine disphosphate choline (CDP-choline, 0.6 micromol/brain, 3 microliter) was given to groups of animals. Control animals, with and without CDP-choline, together with the ischemic groups, were decapitated directly into liquid nitrogen; 10 min after arterial ligation. Brain free fatty acids, neutral lipids and phospholipids, which were labeled in vivo by the intraventricular injection of [1-14C]arachidonic acid (0.4-0.6 micro Ci, 6-9 nmol) 2 hr prior to ligation, were extracted, purified, and separated by thin-layer chromatographic procedures. The CDP-choline treatment noticeably corrected the increase of total and individual fatty acids due to ischemia and the increase of their radioactivity content. The changes in neutral lipids, particularly in the diacyl glycerol fraction, were also corrected by the injection of the nucleotide. CDP-choline partially reversed the decreased of brain phosphatidylcholine and of its labeling, which was due to ischemia. All the data indicate that the prior injection of CDP-choline stimulates the choline phosphotransferase reaction of brain towards synthesis of phosphatidylcholine and prevents the release of free fatty acids, particularly of arachidonic acid, associated with ischemia.

Animals↗
PubMed1983

Interaction of atropine with naloxone to alter anterior pituitary hormone secretion.

The effects of third ventricular injection of naloxone and atropine, alone and together, on plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH) were studied in conscious, ovariectomized (OVX) rats. Samples were removed from unrestrained rats that had been previously implanted with an atrial cannula, and plasma hormone levels were determined by radioimmunoassay. Intraventricular injection of naloxone (30 micrograms) induced increases in plasma LH and GH concentrations, decreased plasma PRL levels, but did not alter plasma TSH. When atropine (100 micrograms) was injected intraventricularly, there was a decrease in plasma LH and an increase in PRL levels but no alterations in the levels of the other hormones. The action of naloxone on PRL and GH release was eliminated by simultaneous administration of atropine, but there was only a slight reduction in its effect on LH. The results indicate that central cholinergic neurons may play an important role, via muscarinic type receptors, in mediation of the effects of naloxone and presumably opiates on PRL and GH release, whereas the effects on LH appear to proceed independently of cholinergic neurons.

Animals↗
PubMed1985

Release of immunoreactive Met-enkephalin from the spinal cord by intraventricular beta-endorphin but not morphine in anesthetized rats.

Effect of beta-endorphin and morphine injected intraventricularly on the release of immunoreactive Met-enkephalin, Leu-enkephalin and dynorphin1-13 from the spinal cord was studied in anesthetized rats. Intraventricular beta-endorphin, 16 micrograms, caused a marked spinal release of immunoreactive Met-enkephalin and to a much lesser extent, of immunoreactive Leu-enkephalin while intraventricular morphine, 40 micrograms, did not cause any significant release of immunoreactive enkephalins. The release of immunoreactive Met-enkephalin was not blocked by the pretreatment with 5 mg/kg naloxone, i.p. Immunoreactive dynorphin1-13 was not released by either beta-endorphin or morphine. High performance liquid chromatographic analysis indicated that immunoreactive Met-enkephalin released by beta-endorphin had a retention time identical to [3H]Met-enkephalin. These findings in conjunction with previous pharmacological studies suggest different modes of pharmacological action for beta-endorphin and morphine.

Animals↗
PubMed1970

Central effects of 6-hydroxydopamine on the body temperature of the rat.

1. Rats which had been pretreated with intraventricular injections of 6-hydroxydopamine (6-OHDA) to cause a selective depletion of brain noradrenaline (NA) to 20.7% of control brain NA and brain dopamine (DA) to 34.6% of control brain DA retained an unimpaired ability to regulate their body temperatures on exposure to heat or cold. This is discussed in relation to the possible role of brain NA in the central control of body temperature.2. Intraventricular injections of 6-OHDA in normal rats at room temperature caused an acute, dose dependent hypothermia of up to 4.5 degrees C which lasted for 4-5 hours. Depletion of brain NA and DA by prior treatment with 6-OHDA markedly reduced the hypothermic response to a subsequent dose of 6-OHDA. Selective depletion of brain NA without affecting brain DA did not reduce the response to 6-OHDA. The acute hypothermic response to 6-OHDA, may therefore, be related to a release of DA in the brain.

