Is taurine involved in cerebral osmoregulation?
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Animals↗
Biomedical subjects
S R Nelson
Publications and source records attributed to S R Nelson.
Vasculature of the paraphysis cerebri of the frog.
The paraphysis cerebri is a glandular structure found in the third ventricle of lower vertebrates. It is well-developed in amphibians and reptiles. The function of the gland is not substantiated, but may play a role in calcium metabolism. To further elucidate its possible endocrine role, the paraphyseal vasculature was examined using casting techniques as well as transmission electron microscopy. Perfusion-fixed paraphyses of Rana pipiens and Rana catesbeiana were either: a) cast with Microfil (with subsequent dehydration, clearing, and macroscopic examination) or Batson's compound (followed by tissue digestion and examination by scanning electron microscopy); or b) processed for transmission electron microscopy. The paraphyseal capillary bed consists of a sinusoidal portal system which receives afferent blood from its associated choroid plexus. The choroid plexus of the third ventricle receives its blood supply via arterioles from the posterior telencephalic artery. These arterioles traverse in the periphery of the paraphysis to branch and supply the choroid plexus. Numerous venules exit from the choroid plexus and drain into sinusoids of the paraphysis. The sinusoid venules appear to empty into a midline venous structure which passes tangentially through the paraphysis. The sinusoids consist of fenestrated endothelium which is indicative of transport vessels. Nerve fibers were observed in the paraphysis, however, histofluorescence revealed no monoaminergic sympathetic innervation of the paraphyseal vasculature.
Animals↗
Kainic acid-induced seizures: changes in brain extracellular ions as assessed by intracranial microdialysis.
The effect of kainic acid on extracellular [K+], [Ca2+], and [Na+] in the rat piriform cortex and hippocampus was studied by means of intracranial microdialysis. Either a dialysis fiber loop or horizontal Vita fiber were stereotaxically implanted within the piriform cortex or hippocampus, respectively. About 24 h later, fibers were perfused (1 ml/min) with Krebs-Ringer bicarbonate solution. Effluent samples were collected before (four at 30 min intervals), and after (six at 30 min intervals) administration of kainic acid (16 mg/kg, i.p.) or kainic acid vehicle. Kainic acid induced sequential signs of lethargy, staring, "wet-dog shakes," forepaw clonus, and tonic-clonic convulsions. In these awake free-moving rats, kainic acid induced a rapid and prolonged increase in extracellular [K+] and an apparent, but not statistically significant, decrease in extracellular [Ca2+] within the hippocampus. In the piriform cortex, kainic acid induced increases in extracellular [K+] and [Na+], which were associated with early pre-convulsive signs. In contrast to the pronounced ion changes commonly seen when the brain is activated by factors such as local application of excitatory substances or when the brain is made ischemic or hypoxic, extracellular ion concentrations are relatively well maintained during parenteral kainic acid-induced seizures.
Animals↗
A man who loves change. Interview by Richard L. Reece.
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Cost Control↗
Soman-induced convulsions affect the inositol lipid signaling system: potentiation by lithium; attenuation by atropine and diazepam.
Effects of atropine or diazepam pretreatment on soman-induced convulsions and brain phosphoinositide (PI) metabolism, as assessed by brain regional inositol-1-phosphate (IP1) levels, were studied in saline and LiCl-pretreated rats. IP1, an intermediate in PI turnover, was measured in cortex, caudate, thalamus, hippocampus, and cerebellum. Soman (100 micrograms/kg; sc) produced convulsions in 63% of the saline-pretreated rats, whereas with LiCl pretreatment all rats exposed to 100 micrograms/kg of soman had tonic-clonic convulsions. Thus, LiCl pretreatment potentiated soman-induced convulsions. Tissue IP1 increased severalfold in soman-exposed convulsing rats with the highest increases being in frontal cortex and caudate. In contrast, no marked increases of IP1 occurred in similarly treated nonconvulsing rats. LiCl treatment itself increased IP1 levels without causing convulsions. In LiCl-pretreated rats, soman again markedly elevated IP1 levels above LiCl alone in convulsing rats, whereas no such effect occurred in nonconvulsing rats. In LiCl-pretreated rats, the increased IP1 levels associated with soman-induced convulsions were greatest in hippocampus and piriform cortex. Thus, LiCl appears to lower the threshold for the spread of seizure activity through limbic structures, thereby potentiating cholinergic-induced convulsions. Diazepam and atropine both blocked soman-induced convulsions, and brain regional IP1 elevations were concomitantly abolished as well. These results indicate that soman-induced convulsions involve the inositol lipid signaling system. This involvement is potentiated by lithium but attenuated by atropine and diazepam.
