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PubMed1982

Cell size changes in the lateral geniculate nuclei of normal and monocularly deprived cats treated with 6-hydroxydopamine and/or norepinephrine.

Given the proposed role of catecholamines in controlling cortical plasticity in the cat (Kasamatsu, T., J. D. Pettigrew, and M. Ary (1979) J. Comp. Neurol. 185: 163-182), we were interested in whether evidence of such control also could be found in the dorsal lateral geniculate nucleus. We undertook geniculate cell size measurements in 26 normal or monocularly deprived cats, 23 of which had been used in cortical recording studies concerned with catecholamine-induced plasticity. For animals grouped according to experimental treatments, the results can be summarized as follows: (1) in visually normal animals, neither intraventricular injections of 6-hydroxydopamine (6-OHDA) nor local perfusions of norepinephrine (NE) cause changes in geniculate cell size. (2) In otherwise untreated kittens, 1 week of monocular deprivation begun in the 6th week of life results in quite obvious changes in geniculate cell size. (3) Intraventricular injections of 6-OHDA do not appear to prevent deprivation-induced changes in geniculate cell size. (4) Older NE-treated kittens and adult cats that are monocularly deprived for a brief period either late in the critical period or after the critical period has ended do not show deprivation-induced changes in geniculate cell size in either hemisphere. (5) In younger kittens which had been first injected with 6-OHDA intraventricularly and then monocularly deprived for a brief period early in the critical period, there is no evidence to suggest that a local perfusion of NE enhances deprivation-induced changes in geniculate cell size.

Animals↗
PubMed1991

Effect of recombinant human nerve growth factor on presynaptic cholinergic function in rat hippocampal slices following partial septohippocampal lesions: measures of [3H]acetylcholine synthesis, [3H]acetylcholine release and choline acetyltransferase activity.

To determine whether intraventricular administration of nerve growth factor alters presynaptic cholinergic function in the intact hippocampus or following partial lesions of the fimbria, we investigated the effects of recombinant human nerve growth factor treatment on [3H]acetylcholine synthesis and release by hippocampal slices following various treatment regimens. For chronic nerve growth factor treatment, 1 microgram of recombinant human nerve growth factor was injected intraventricularly every second day. Lesions reduced [3H]acetylcholine synthesis (by 48%) and spontaneous and evoked [3H]acetylcholine release by 35 and 61%, respectively. Chronic nerve growth factor treatment over three weeks elevated [3H]acetylcholine synthesis (by 39%) and spontaneous and evoked [3H]acetylcholine release by 27 and 64%, respectively, over values in lesioned hippocampi of animals treated with a control protein (cytochrome c). The nerve growth factor-induced enhancement of presynaptic cholinergic function persisted for three weeks following the termination of nerve growth factor administration. Furthermore, chronic (nine-week) treatment with nerve growth factor increased [3H]acetylcholine by 118% over values in lesioned hippocampi of animals treated with cytochrome c. These findings indicate that chronic treatment with recombinant human nerve growth factor increases the capacity of hippocampal cholinergic neurons surviving a partial fimbrial transection to synthesize, store and release acetylcholine. Application of recombinant human nerve growth factor during the initial weeks after lesioning was necessary to product significant elevations in acetylcholine synthesis, since chronic recombinant human nerve growth factor treatment after delays of three or more weeks were ineffective. Furthermore, chronic nerve growth factor treatment failed to stimulate acetylcholine synthesis and release in intact hippocampal cholinergic systems. Single intraventricular injections of recombinant human nerve growth factor at the time of lesioning resulted in a small decrease in acetylcholine synthesis which, however, was not accompanied by a change in the rate of evoked acetylcholine release from cholinergic neurons surviving the lesion. The study indicates that chronic or repeated administration of nerve growth factor during the onset of degenerative events is necessary for the stimulation of presynaptic cholinergic function in the hippocampus of adult rats with partial fimbrial transections.

Acetylcholine↗
PubMed1994

Toxicity of an antitumor ribonuclease to Purkinje neurons.