Animals↗
PubMed1979

Muscimol antagonism of morphine analgesia in rats.

1 Muscimol, a gamma-aminobutyric acid (GABA) receptor agonist, when injected intraventricularly antagonizes the antinociceptive effect of morphine given either subcutaneously or intraventricularly. The antagonistic effect of muscimol on morphine analgesia appears to be linearly related. 2 This finding provides support for the view that a GABA-ergic system is involved in morphine analgesia.

Animals↗
PubMed2004

Effects of progesterone derivatives, dihydroprogesterone and tetrahydroprogesterone, on the subependymal layer of the adult rat.

Indirect evidence suggests that in the subependymal layer (SEL) steroid hormones could be partially involved in the modulation of neurogenesis, but little or nothing is known about a direct effect of these molecules on this cellular system. The possible effect of progesterone (P) and/or its neuroactive metabolites, dihydroprogesterone (DHP) and tetrahydroprogesterone (THP), on the two cellular components of the SEL (i.e., proliferating/migrating neuroblasts and protoplasmic astrocytes) has been analyzed in adult male rat. P, DHP, and THP were administered by intraventricular injections and after 2 days the SEL was analyzed by immunohistochemistry by using anti-glial fibrillary acidic protein (GFAP) and anti-vimentin antibodies, to label the glial compartment, anti-polysialylated form of the neural cell adhesion molecule (PSA-NCAM), anti-Stathmin, and anti-beta III Tubulin antibodies to label the migrating neuroblasts. Furthermore, the newly formed cells were identified by using intraventricular injections of 5-bromo-2'-deoxyuridine (BrdU) detected immunohistochemically. Our results demonstrate that DHP and THP treatments drastically decrease the number of BrdU-labeled cells within the SEL. THP, DHP, and to a lesser extent P, administrations also induce molecular and structural modifications of the SEL glial compartment. On the whole, the present results indicate that neuroactive derivatives of P (i.e., DHP and THP) exert direct effects on adult neurogenesis, strongly affecting both neuroblasts and astrocytes of the SEL.

20-alpha-Dihydroprogesterone↗
PubMed1992

Control of anterior pituitary hormone secretion by neurotensin.

Neurotensin is localized in discrete populations of neuronal cell bodies with terminals in the hypothalamus and median eminence. High-affinity binding sites for neurotensin have been demonstrated not only in the hypothalamus but also in the pituitary gland. These studies suggest a role for neurotensin in control of hypothalamic-pituitary function. We initially demonstrated that neurotensin could block the release of prolactin in conscious, ovariectomized and male rats after its injection into the third ventricle, whereas intravenous injection of the peptide significantly elevated plasma prolactin and increased prolactin release by pituitaries incubated in vitro. These results suggested that neurotensin had opposite actions on prolactin release, an inhibitory effect at a hypothalamic site and an excitatory one at the pituitary. Further studies employing dopamine receptor blockers and inhibitors of catecholamine synthesis indicated that the action of the peptide to block prolactin release was probably mediated by release of dopamine, which then inhibited prolactin release by the pituitary gland directly. We have evaluated the physiological significance of the peptide in control of prolactin release by intraventricular injection of highly specific antiserum against neurotensin. The antiserum evoked dose-related elevations in plasma prolactin in intact males that were significant but smaller in magnitude than those seen in females, actions opposite to those of the peptide itself, which indicates that the inhibitory action of the peptide within the brain is physiologically significant. Intravenous injection of this antiserum produced a significant suppression of plasma prolactin in females but not males, which indicates that the previously demonstrated stimulatory effect of the peptide on prolactin release by the gland is also physiologically significant because immunoneutralization of the peptide resulted in a decline in plasma prolactin. Our earlier experiments revealed that neurotensin had a dose-related ability to inhibit LH release in ovariectomized and ovariectomized, estrogen progesterone-treated rats. Since it had no effect on the release of LH in vitro, we assigned a hypothalamic site for this action. It appears that this inhibitory effect of the peptide to suppress LH release is also physiologically significant since the intraventricular injection of the antiserum against the peptide produced a dose-related stimulation of LH release in ovariectomized and ovariectomized, estrogen progesterone-blocked rats. The mechanism by which endogenous neurotensin inhibits the release of LHRH has yet to be evaluated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1980

Effects of 5-hydroxytryptamine on defecation in open-field behavior in rats.

