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PubMed1987

Modulation of the vestibulo-ocular reflex by serotonin in the rat.

The effects of intraventricular injection of serotonin (5-HT) and its agonists and antagonists on the amplitude of the vestibulo-ocular reflex were studied in chronic implanted rats. 5-HT (10(-5) M) triggers an increase of the amplitude of the reflex which lasts 30 min. Similar results are obtained when N,N-dimethyl-5-methoxytryptamine (10(-3) M) is introduced into the ventricular cannula. The increasing effects observed both with 5-HT and N,N-dimethyl-5-methoxy-tryptamine are abolished by methiothepin, a potent antagonist of 5-HT receptors. Injection of indirect agonists like pargyline, a monoamine oxidase inhibitor, or fluoxetine, a potent inhibitor of 5-HT reuptake, is followed by an increase of the amplitude of the vestibulo-ocular reflex. These results indicate that 5-HT can modulate the activity of the vestibulo-ocular pathway and muscular tone of extraocular muscles. Location and involvement of various modulating 5-HT sites are discussed.

Animals↗
PubMed1979

The synthesis and turnover of spermidine and spermine in mouse brain.

Following the administration to mice of radiolabeled putrescine by intraventricular injection, changes in the specific radioactivity of putrescine, spermidine, and spermine have been measured. Putrescine decline was biphasic, being more rapid over the first 12 hr(t 1/2 = 5 hr) than over the remainder of the 48-hr period (t 1/2 = 11 hr) that significant labeling was detected. Spermidine was rapidly labeled during the decline in putrescine radioactivity and maximum incorporation of label occurred at 18 hr. Subsequently, spermidine specific activity declined with a half-life of 22 days. Spermine synthesis was slower, with maximum labeling occurring after 4 days. Spermine turnover, measured at a time when spermidine radioactivity had substantially declined, was extremely slow (t 1/2 = 92 days). The data supports the view that putrescine is a precursor of spermidine which in turn is required for spermine synthesis.

Animals↗
PubMed1979

Dopa accumulation is a measure of dopamine synthesis in the median eminence and posterior pituitary.

A radioenzymatic assay was employed to measure the accumulation of DOPA in a variety of rat brain tissues 30 min after the administration of a decarboxylase inhibitor in order to estimate the activity of dopamine (DA) nerves which terminate in these regions. In the median eminence and posterior pituitary the accumulation of DOPA appears to occur primarily in DA nerves since: (1) the rate of synthesis of norepinephrine (NE), as estimated from the alpha-methyltyrosine-induced decline of catecholamines, accounts for less than 10% of total catecholamine synthesis in these two brain regions; and (2) the accumulation of DOPA is not significantly altered when the NE concentrations in these regions are reduced to 40--50% of control by prior intraventricular injections of 6-hydroxydopamine. These results suggest that the accumulation of DOPA in the median eminence and the posterior pituitary can be used to estimate the activity of tubero-infundibular and tuberohypophyseal DA nerves, respectively.

Animals↗
PubMed1975

Acetylcholine induced responses of plasma LH and prolactin in normal and 6-hydroxydopamine-treated rats.

The effects of intraventricular injection of acetylcholine at doses of 50 mug were studied in male rats. Under ether anesthesia, acetylcholine did not modify plasma prolactin and LH levels. Contrarily, in rats anesthetized with pentobarbital, acetylcholine at the same doses induced significant decreases of prolactin from 10 to 60 min postinjection. LH levels were not modified by treatment. Prolactin responses to acetylcholine were absent during the first 30 min postinjection in 6-hydroxydopamine-treated rats. Only a delayed response was detected. In these animals, icv administration of dopamine caused a clear decrease of plasma prolactin levels. A marked rise of LH at 30 and 60 min following acetylcholine injection was found in 6-hydroxydopamine-treated rats. Results suggest a catecholaminergic mediation of the prolactin and LH responses induced by acetylcholin in male rats.