Purkinje cell toxicity is one of the characteristic features of the Gordon phenomenon, a syndrome manifested by ataxia, muscular rigidity, paralysis, and tremor that may lead to death (Gordon, 1933). Two members of the RNase superfamily found in humans, EDN (eosinophil-derived neurotoxin) and ECP (eosinophil cationic protein), cause the Gordon phenomenon when injected intraventricularly into guinea pigs or rabbits. We have found that another member of the RNase superfamily, an antitumor protein called onconase, isolated from Rana pipiens oocytes and early embryos, will also cause the Gordon phenomenon when injected into the cerebrospinal fluid of guinea pigs at a dose similar to that of EDN (LD50, 3-4 micrograms). Neurologic abnormalities of onconase-treated animals were indistinguishable from those of EDN-treated animals, and histology showed dramatic Purkinje cell loss in the brains of onconase-treated animals. The neurotoxic activity of onconase correlates with ribonuclease activity. Onconase modified by iodoacetic acid to eliminate 70% and 98% of the ribonuclease activity of the native enzyme displays a similar decrease in ability to cause the Gordon phenomenon. In contrast, the homologous bovine pancreatic RNase A injected intraventricularly at a dose 5000 times greater than the LD50 dose of EDN or onconase is not toxic and does not cause the Gordon phenomenon. A comparison of the RNase activities of EDN, onconase, and bovine pancreatic RNase A using three pancreatic RNA substrates demonstrates that onconase is orders of magnitude less active enzymatically than EDN and RNase A. Thus, another member of the RNase superfamily in addition to EDN and ECP can cause the Gordon phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1984

Both dopaminergic and adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl 3',5'-adenosine monophosphate and aminophylline in the rat.

Following administration of dibutyryl cyclic-AMP or aminophylline, but not vehicle solution, into the lateral cerebral ventricle of rats produced locomotor stimulation, head and body rearing, circling, (as indicated by an enhancement of gross movement), increased grooming, head swaying and scratching (as indicated by an enhancement of fine movement), tail elevation, piloerection and convulsion. The behavioural excitation produced by either dibutyryl cyclic-AMP or aminophylline was antagonized by pretreatment with intraventricular injection of either two alpha-adrenergic antagonists (phentolamine and yohimbine) or a dopaminergic antagonist (haloperidol), but not with either a beta-adrenergic antagonist (propranolol) or a narcotic antagonist (naloxone). In addition, direct administration of dibutyryl cyclic-AMP into either the anterior hypothalamus, the nucleus accumbens or the caudate-putamen complex of rats produced the same behavioural responses as those produced by the intraventricular injection. Again, the behavioural responses induced by intracerebral injection of dibutyryl cyclic-AMP was antagonized by pretreatment with either alpha-adrenergic antagonists or a dopaminergic antagonist. The present data indicate that both the dopaminergic and the adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl cyclic-AMP and aminophylline in the rat.

Aminophylline↗
PubMed1975

[Hydrodynamic of the C.S.E. under experimental occlusion of superior sagittal sinus (author's transl)].

It is recognized that absorption of C.S.F. occurs mainly at the superior sagittal sinus through arachnoid villi after study of the Retzius (1875) and Weed (1914). We are interested in C.S.F. circulation and pathway on the obstructed superior sagittal sinus. At the border of middle one third and posterior one third of the superior sagittal sinus was obstructed experimentally. 1. When evans blue 0.5 to 1.0 ml was injected into lateral ventricle or cisterna magna, the evans blue was recognized on basal surface in either normal and obstructed dog of the superior sagittal sinus. Evans blue stained the convexity of normal dog, however, did not stain the convexity in the dog of obstructed superior sagittal sinus contrally. This was caused by the disturbance of C.S.F. circulation toward superior sagittal sinus. On the intraventricular injection of evans blue, it infiltrated into parenchym from ventripcle due to C.S.F. circulatory disturbance. 2. Study of radioactivity in the peripheral blood after intracisternal or intraventricular injection of RISA 100 muCi revealed that the radioactivity in the blood lowered with day after obstruction of superior sagittal sinus comparing with normal dogs. 3. Macroautoradiography after intracisternal or intraventricular injection of P 2mCi showed lower RI activity at the convexity, but increased activity at the basal brain in the obstructed dogs of superior sagittal sinus. These results showed that C.S.F. in normal dog was absorbed through the brain surface, expecially the basal surface of brain, other than through the superior sagittal sinus. Absorption of C.S.F. through the convexity of brain was disturbed significantly in the obstructed dogs of superior sagittal sinus. C.S.F. absorption into peripheral blood decreased in chronic stage after occlusion of surperior sagittal sinus and it suggested that the absorptive function of C.S.F. through the basal surface of brain was restricted.

