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1. The role of the kidney and vasopressin in the increase of blood pressure obtained when angiotensin II is injected intraventricularly into rats has been investigated. 2. Intraventricular injection of angiotensin II led to a significant increase in blood pressure in the control and all sham-operated rats compared with that in unilaterally nephrectomized, one-kidney denervated rats and bilaterally nephrectomized rats. The degree of increase in blood pressure in unilaterally nephrectomized, one-kidney denervated rats was equal to that in bilaterally nephrectomized rats. 3. The increase in blood pressure in the bilaterally nephrectomized rats lasted significantly longer than that in the control and unilaterally nephrectomized, one-kidney denervated rats. 4. In the bilaterally nephrectomized rats plasma vasopressin was still higher 30 min after the intraventricular injection of angiotensin II than that of the control and unilaterally nephrectomized, one-kidney denervated rats. 5. These results suggest that the rise in blood pressure observed after intraventricular injection of angiotensin II is due partly to stimulation of the renal sympathetic nervous system and partly to increase in plasma vasopressin concentration.
To determine the role of the Tat protein of the human immunodeficiency virus type 1 (HIV-1) in the pathogenesis of HIV-1 associated dementia, recombinant Tat was injected intraventricularly as a single or repeated dose into male Sprague-Dawley rats. Histopathological evaluation showed an initial infiltration of neutrophils one day after Tat injection, followed by macrophages and lymphocytes by 7 days. Tat-injected brains also exhibited astrocytosis, apoptotic cells, and ventricular enlargement 7 days following the last injection. Nuclear magnetic resonance spectroscopic analysis of tissue extracts of hippocampi from Tat-injected rats showed a decrease in the glutamate/g aminobutyric acid ratio. We conclude that the transient extracellular exposure of the central nervous system to Tat protein of HIV can cause a cascade of events leading to the influx of inflammatory cells, glial cell activation, and neurotoxicity.
In rats dehydrated for 48 h and injected intraventricularly with L-cysteine-35S-hydrochloride, the specific activity of TCA-precipitable material, both in the hypothalamus and neurohypophysis, was found to diminish under reserpine treatment.
Ricin, a protein from the seeds of Ricinus communis which inhibits protein synthesis by eukaryotic ribosomes, is highly toxic when injected intraventricularly to rats, the LD50 being 0.241 micrograms/rat at 72 hr and 0.084 micrograms/rat at 7 days. Poisoned animals showed signs of central depression; they did not die before 20 hr of intoxication. Incorporation of amino acids in vivo into brain total protein and into brain ribosomes was impaired, as was protein synthesis in vitro by microsomes isolated from the brain of poisoned rats.
Nerve growth factor (NGF) was injected intraventricularly during 4 weeks into adult rats with unilateral partial lesions of the cholinergic septo-hippocampal pathway. On the lesioned side, NGF treatment elevated choline acetyltransferase (ChAT) activity up to 60% above the activity measured on the lesioned side of cytochrome c-treated controls. On the unlesioned side, NGF treatment increased ChAT activity only to an insignificant degree. ChAT activity in the septum of NGF-treated animals was increased by 60% as compared to controls. The NGF-induced increases on the lesioned side and in the septum were not accompanied by elevations in acetylcholinesterase (AChE) activity. Furthermore, histochemical analysis revealed no difference in AChE staining pattern or intensity between NGF-treated and control animals. The lack of effect on AChE strongly suggests that the increases in ChAT activity in hippocampus and septum are due to an elevation of ChAT activity within cholinergic neurons surviving the lesion rather than to a promotion of sprouting of cholinergic fibers.
The analysis of the behavioral effect of the nicotinic acetylcholine receptor (nAChR) antagonists has been generally based on drugs which act at the associated ion channel. In contrast dihydro-beta-erythroidine (DH beta E) is a competitive antagonist at the nAChR. Using rats, DH beta E was injected intraventricularly prior to training in two spatial tests, the Morris Water Maze and a Win-Stay radial maze. In addition DH beta E 300 nmol was used to reverse the effect of (-)-nicotine on locomotor activity. In the Morris Water Maze DH beta E (300 nmol) disrupted memory of the platform location as measured by crosses of the area in a probe trial. At 300 nmol DH beta E showed no sensorimotor effects in a visible platform test. In the Win-Stay task there was a significant, dose dependent disruption of spatial memory. A dissociation of nicotine's effects on locomotor activity was observed, in that DH beta E 300 nmol was able to significantly attenuate (-)-nicotine enhancement of horizontal motor activity, but did not affect the initial reduction of vertical activity. Nicotinic processing of memory appears to be involved in these tests of spatial memory.