An attempt was made to elucidate the role of the serotonergic nervous sytem in defecation resulting from environmental stimulation in rats. The open-field (OF) test and shuttle box method were used to study the defecation. 5-Hydroxytryptophan (5-HTP) significantly decreased the number of fecal boluses excreted in both emotional situations, namely, in both OF and shuttle box. The fecal excretion was significantly reduced compared with the controls after intraventricular injection of 5-hydroxytryptamine (5-HT). Animals pretreated with p-chlorophenylalanine (pCPA) and 5,6-dihydroxytryptamine (5,6-DHT) tended to show a slight increase in the OF defecation. 5-HTP was equally effective in diminishing the OF performance of pCPA-treated rats. The inhibitory effects of 5-HTP on the defecation were also observed after depletion of biogenic amines by reserpine treatment. Home cage defecation was increased after 5-HTP administration, decreased under pretreatment with pCPA and not influenced by intraventricular injection of 5-HTP. These results suggested that the defecation after environmental stimuli was due to a change in 5-HT levels in the brain.

5,6-Dihydroxytryptamine↗
PubMed1984

Loss of vision-guided adaptation of the vestibulo-ocular reflex after depletion of brain serotonin in the rabbit.

Brain serotonin in pigmented rabbits was depleted by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT). Before depletion, an adaptive increase in the gain of the horizontal vestibulo-ocular reflex (HVOR) could be induced regularly by continuously rotating the animals in combination with optokinetic stimulus. After the depletion, such an increase in HVOR gain did not occur, even though dynamic characteristics of the HVOR and of the optokinetic eye movement were not altered. 5,7-DHT treatment also reduced brain norepinephrine, but depletion of norepinephrine to a similar extent by intraventricular injection of 6-hydroxydopamine in other rabbits did not affect the HVOR adaptation. These results suggest that brain serotonin plays an important role in maintaining adaptive modifiability of the HVOR.

5,7-Dihydroxytryptamine↗
PubMed2006

Hyperphosphorylation at serine 199/202 of tau factor in the gerbil hippocampus after transient forebrain ischemia.

We examined the phosphorylation state of tau factor in hippocampal delayed neuronal death (DND) after transient forebrain ischemia. A transient phosphorylation increase at serine 199/202 but not serine 396 of tau factor after transient ischemia was clearly observed. Intraventricular injections of olomoucine and U-0126 (CDK5 and MAP kinase inhibitors, respectively) inhibited hyperphosphorylation. In contrast, wortmannin (PI3 kinase inhibitor) increased phosphorylation at serine 199/202 and corresponded with an increase in GSK3 phosphorylation. Our findings suggest that CDK5, MAP kinase, and GSK3 phosphorylate these sites after ischemia. We prepared recombinant normal human tau (N-Tau40) with TAT-HA protein and dephosphorylated-form human Tau-40 (D-tau40) in which 199/202 serines were changed to alanine by site-directed mutagenesis. Intraventricularly injected D-tau40 protected somewhat against DND while N-Tau40 did not. These data suggest that hyperphosphorylation at serine 199/202 of tau factor is induced by MAP kinase, CDK5, and GSK3, and contributes to ischemic neuronal injury.

Animals↗
PubMed1984

Evidence that spinal endorphin mediates intraventricular beta-endorphin-induced tail flick inhibition and catalepsy.

Naloxone injected intrathecally had a different effect on the inhibition of the inhibition of the tail flick response produced by beta-endorphin and morphine injected intraventricularly. The intrathecal naloxone completely antagonized the effect of beta-endorphin but had only a very weak effect on morphine. In the same rats the cataleptic response to beta-endorphin was antagonized as well; however no definitive conclusion could be made regarding the antagonism of the morphine-induced catalepsy. The results indicate that spinal endorphin is involved in the production of intraventricular beta-endorphin-induced spinal tail flick inhibition and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological action via the activation of different descending inhibitory systems.

Animals↗
PubMed1977

Possible physiological significance of the initial step in the catabolism of noradrenaline in the central nervous system of the rat.