Absorption↗
PubMed1994

Neurotoxicity in conscious rats following intraventricular SNAP, a nitric oxide donor.

A solution containing S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO.-releasing compound, was microinjected in doses of 0.25-2 mumol into a lateral ventricle of conscious rats. SNAP produced dose-dependent convulsions similar to those associated with limbic stimulation, such as tonic extension of the hindlimbs and tail, and dystonia of the forepaws. At 2 mumol, SNAP evoked hyperventilation (arterial hypocapnia), arterial hyperglycemia and caused necrotic lesions of periventricular gray (e.g. lateral septal nucleus) and white matter structures. In the caudate nucleus and lateral septal nucleus ipsilateral to injection, SNAP elicited a bipolar metabolic pattern of low glucose metabolism proximal to the ventricle with higher values occurring more distally. In control studies, we proved that the residue of SNAP decomposition, N-acetylpenicillamine disulfide injected intraventricularly (2 mumol), was without physiological, behavioral, or histological effects. Ventricular pretreatment with methylene blue (2 nmol), a putative inhibitor of guanylate cyclase and superoxide generator, suppressed several of the behavioral manifestations of 1 mumol SNAP, such as the forepaw dystonia, squinting, and facial clonus, but was ineffective on the physiological and histological variables affected by the 2 mumol SNAP dose. Another NO. donor, sodium nitroprusside (2 mumol), produced fewer behavioral and cytotoxic effects over a 55-min observation period, but caused more intense and widely distributed metabolic stimulation, especially in commissural and projection white matter tracts. The results are the basis for a conscious rat model using intraventricular injection of nitrocompounds to examine the physiological, behavioral, metabolic and cytotoxic properties of NO. in the brain.

Acid-Base Equilibrium↗
PubMed1987

Nicotine cue in rats: effects of central administration of ganglion-blocking drugs.

In rats trained to discriminate nicotine from saline, a single intraventricular injection of a small dose of the quaternary ganglion-blocking drug chlorisondamine blocked the response to nicotine for four weeks. pentolinium was only weakly active and hexamethonium was inactive as a nicotine antagonist under the conditions used, even in doses that were just below those producing myoclonic jerks. Chlorisondamine had no blocking effect in rats trained to discriminate the non-nicotinic drugs midazolam or morphine from saline. Intraventricular injections of chlorisondamine have a specific and unusually persistent nicotine-blocking action, the mechanism of which requires further investigation.

Animals↗
PubMed1979

Brain angiotensin II binding and central [Sar1,Ala8]angiotensin responses in normal rats and the New Zealand strain of genetically hypertensive rats.

1. Specific angiotensin II (ANGII) receptor binding was measured in regions of the brains of the New Zealand gentically hypertensive and normal rats. 2. ANGII receptor binding was consistently lower in the septum, midbrain, thalamus and posterior medulla of the genetically hypertensive rats than in normal rats. 3. Blood pressure responses to intraventricular injections of ANGII and an ANGII antagonist [Sar1,Ala8]angiotensin were studied in conscious and pentobarbitone-anaesthetized genetically hypertensive and normal rats. In conscious rats no significant difference between the two strains of rat was detected. 4. In pentobarbitone-anaesthetized rats intraventricular injection of 40 microgram of [Sar1,Ala8]angiotensin had a hypotensive effect which was three times greater in the genetically hypertensive rats than that observed in normal rats. The latency of this hypotensive effect was longer than the latency of the hypertensive effect of ANGII. 5. The drinking responses to intraventricular injections of ANGII were similar in genetically hypertensive and normal rats. 6. The physiological role of the ANGII system is discussed and it is concluded that an abnormality of this system in the brain may well be responsible for the hypertension found in the genetically hypertensive rat.