Acetylcholine↗
PubMed1984

The effect of pyridoxal phosphate-induced convulsive seizures on rat brain phospholipid metabolism.

The intraventricular injection of pyridoxal phosphate (PLP; 1 mumole/brain) to rats causes convulsive seizures beginning 3 min after injection and lasting for about 20 min. The incorporation of [2-3H] glycerol into rat brain glycerides has been studied to ascertain whether treatment with PLP affects the incorporation of label into various lipid classes. The labeling pattern of glycerides is changed by the administration of PLP. The observed alterations begin a few min after injection, together with the convulsive seizures. 1 h after the injection the pattern of labeling of brain glycerides returns to normal. Different glycerides are differently affected by PLP. This work demonstrates that the labeling of diglyceride increases whereas that of phosphatidylethanolamine decreases following PLP administration.

Animals↗
PubMed1992

Effects of biperiden on sleep at baseline and after 72 h of REM sleep deprivation in the cat.

We examined the effects of the muscarinic M1 antagonist biperiden in cats. In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden. In the second experiment after REM sleep deprivation cats were injected with either biperiden (0.1 mg/kg) or saline. Biperiden produced a reduction in REM sleep percentage and an increase in REM sleep latency with these high doses. The 0.1 mg/kg biperiden dose, which did not suppress REM sleep at baseline, did reduce the REM sleep rebound. The present study suggests a modulatory role of biperiden on REM sleep regulatory processes. The fact that an effect of biperiden is noted only at the high doses suggests that at these doses the drug is influencing non-M1 receptors. Changes in the sensitivity of these receptors as a result of REM sleep deprivation might explain why a dose of biperiden will reduce REM sleep rebound, while being ineffective in suppressing REM sleep at baseline.

Animals↗
PubMed1987

Microglia in the hypendyma of the rat subcommissural organ following brain lesion with serotonin neurotoxin.

The population of microglial cells in the subependymal layer of the subcommissural organ is sparse in normal adult rats. The number of microglial cells was substantially increased in this area following intraventricular injection of the serotonin neurotoxin 5,6-dihydroxytryptamine (5,6-DHT). In sections of plastic embedded material, 1 micron thick, the majority of phagocytic cells scattered in the subependymal layer had an appearance similar to that described in classical studies of microglial cells. At the electron microscopic level microglial cells exhibited the characteristic elongate nucleus with peripheral chromatin condensation. The perikaryon was scanty, containing strands of rough endoplasmic reticulum. The abundant organelles in the processes included Golgi complexes, mitochondria, rough and smooth endoplasmic reticulum as well as dense and multivesicular bodies. In addition, the processes contained phagocytosed axon terminals originating from the dense serotoninergic input to the subcommissural organ, which had degenerated on accumulating the serotonin neurotoxin. A fraction of the phagocytosed material was contained in subependymal subcommissural organ cells, astrocytes and oligodendrocytes. At the light microscopic level the phagocytosed terminals were visualized histochemically with Schmorl's reaction, which resulted in Prussian Blue precipitates. This allowed screening of microglial cells in complete series of sections through the well-defined subependymal layer of the subcommissural organ.

5,6-Dihydroxytryptamine↗
PubMed1981

Calcium-dependent turnover of brain polyphosphoinositides in vitro after prelabelling in vivo.