The hypothalamus, the cerebral cortex and the cerebellar cortex of the rat were labelled in vitro with 3H-noradrenaline (3H-NA) and the metabolism of the tritiated transmitter was studied during spontaneous outflow and under conditions of release elicited by exposure to 20 mM K+. In the three areas of the central nervous system of the rat 3H-NA accounted for approximately 40% of the total radioactivity in spontaneous outflow while the 3H-O-methylated deaminated fraction (3H-OMDA) and 3H-3,4-dihydroxyphenylglycol (3H-DOPEG) were the main metabolites. Exposure to the reserpine-like agent, Ro 4-1284 induced a selective increase in the spontaneous outflow of 3H-DOPEG, while the contribution of the 3H-OMDA metabolites to the release induced by Ro 4-1284 was very small. During 3H-transmitter release elicited by exposure to 20 mM K+, approximately 80% of the radioactivity was collected as unmetabolized 3H-NA, while 3H-DOPEG was the main metabolite formed under these experimental conditions. Exposure to cocaine prevented 3H-DOPEG formation from 3H-NA released by K+, indicating that 3H-DOPEG was formed after neuronal reuptake of the transmitter released by K+. After in vitro labelling with 3H-NA, the unmetabolized transmitter represented approximately 70% of the total radioactivity retained in the tissue. However, when 3H-NA was administered in vivo, by intraventricular injection, only 30% of the total radioactivity retained by the tissue was accounted for by 3H-NA, and 60% of the radioactivity corresponded to the 3H-OMDA fraction, most of which was retained as 3H-MOPEG sulfate. When the rats were pretreated with pyrogallol, free 3H-DOPEG accounted for nearly 50% of the radioactivity retained in the three areas of the central nervous system after in vivo labelling with 3H-NA. When monoamine oxidase was inhibited by pargyline and 3H-NA was administered by intraventricular injection, 3H-NMN accounted for approximately 50% of the total radioactivity retained in the three areas of the central nervous system of the rat. The results obtained are compatible with the view that formation of the deamined glycol is the first step in the metabolism of 3H-NA in the rat central nervous system. In addition, it is concluded that the determination of the levels of some NA metabolites retained in the central nervous system does not necessarily represent an accurate reflection of the degree of central noradrenergic activity or of selective metabolic pathways. Consequently, in studies on the metabolism of NA it is important to take into account not only the transmitter and its metabolites in the tissue but also in the outflow from the structures studied either under in vivo or in vitro conditions.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1983

Involvement of preoptic-anterior hypothalamic GABA neurons in the regulation of pituitary LH and prolactin release.

The effects of intraventricular injections of the highly specific gamma-amino-butyric acid (GABA) agonist muscimol (5 nmol/animal) on blood LH and prolactin levels were measured in ovariectomized (ovx) and in ovx estrogen-progesterone (OEP) primed rats. While the drug stimulated pituitary prolactin release in both experimental groups, pituitary LH release was significantly inhibited in the ovx animals. Muscimol was without any effect on LH levels in ovx-OEP primed rats. Bilateral implantation of tubes containing a muscimol-mannitol mixture into the medial preoptic/anterior hypothalamic (MPO/AH) area abolished pulsatile LH release whereas blood prolactin values were elevated. The intraventricular injection of GABA (8 mumol) also reduced LH and increased prolactin levels in the blood. Measurements of catecholamine turnover rates in the MPO/AH and in the mediobasal hypothalamus (MBH) yielded reduced preoptic but unchanged hypothalamic norepinephrine (NE) and stimulated hypothalamic dopamine (DA) turnover. In view of the well known stimulatory involvement of the NE system in the mechanism of pulsatile LH release and the inhibitory effect of GABA and its agonist muscimol on pulsatile LH release, it is suggested that GABA inhibits NE release in the MPO/AH by the mechanism of presynaptic inhibition. The observation that muscimol is unable to suppress LH release in vox OEP-primed rats may indicate that those estrogen receptive neurons in the MPO/AH which mediate the negative feedback action of the steroid may use GABA as neurotransmitter and that they are the neurons which inhibit NE release. The inhibitory effect of locally implanted muscimol into the MPO/AH also supports this hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