Angiotensin II↗
PubMed1994

Na,K-ATPase is decreased in hippocampus of kainate-lesioned rats.

The effects of intraventricular injection of kainic acid on the Na,K-ATPase (Na,K pump) were examined in discrete pyramidal cell regions of rat hippocampus. [3H]Ouabain binding was used to quantitate Na,K-ATPase catalytic subunits and in situ hybridization was used to determine Na,K-ATPase mRNA levels. Large decreases were found in both [3H]ouabain binding and alpha 3 isoform mRNA in hippocampus areas, especially in the CA3 pyramidal cell layer, which sustains heavy cell losses as a result of bilateral, intraventricular injection of kainic acid. Substantial decreases in the high affinity component of ouabain binding and in the alpha 3 isoform mRNA (but not isoforms for other Na,K-ATPase subunits) were also observed in the CA1 region of hippocampus, an area preserved in this model. High affinity [3H]ouabain binding was decreased 25-33% in the stratum pyramidale and stratum radiatum after treatment with kainic acid, and alpha 3 mRNA was decreased by 26-50%. To further characterize the decrease in alpha 3 mRNA, animals were killed at 1, 2, and 3 weeks after injection of kainate and results show a large decrease in alpha 3 mRNA only at 2 weeks recovery time. While the pathology underlying temporal lobe epilepsy is unclear, changes in the Na,K-ATPase may be involved in abnormal firing characteristics of cells in epileptic tissue.

Animals↗
PubMed1982

Effect of opioid peptides on gonadotrophin secretion.

The intraventricular injection of 25 micrograms of Methionine-Enkephalin (Met-Enk) induces a significant increase of serum LH levels in long-term ovariectomized rats 15, 30 and 60 min following administration. The synthetic Met-Enk agonistic analogue [D-Ala2] methionine-Enkephalinamide ([D-Ala2]Met-Enk) also enhances significantly serum LH levels at 30 and 60 min; under the same experimental conditions neither Met-Enk nor [D-Ala2]Met-Enk modifies serum levels of FSH following intraventricular injections into ovariectomized animals. It is concluded that, under particular circumstances, opioid peptides of the Met-Enk family may stimulate LH release.

Animals↗
PubMed2003

Selective neuromicrovascular endothelial cell death by 8-Iso-prostaglandin F2alpha: possible role in ischemic brain injury.

BACKGROUND AND PURPOSE: Free radical-induced peroxidation is an important factor in the genesis of hypoxic-ischemic encephalopathy, including that of the preterm infant. Isoprostanes are major peroxidation products. Since microvascular dysfunction seems to contribute to ischemic encephalopathies, we studied the cytotoxicity of 8-iso-prostaglandin F2alpha (PGF2alpha) on cerebral microvascular cells. METHODS: Microvascular endothelial, astroglial, and smooth muscle cells from newborn brain were cultured. The cytotoxicity of 8-iso-PGF2alpha on these cells was determined by MTT assays and lactate dehydrogenase (LDH) release, propidium iodide incorporation, and DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling [TUNEL]). In addition, effects of intraventricular injections of 8-iso-PGF2alpha and possible involvement of thromboxane in 8-iso-PGF2alpha-induced cytotoxicity were determined. RESULTS: 8-Iso-PGF2alpha induced time- and concentration-dependent endothelial cell death (EC50=0.1 nmol/L) but exerted little effect on smooth muscle and astroglial cells; endothelial cell death seemed mostly of oncotic nature (propidium iodide incorporation and LDH release). Cell death was associated with increased endothelial thromboxane A2 (TXA2) formation and was prevented by TXA2 synthase inhibitors (CGS12970 and U63557A); TXA2 mimetics U46619 and I-BOP also caused endothelial cell death. Intraventricular injection of 8-iso-PGF2alpha induced periventricular damage, which was attenuated by CGS12970 pretreatment. CONCLUSIONS: These data disclose a novel action of 8-iso-PGF2alpha involving TXA2 in oxidant stress-induced cerebral microvascular injury and brain damage.