Rat brain phospholipids were labelled in vivo by an intraventricular injection of 32P. The radioactivity was found to accumulate predominantly in limbic structures, particularly hippocampus and diencephalon. A rapid and high specific labelling of the inositol phospholipids and phosphatidic acid was observed. The rate of incorporation into a crude myelin fraction was similar to that into a mitochondrial/synaptosomal fraction although phosphatidyl-myo-inositol 4,5-diphosphate was especially enriched in myelin. Upon incubation in vitro high specific labelling of the inositol phospholipids and phosphatidic acid was observed. The rate of incorporation into a crude myelin fraction was similar to that into a mitochondrial/synaptosomal fraction although phosphatidyl-myo-inositol 4,5-diphosphate was especially enriched in myelin. Upon incubation in vitro high specific labelling of the inositol phospholipids and phosphatidic acid was observed. The rate of incorporation into a crude myelin fraction was similar to that into a mitochondrial/synaptosomal fraction although phosphatidyl-myo-inositol 4,5-diphosphate was especially enriched in myelin. Upon incubation in vitro of the brain fraction after 2 h prelabelling in vivo, both phosphatidyl-myo-inositol 4-phosphate and phosphatidyl-myo-inositol 4,5-diphosphate rapidly lost their radioactivity. Half of the labile fraction of the incorporated 32P was removed within 2 min. None of the other phospholipids changed in the 30 min in vitro incubation period. The metabolism of the polyphosphoinositide proceeded at a lower rate when the temperature was lowered, and was Ca2+-dependent. Further subcellular fractionation revealed that purified synaptosomes and myelin contained highly labelled phosphatidyl-myo-inositol 4-phosphate or phosphatidyl-myo-inositol 4,5-diphosphate. Mitochondria contained highly labelled phosphatidyl-myo-inositol but no phosphatidyl-myo-inositol 4-phosphate or phosphatidyl-myo-inositol 4,5-diphosphate. ACTH1-24 did not inhibit the in vitro dephosphorylation of prelabelled polyphosphoinositide, confirming previous findings that the peptide affects the polyphosphoinositide kinases and not the respective phosphatases.

Animals↗
PubMed1976

Monoamine neurotoxins: selective and delayed effects on behavior in colonies of laboratory rats.

Male laboratory rats were raised in two colonies, each of 27 rats, and then given intraventricular injections of the norepinephrine neurotoxin 6-hydroxydopamine (6-OHDA) or the serotonin neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) or saline. They were then returned to their enclosure and behavior during the next 50 days was observed. Shortly after neurotoxin injections the 6-OHDA rats spent more time in the burrows than controls and when out were inactive. The 5,6-DHT rats in contrast spent more time in the open than controls, ran more in activity wheels, approached humans, and fought more. Fighting, mounting, and hoarding in the colony gradually increased for 25 days; during this time the status of the 6-OHDA animals fell progressively whereas the 5,6-DHT animals increased in dominance. Social behavior returned to more normal levels after 50 days. Several successive stages of behavioral alterations occur following neurotoxin injections.

Aggression↗
PubMed1977

The metabolism of nerve terminal glycoproteins in the rat brain.

The fate of [3H]fucose in subcellular fractions has been followed for a period of three weeks after intraventricular injection in the rat brain. Isolated synaptosomal membranes were examined by gel electrophoresis. Seven fucosyl glycoproteins with molecular weights ranging from 123,000 to 31,000 were detected by scintillation counting of transversely sliced gels and their specific activities determined. The half-lives of 6 of the membrane glycoproteins fell within the range 11-22 days. The smallest glycoprotein showed anomalous behaviour; its radioactivity did not fall significantly over the period of study. The results are discussed in relation to current concepts of fast axonal transport.

Animals↗
PubMed1979

ACTH-like neurotropic peptides: possible regulators of rat brain cyclic AMP.