A peptide material with opiate-like activity in the guinea-pig ileum was extracted from porcine pituitaries using a hot glacial acetic acid extraction method and was partially purified by gel filtration. When injected intraventricularly in rats, these purified peptides induced strong analgesia, catelepsy, respiratory depression and other opiate-like effects, which lasted for several hours.
Intraventricular injection of 250 microgram of 5 HTP induces both slow wave and paradoxical sleep, after 20-60 min. latencies, in insomniac Cats pretreated with P-chlorophenylalanine. Direct injections of 5 HTP in several brain stem structures do not induce sleep. The long latency or paradoxical sleep induction and its suppression with chloramphenicol suggest that indolamines are not directly responsible for paradoxical sleep, but that they act by controlling the synthesis and/or the liberation in the periventricular system of some specific paradoxical sleep inducing factor.
Glutamate and GABA content in different regions of adult female rat brain were determined at 10 and 30 min following intraventricular injection of LHRH or somatostatin. Cerebral cortex, cerebellar and hypothalamic glutamate levels were significantly elevated at 30 min following injection of 1 micrograms somatostatin, whereas hypothalamic glutamate levels were elevated at 10 min following a 0.5 micrograms dose. LHRH at a dose of 1 micrograms elevated cerebellar and brain stem glutamate levels at 10 and 30 min, whereas a 0.5 micrograms dose significantly elevated cerebral cortex, cerebellar and hypothalamic glutamate levels at 30 min. Third ventricular injection of 1 micrograms somatostatin produced a significant decrease in hypothalamic GABA levels at 10 and 30 min, whereas a 0.5-microgram dose decreased brain stem GABA levels at 10 min. LHRH at a dose of 0.1 microgram significantly increased cerebral cortex and cerebellar GABA levels at 10 min and brain stem GABA levels at 10 and 30 min following injection. Intraventricular injection of LHRH at a dose of 0.5 microgram significantly elevated cerebral cortex, cerebellar and brain stem GABA levels at 30 min. Hypothalamic GABA levels were elevated at 10 and 30 min following 0.5 and 1 microgram intraventricular LHRH injection. The implications of these results are discussed in relation to probable interaction between these neuroactive amino acids and neuropeptides in the rat brain.
The present study determined the topographical distribution profile for [125I]-glial cell line-derived neurotrophic factor in unlesioned and MPTP-lesioned (unilateral intracarotid injection) rhesus monkeys following an intraventricular injection. Autoradiographic analysis showed that following a bolus intraventricular injection, there was widespread distribution of [125I]-glial cell line-derived neurotrophic factor throughout the ventricular system (walls of lateral, third, and fourth ventricles and aqueduct), with some accumulation at the lateral ventricle injection site, possibly associated with the ependymal cell layer. In both unlesioned and MPTP-lesioned monkeys, there was labelling of the cerebral cortex, substantia nigra/ventral tegmental area and sequestration of [125I]-glial cell line-derived neurotrophic factor adjacent to the hippocampal formation, globus pallidus, ventral to and in the substantia nigra. However, [125I]-glial cell line-derived neurotrophic factor did not appear to diffuse readily or accumulate in the caudate-putamen even though there was some penetration away from the ventricular walls. Throughout the brain, there was also substantial non-parenchymal labelling of [125I]-glial cell line-derived neurotrophic factor, possibly associated with extracellular matrix components, meninges and vasculature due to the heparin binding properties of glial cell line-derived neurotrophic factor. In addition to the extensive loss of tyrosine hydroxylase immunoreactivity within the substantia nigra, there was also decreased accumulation of [125I]-glial cell line-derived neurotrophic factor and reduced glial cell line-derived neurotrophic factor immunoreactivity ipsilateral to the lesion. Microscopic analysis showed that glial cell line-derived neurotrophic factor immunoreactivity was associated with upper cortical layers including a high density of immunoreactivity at the surface of the cortex (meningeal, pial layer, vasculature) and around the ventricular walls (with some cellular labelling and labelling of vasculature). Moderate staining was observed in nigral cells contralateral to the MPTP-lesion, whereas only minimal levels of that glial cell line-derived neurotrophic factor immunoreactivity were detected ipsilateral to the lesion. This study shows that intraventricularly injected glial cell line-derived neurotrophic factor accumulates not only around the ventricular walls, but also in specific brain regions in which sub-populations of cells are more readily accessible than others. The presence of cells labelled with [125I] and immunopositive for glial cell line-derived neurotrophic factor in the substantia nigra indicates that these cells are a target for the trophic factor following intraventricular administration. Thus, the behavioral improvement observed in MPTP-lesioned monkeys following an intraventricular injection of glial cell line-derived neurotrophic factor is likely the result of activation of nigral cells.