Animals↗
PubMed1990

Regulation of Nerve Growth Factor (NGF) Synthesis in the Rat Central Nervous System: Comparison between the Effects of Interleukin-1 and Various Growth Factors in Astrocyte Cultures and in vivo.

In order to obtain information on the physiological regulation of NGF-synthesis in the central nervous system (CNS) we investigated the effects of a series of growth factors (known to be present in the CNS) in cultures of purified rat astrocytes and compared these effects with those observed after intraventricular injection of the same molecules. After preliminary experiments had shown that 10% fetal calf serum (FCS) produced a marked increase in NGF-mRNA levels in astrocytes (but neither in microglia nor oligodendrocytes) as demonstrated by Northern blot analysis and in situ hybridization the experiments were performed at low (0.5%) FCS concentrations. Supramaximal concentrations of IL-1 and various growth factors caused a 5- to 7-fold increase in NGF-mRNA after 6 h. By 24 h the NGF-mRNA levels approached control values again, most probably due to inactivation of the added factors since after readdition after 24 h the response was about the same as the initial one. Norepinephrine and 8-bromo-cAMP did not change NGF-mRNA levels. The growth factor-mediated changes in NGF-mRNA levels in astrocyte cultures were not consistently reflected by the changes observed after intraventricular injection. IL-1 produced by far the largest increase in hippocampal NGF-mRNA after intraventricular injection. This large response to IL-1 could result from a positive feedback mechanism, since IL-1beta injection not only increases NGF-mRNA but also IL-1beta-mRNA in the hippocampus. The understanding of the physiological regulation of NGF synthesis in the CNS is the basis for a rational approach to its pharmacological modification. This, in turn, is an attractive alternative to the (long-term) infusion of NGF or the transplantation of NGF-secreting cells with the goal of providing trophic support to the cholinergic neurons of the basal forebrain nuclei. These neurons are consistently affected in the early stages of Alzheimer's disease, their impaired function being essentially responsible for the cognitive deficits.

Journal Article↗
PubMed1970

Temperature responses and other effects of 5-hydroxytryptophan and 5-hydroxytryptamine when acting from the liquor space in unanaesthetized rabbits.

1. In unanaesthetized rabbits 5-hydroxytryptophan (5-HTP) and 5-hydroxytryptamine (5-HT) were injected into the cisterna magna or into the cannulated left lateral cerebral ventricle while rectal temperature was recorded.2. 5-HTP injected intracisternally in a dose of 1.5-3 mg produced a fall in temperature often followed by a rise beyond the pre-injection level. With 6 mg the main effect was a rise in temperature. The intraventricular injection of 1-2 mg 5-HTP usually produced a fall followed by a rise.3. 5-HT injected intracisternally in a dose of 0.2 mg produced a fall in temperature similar to that produced with this dose injected intraventricularly. Following an intracisternal injection of 1-4 mg 5-HT there was either a fall, or a fall followed by a rise, but in a few experiments the effect consisted mainly of a rise in temperature.4. Additional effects regularly observed with these injections were tachypnoea, ear twitching, rapid movements of the vibrissae, shaking of the head, wiping and scratching movements, ataxia, nodding and sideways movements of the head and long-lasting catalepsy.5. The sites where 5-HTP and 5-HT act when producing the temperature responses and the various behavioural effects are discussed.

5-Hydroxytryptophan↗
PubMed1993

Evidence for an involvement of the mu-type of opioid receptor in the modulation of learning.