The influence of behaviorally active, N-terminal fragments of ACTH on the accumulation of cAMP in rat brain investigated in broken cell preparations of subcortical tissue, in slices of neostriatum and in vivo. ACTH1--24 has a biphasic effect on the activity of adenylate cyclase in broken cell preparations of rat brain subcortical tissue: concentrations below 25 micrometer stimulated, whereas concentrations of 0.1 mM and higher inhibited adenylate cyclase activity. The magnitude of the stimulation was dependent on the concentrations of ATP and Mg2+ in the incubation medium. Structure activity studies revealed that at a concentration of 10(-4) M ACTH1--16-NH2 and ACTH4--7 also inhibited the activity of adenylate cyclase, whereas ACTH11--24, ACTH1--10, ACTH4--10, [D-Phe7]ACTH1--10 and [D-Phe7]ACTH4--10 were inactive in this respect. Addition of 0.8 mM EGTA but not of 0.25 mM Ca2+ prevented the inhibition by 10(-4) M ACTH1--24. GMP-N-P (10(-5) M), naltrexone (10(-3) M) and ergometrine (10(-3) M) did not influence the inhibitory effect. ACTH1--24 enhanced the accumulation of cAMP in slices from rat brain neostriatum in a dose-dependent manner. This effect was already maximal 7.5 min after the addition of the peptide and was potentiated by isobutylmethylxanthine, a potent inhibitor or phosphodiesterase. Intraventricular injection of 1 microgram ACTH1--16-NH2 in rats significantly elevated (+ 27%) the concentration of cAMP in the septal region 60 min after the injection of the peptide. The results are discussed in terms of a possible involvement of cAMP as a second messenger in the central nervous system for N-terminal fragments of ACTH.

Adenosine Triphosphate↗
PubMed1979

Immune lesions of central noradrenergic neurons produced by antibodies to dopamine-beta-hydroxylase.

(1) Intraventricular injection of antibodies to dopamine-beta-hydroxylase (DBH) caused degeneration of central noradrenergic nerve terminals in rats and guinea-pigs. In rats it was necessary to infuse exogenous complement in the form of guinea-pig serum together with the anti-DBH, whereas in guinea-pigs the anti-DBH was effective on its own. Control animals were infused with equivalent amounts of non-immune serum and complement and showed no signs of degeneration other than in the region of the needle tract. (2) There was a loss of varicosities in most terminal fields of the noradrenergic projections and swollen distorted axons were seen in both ascending and descending noradrenergic pathways. Noradrenergic cell bodies in the locus coeruleus and subcoeruleus appeared unaffected. No histochemical changes were observed in dopaminergic neurons. (3) The ultrastructural changes in degenerating axons that were first identifided by fluorescence histochemistry included swelling, vacuolation, accumulation of dense cored vesicles, lysosome-like bodies and smooth membranous sacs. The surrounding neuropil appeared normal. (4) There was a significant depletion of noradrenaline in all regions of the rat brain ranging from 20% in the hypothalamus to 80% in the neocortex. Dopamine concentrations were unaffected. (5) These observations provide a new approach to the production of selective lesions in specific neurotransmitter pathways that could be extended to non-adrenergic neurones. They may also be useful as a model for the study of autoimmune diseases of the nervous system.

Animals↗
PubMed1980

Selective reinnervation of hippocampal area CA1 and the fascia dentata after destruction of CA3-CA4 afferents with kainic acid.

Intraventricular injections of kainic acid were used to destroy the hippocampal CA3-CA4 cells, thus denervating the inner third of the molecular layer of the fascia dentata and stratum radiatum and stratum oriens of area CA1. The responses of intact afferents to such lesions were then examined histologically. The hippocampal mossy fibers densely reinnervated the inner portion of the dentate molecular layer after bilateral destruction of CA4 neurons and to a lesser extent after unilateral destruction. Septohippocampal fibers replaced CA4-derived fibers in the dentate molecular layer only after particularly extensive bilateral CA4 lesions. Medial perforant path fibers showed no anatomical response to any of these lesions. Neither septohippocampal, temporoammonic nor mossy fibers proliferated in or grew into the denervated laminae of area CA1. These results show a preferential ordering in the reinnervation of dentate granule cells which is not readily explained by proximity to the degenerating fibers and also that removal of CA3-CA4-derived innervation more readily elicits translaminar growth in the fascia dentata than in area CA1. These results may be relevant to clinical situations in which neurons of the hippocampal end-blade are lost.

Afferent Pathways↗
PubMed1980

Loss and reacquisition of hippocampal synapses after selective destruction of CA3-CA4 afferents with kainic acid.