1. Cholinergic synapses in the hypothalamus may transmit information in those thermoregulatory pathways which function to raise body temperature. The effect of atropine, administered intracranially, on the febrile response to intravenous leucocyte pyrogen or intracranial prostaglandin E1 was therefore examined in conscious rabbits. 2. In rabbits exposed to a thermoneutral environment, micro-injections of PGE1, into the anterior hypothalamus, intraventricular injections of PGE1, and intravenous injection so leucocyte pyrogen all caused fever accompanied by vasoconstriction in the ears and reduced respiratory rate. Intraventricular injection of 200 mug atropine during such fevers attenuated their development. This was due to the activation of heat loss mechanisms through vasodilatation in the ears and an increase in the frequency of respiration. This suggests a similarity in the pattern of neuronal activity evoked by PGE1 and leucocyte pyrogen, at least at the site(s) where atropine directly or indirectly exerted its effect and in the efferent pathways from this site. 3. In rabbits exposed to a cold environment, intraventricular injection of PGE1 caused fever through the activation of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shievering and a decrease in O2 consumption so that temperature ceased to rise and returned to normal. 4. During fever, reversal by atropine of the increased heat conservation of rabbits in a neutral environment, and of their increased heat production in a cold environment adds further support to the concept that cholinergic synapses provide an important link in central temperature-rasising pathways.
1. Intraventricular injection of rabbit and human serum albumin, and rabbit endogenous pyrogen produced dose-dependent fevers in rabbits. The pyrogenicity of albumin was less than one-twentieth of the pyrogenicity of endogenous pyrogen. 2. Fevers induced by ventricular albumin were significantly suppressed by intraventricular injection of indomethacin which is a cyclooxygenase inhibitor. In contrast, subcutaneous injection had no effect. 3. Ventricular endogenous pyrogen induced several of the acute phase responses, i.e. decreases in the plasma concentration of iron and zinc, and increases in both the plasma concentration of copper and the white blood cell count. Albumin induced none of these responses. 4. It is concluded that fever induced by ventricular albumin is processed by prostaglandins synthesized within the central nervous system. However, ventricular albumin does not activate the central mechanism to induce acute phase responses.
Intraventricular injection into the rat brain of four trace amines and a catecholamine resulted in rapid exponential loss of the amines in the first 30 minutes after injection. The half-lives were: phenylethylamine 3.8 min, para-tyramine 5.1 min, meta-tyramine 7.4 min and dopamine 8.0 min. Tryptamine showed a biphasic loss with half-lives of 4.7 min (over the 5 to 10 min period) and 14.1 min (10 to 30 min). The half-lives were substantially increased by deuterium labeling at the alpha carbon position: phenylethylamine 4.8 min, para-tyramine 8.8 min, meta-tyramine 14.1 min, dopamine 13.0 min and tryptamine 6.0 min (5 to 10 min period) and 28.7 min (10 to 20 min). The loss of the amines was reduced by monoamine oxidase inhibition by pargyline hydrochloride and the deuterium isotope effect was abolished. It is noteworthy that the half-life of dopamine was similar to those of the trace amines in this time period and that the trace amine half-lives after i.v. injection was longer than those obtained from measurements of increases of concentrations of endogenous amines after MAOI in vivo and that of dopamine shorter than values calculated from turnover measurements.