Pavlovian conditioning of the rabbit's nictitating membrane response was used to determine whether the retardation of learning produced by enkephalin derivatives was mediated through an action on mu- or delta-opioid receptors. Intraventricular injection of the highly selective mu-agonist, [D-Ala2, MePhe4, Gly-ol5] enkephalin (DAMGO) significantly retarded (2 nmol) or completely blocked (20 nmol) the acquisition of conditioned responses. The retarded or blocked acquisition of conditioned responses produced by DAMGO could still be detected when the rabbits were tested two days after cessation of drug injections, suggesting that DAMGO had affected learning and not simply performance of conditioned responses. Intraventricular injection of a comparable dose (20 nmol) of the highly selective delta-agonist, [D-Pen2,5] enkephalin (DPDPE) did not retard learning. A higher dose of DPDPE (200 nmol), which would be expected to act at both mu- and delta-receptors, did produce a retardation of acquisition that was comparable to the effects of a 2-nmol dose of DAMGO. However, unlike DAMGO, the retardation of learning produced by this dose of DPDPE appeared to be due, at least in part, to a reduction in the aversive properties of the unconditioned stimulus. The retardation of learning produced by 2 nmol of DAMGO and 200 nmol of DPDPE was due to an action on an opioid receptor because this effect was blocked by a subcutaneous injection of naloxone (2.5 mumol/kg), a specific opioid antagonist. The stereoselective effects of the mu-opioid agonist levorphanol further confirmed that the retarded learning was mediated through actions at the mu-opioid receptor. Autoradiographic studies indicated that a 2-nmol, intraventricular dose of DAMGO achieved contents greater than 1 pmol/mg in tissue lying within 2 mm of the lateral ventricle, third ventricle and cerebral aqueduct. These data suggest that enkephalins produce a retardation of learning through an effect on the mu-type of opioid receptor and that at least one locus of their actions is produced at periventricular sites lying within 2 mm of the ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Actions of endogenous vasopressin and oxytocin on anterior pituitary hormone secretion.

To evaluate the significance of endogenous vasopressin and oxytocin in control of anterior pituitary hormone release, antiserum against vasopressin (AB-VP) or oxytocin (AB-OT) were microinjected into the third ventricle (3V) of conscious, ovariectomized rats to immunoneutralize endogenous VP or OT, respectively. Blood samples were collected just before and at different times after the microinjections. There were no differences in the plasma LH, FSH, PRL and TSH concentrations between control groups injected into the 3V with normal rabbit serum (NRS) and groups submitted to the intraventricular injection of AB-OT or AB-VP for 24 h after the injections. Plasma growth hormone (GH) declined significantly by 4 h after NRS injection, remained low at 6 h and had rebounded to nearly initial levels at 24 h. This pattern was not changed by microinjection of AB-VP, but plasma GH increased significantly compared to initial values in the period from 1 to 24 h after intraventricular microinjection of AB-OT. The intraventricular injection of AB-VP or AB-OT significantly decreased plasma ACTH; however, the effect of AB-VP was more prolonged and persisted for 6 rather than 4 h after injection. Thus, endogenous oxytocin may play a role in the control of basal GH release probably by stimulating somatostatin secretion and/or inhibiting GH-releasing hormone secretion or by both actions. On the other hand, both endogenous vasopressin and oxytocin play a physiologically significant stimulatory role in the control of basal ACTH release.

Adrenocorticotropic Hormone↗
PubMed1995

Selective lesioning of the basal forebrain cholinergic system by intraventricular 192 IgG-saporin: behavioural, biochemical and stereological studies in the rat.