Intraventricular injections of kainic acid were used to destroy the hippocampal CA3-CA4 cells bilaterally in rats, thus denervating the inner third of the molecular layer of the fascia dentata and stratum radiatum of area CA1. Electron microscopic studies showed that this lesion reduced the synaptic density of the CA1 stratum radiatum by an average of 86%. The synaptic density of the inner third of the dorsal dentate molecular layer declined by two-thirds and the corresponding zone of the ventral dentate molecular layer by about half. Within 6-8 weeks the synaptic density of these laminae had been restored to the control value or nearly so. In the CA1 stratum radiatum about 72% of the synaptic contacts destroyed by the lesion were replaced, the inner third of the ventral dentate molecular layer recovered 75% of its lost synapses and the inner third of the dorsal dentate molecular layer apparently recovered virtually all of them. The newly formed synapses did not differ noticeably from those normally present. A kainic acid lesion reduced the synaptic density of the outer two-thirds of the dentate molecular layer by 30% within 3-5 days, despite a virtual absence of presynaptic degeneration in that zone. This result implies a substantial disconnection of perforant path synapses. It did not appear to depend on the extent of denervation of the inner zone. The loss of perforant path synapses was completely reversible. We suggest that the dentate granule cells shed a portion of their synapses in response to a substantial loss of neurons to which they project and regained them when their axons had formed new synaptic connections.

Afferent Pathways↗
PubMed1982

Dehydration attenuates panting response to intraventricular 5-hydroxytryptamine in the rabbit.

Panting response and a fall in rectal temperature following intraventricular injection of 5-hydroxytryptamine (5-HT) were significantly reduced in dehydrated rabbits as compared with normally hydrated animals. The vasomotor heat loss response to 5-HT was essentially similar in both groups. These as well as earlier findings suggest that dehydration may modify signals generated in brain thermoregulatory centers controlling evaporative but not the vasomotor heat loss.

Animals↗
PubMed1984

Corticotropin releasing factor administered into the ventricular CSF stimulates the pituitary-adrenal axis.

Ovine corticotropin releasing factor (CRF) given intracerebroventricularly to rhesus monkeys at doses of 0.1-1 microgram/kg activates the pituitary-adrenal axis. The increases of plasma cortisol concentrations after intraventricular injection of CRF were similar to those observed after intravenous administration of this releasing factor and occurred without elevation of plasma concentrations of CRF, measured by radioimmunoassay. Thus, the cerebrospinal fluid (CSF) can serve as a conduit for delivery of CRF to the pituitary gland.

Animals↗
PubMed1987

Effects of substance P and neurokinin A (substance K) on motor behavior: unique effect of substance P attributable to its amino-terminal sequence.

The effects of intraventricular injections of the neuropeptides substance P (SP) and neurokinin A (NK-A; also called substance K) on spontaneous motor behavior were examined in mice. SP and NK-A were essentially equipotent at enhancing grooming and scratching behavior, and at reducing sniffing behavior. However, SP significantly enhanced hindlimb rearing behavior, while NK-A reduced this behavior. The effects of 3 other tachykinins, physalaemin, eledoisin and kassinin, were comparable to those of NK-A, including the reduction in rearing. Thus, SP is unique among tachykinins in its potentiation of rearing behavior. It was further demonstrated that carboxy-terminal SP fragments with tachykinin activity on smooth muscle resemble NK-A, and not SP, in their effects on motor behavior. In contrast, amino-terminal SP fragments, devoid of tachykinin-like activity, reproduced the one motor effect unique to SP, enhanced rearing, while lacking those actions common to all tachykinins. The structural requirements for enhanced rearing behavior by amino-terminal fragments were quite specific, in terms of chain length and sensitivity to D-amino acid substitutions, with the natural amino-terminal hexa- and heptapeptides being most active. The implications of these findings are discussed in light of recent observations that these same amino-terminal SP fragments are produced in vivo as metabolites of SP.

Animals↗