Effects of intraventricularly injected spermine on behavior and electrocortical activity and gamma-aminobutyric acid (GABA) metabolism after a single dose of 1.13 mumol/animal were studied. Decrease in locomotor activity, sedation or sleep, and electrocortical synchronization that lasted approximately 2 h were observed. In addition spermine caused a significant increase in GABA content in diencephalon and brainstem, 30 min after administration. Concomitantly a significant increase of glutamate decarboxylase (GAD) activity was observed in cerebral hemispheres, diencephalon, and brainstem. Reduction in gamma-aminobutyrate: alpha-oxoglutarate amino-transferase (GABA-T) levels occurred in the diencephalon along with a significant increase of GABA-T in the brainstem. The present results demonstrate that spermine has the capacity to affect GABA metabolism and are in favor of the suggestion that endogenous polyamines may modulate GABAergic mechanisms.
In adult fowls intravenous but not intraventricular injection of diazoxide produced hypotension and a rise in blood glucose concentration. Since noradrenaline microinfused into the hypothalamus produced a fall in blood pressure, it does not seem that hypotensive effects of diazoxide are mediated through release of noradrenaline in areas of the luain accessible from the ventriculus tertius cerebri. Present experiments also indicate that the hyperglycemic effects of diazoxide is unlikely to be due to an action on central adrenergic receptors.
The effects of intraventricular injection of adenosine and its analogues on renal sympathetic nerve activity (RSNA) were examined in sinoaortic denervated and vagotomized anesthetized rats. In response to intraventricular bolus injection of adenosine, RSNA was increased by 41.9 +/- 6.08% (P < 0.001), mean arterial pressure (MAP) was initially increased by 1.39 +/- 0.19 kPa (P < 0.001) and subsequently decreased by 3.74 +/- 0.64 kPa (P < 0.001), and heart rate (HR) was reduced by 95 +/- 14 bpm (P < 0.001). To determine the adenosine-receptor subtype which mediates the response of RSNA to adenosine, we used selective A1-receptor agonist (R-PIA) and A2-receptor agonist (NECA) and found that MAP and HR were reduced by R-PIA and NECA. The effects lasted significantly longer than those of adenosine. R-PIA induced an increase in RSNA by 31.6 +/- 5.21% (P < 0.001), while NECA showed no effect on RSNA. The renal sympathoexcitatory response to intraventricular injection of adenosine was completely inhibited by pretreatment with a selective A1-receptor antagonist (DPCPX). Following the bilateral stellate ganglionectomy, intraventricular injection of adenosine failed to induce the increase in RSNA. The results indicate that adenosine may activate cardiac sympathetic afferents through A1-receptor, resulting in a reflex augmentation of RSNA.
Intraventricular injections of the tachykinin NK3 receptor (NK3-R) agonist, senktide, suppress the ingestion of hypertonic (0.5 M) NaCl by decreasing the initial lick rate and accelerating the decay in lick rate in sodium deficient rats. The present experiment examined whether the effects of intraventricular injections of senktide on lick rate were selective for NaCl solution, or if the ability of NK3-R agonists to inhibit intake generalizes other sodium-containing solutions. The effects of lateral ventricular injections of isotonic saline or senktide (200 ng) on intake and lick rate of 0.5 M solutions of sodium chloride (NaCl), sodium acetate (Na acetate), sodium bicarbonate (Na bicarbonate), and monosodium glutamate (MSG) were measured in sodium deficient rats. Compared to saline injection, senktide injection had no effect on the lick rate or intake of Na bicarbonate. In contrast, intraventricular injection of senktide suppressed the intake of NaCl, Na acetate, and MSG compared to saline injection. Senktide injection accelerated the decay in lick rate for NaCl, Na acetate and MSG, but only suppressed the initial lick rate for NaCl and Na acetate. The results show that activation of NK3-R in sodium deficient rats suppresses the intake of tastes that are classified as "salty" tasting and that the decrease in intake reflects effects on the initial lick rate, the decay in lick rate, or both.