The elucidation of the functional role of the basal forebrain cholinergic system will require access to a highly specific and efficient cholinergic neurotoxin. Recently, selective depletion of the nerve growth factor (NGF) receptor-bearing cholinergic neurons in the rat basal forebrain and a dramatic loss of cholinergic innervation in the related cortical regions have been obtained following intraventricular injection of a newly introduced immunotoxin, 192 IgG-saporin. Here we extend these initial findings and report that administration of increasing doses (1.25, 2.5, 5.0 or 10 micrograms) of the 192 IgG-saporin conjugate into the lateral ventricles of adult rats induced dose-dependent impairments in the water maze task and passive avoidance retention, but only weak and inconsistent effects on locomotor activity. These behavioural changes were paralleled by a reduction in choline acetyltransferase activity in hippocampus and several cortical areas (up to 97%) and selective depletions of NGF receptor-positive cholinergic neurons in the septal-diagonal band area and nucleus basalis magnocellularis (up to 99%). By contrast, the non-cholinergic parvalbumin-containing neurons in the septum were completely spared, and other cholinergic projection systems (such as in the striatum, thalamus, brainstem and spinal cord) were unaffected even at the highest dose. The observed changes in the water maze and passive avoidance tasks, as well as the cholinergic cell loss, were maintained up to at least 8 months following the intraventricular injection of a single dose (5 micrograms) of the immunotoxin. The results confirm the usefulness of the 192 IgG-saporin toxin for selective and profound lesions of the basal forebrain cholinergic neurons and provide further support for a role of the basal forebrain cholinergic system in cognitive functions.

Acetylcholinesterase↗
PubMed1983

[Pharmacological studies of d1-2-[3-(2'-chlorophenoxy)phenyl]propionic acid. (2) Sites and mechanisms of analgesic and antipyretic effects].

Effects of d1-2-[3-(2'-chlorophenoxy)phenyl]propionic acid (CPP) on the nociceptive response induced by injection of bradykinin (BK) into rabbit femoral artery were studied. When drugs were administered intravenously, the analgesic activity of morphine was 2 to 10 times more potent than that of CPP; but when it was injected into the femoral artery, CPP was approximately 5 times more potent than morphine. Intraventricular injection of a small dose of 10 micrograms/head morphine produced a prominent analgesic activity, while even a large dose of 500 micrograms/head CPP had little effect. Prostaglandin E1 (PGE1) alone in a dose range of 0.1 to 1 microgram i.a. produced no nociceptive response, but an intra-arterial pre-injection of PGE1 enhanced BK-induced nociceptive response. Morphine suppressed the BK-response pretreated with PGE1, but CPP as well as indomethacin had little effect. These results suggest that CPP suppresses BK-induced nociceptive response at the periphery, probably at the paravascular "pain receptor", and the analgesic effect of CPP may be due to inhibition of endogenous PG synthesis. On the other hand, CPP in a dose range of 2.5 to 20 mg/kg, i.v. produced antipyretic effects on the fever induced by typhoid vaccine. Intraventricular injection of 500 micrograms/head CPP produced a slight antipyretic effect. CPP had no effect on PGE1 -induced fever. These results suggest that CPP produces the antipyretic effect acting on the central nervous system, probably due to inhibition of endogenous PG synthesis.

Alprostadil↗
PubMed1989

Rapid activation of gluconeogenesis after intracerebroventricular carbachol.

Intracerebroventricular administration of carbachol (27 nmol in 5 microliters 0.15 M NaCl) produced marked hyperglycemia in 24-h fasted rats, despite the negligible amounts of preformed liver glycosyl residues. To investigate the possibility of a stimulation of gluconeogenesis, conscious unrestrained rats were continuously infused with [14C]bicarbonate (0.51 microliters, 0.18 muCi/min) and label incorporation into circulating glucose determined before and after intraventricular injection. The rate of 14C incorporation into blood glucose of fed rats was not affected by intraventricular injection of 0.15 M NaCl but increased significantly after carbachol administration. In both fed and 24-h fasted rats the hyperglycemia induced by intraventricular carbachol was accompanied by marked increases in plasma lactate. Previous adrenodemedullation prevented both the hyperglycemia and the hyperlactemia. Liver pyruvate kinase activity was reduced in carbachol-treated rats, when the enzyme was assayed with suboptimal concentrations of phosphoenolpyruvate and in the absence of fructose 1,6-biphosphate. Phosphoenolpyruvate carboxykinase activity was not affected. The data suggest that central chemical stimulation with cholinergic agents induces a rapid activation of liver gluconeogenesis, which probably results from an increased sympathetic outflow for epinephrine secretion by the adrenal medulla.

Animals↗