Animals↗
A possible role for taurine in osmoregulation within the brain.
Intracranial microdialysis was used to measure changes in extracellular amino acids within the rat brain during local osmotic alteration of the extracellular microenvironment or during systemic water intoxication. Increased cellular hydration produced by either of these methods was accompanied by a marked increase in extracellular taurine levels without affecting the other amino acids measured. With local osmotic alteration, this increase was osmolarity dependent and reversible. The specificity, sensitivity, and reversibility of the increase in extracellular taurine strongly suggest a functional role in osmoregulation in the brain under normal as well as pathological conditions.
Animals↗
Convulsions and cerebral inositol-1-phosphate levels in rats treated with diisopropyl fluorophosphate.
In order to examine the relationship of organophosphate-induced cholinergic stimulation to phosphoinositide (PI) hydrolysis in the brain, diisopropyl fluorophosphate (DFP; 1.3 or 1.5 mg/kg subcutaneously) was given to rats pretreated with saline or LiCl (5 meq/kg subcutaneously). Behaviour was monitored 60 min. after the administration of DFP, and inositol-1-phosphate (IP1), an intermediate in PI metabolism, was measured in the brain DFP alone caused tremors, whereas with LiCl pretreatment, DFP caused tremors and tonic-clonic convulsions. DFP alone did not increase IP1 above control levels. LiCl alone elevated IP1 2-5 fold but did not alter rat behavior. With LiCl pretreatment, DFP caused IP1 to increase 2-4 fold above LiCl control values in convulsing rats. LiCl increased the potential of DFP to induce convulsions and greatly amplified IP1 elevations induced by DFP.
Animals↗
Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam.
Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself.
Animals↗
Role of early edema in the development of regional seizure-related brain damage.
Kainic acid-induced seizures produced early (2 hr) generalized edema and later (24 and 48 hr) necrotic edema in temporal cortex and hippocampus as measured by specific gravity changes. Mannitol given during the seizure partially protected against the early edema and prevented the necrotic edema indicating early edema may play a role in later brain damage. However, H2O intoxication, causing much greater generalized edema than the kainic acid-induced seizures, caused no necrotic edema in temporal cortex or hippocampus at 48 hr. Thus it appears that mannitol protection against kainic acid-induced brain damage may be by a mechanism in addition to dehydration.
Animals↗
Protein secretion by choroid plexus: isolated apical fragments synthesize protein in vitro.
Protein synthesis was studied in the isolated rat choroid plexus. When the choroid plexus was studied by transmission electron microscopy, membrane-bound structures were often observed in the ventricular space. These structures appear to bud from the apical surface of the epithelial cells. In the present study, we attempted to isolate these membrane-bound cellular fragments from the choroid plexus and to determine their ability to synthesize proteins. The apical fragments (aposomes) were isolated from the choroid plexus by allowing tissue explants to incubate in media (37 degrees C) for 1 h. The tissue was removed and the media, now containing aposomes, was incubated with [S35]methionine (100 microCi). The media was collected and analysed by SDS-PAGE followed by fluorography. Parallel [S35]methionine incubations were done with whole tissue explants. The SDS-PAGE protein derived from the aposomes was similar to the profile derived from the tissue. In addition, proteins detected in CSF had relative molecular weights comparable to the products synthesized by aposomes. These observations suggest that aposomes provide an additional route of entry for proteins into CSF.
Animals↗
Cholinergic systems influence local cerebral glucose use in specific anatomical areas: diisopropyl phosphorofluoridate versus soman.
The organophosphates, diisopropyl phosphorofluoridate and soman have a common mechanism of action (inhibition of acetylcholinesterase), but result in very different behavioral responses in the rat. Soman rapidly produced persistent tonic convulsions whereas diisopropyl phosphorofluoridate only infrequently produced transient convulsive-like activity. Soman increased local cerebral glucose use in most of the cortex, striato-pallido-nigral pathway, limbic system and in specific thalamic nuclei whereas diisopropyl phosphorofluoridate increased glucose use in a limited fashion, primarily in the dorsal striato-pallido-nigral pathway. When diazepam blocked soman-induced convulsions, the pattern of glucose use was strikingly similar to that caused by diisopropyl phosphorofluoridate. Soman or diisopropyl phosphorofluoridate depressed local cerebral glucose use in rats pretreated with the antidotal mixture of trimedoxime, atropine and benactyzine (muscarinic antagonists). Also, this antidotal mixture blocked the increased glucose use in the dorsal striato-pallido-nigral system produced by either acetylcholinesterase inhibitor, indicating that muscarinic receptors mediate the excitation of this pathway. Both diisopropyl phosphorofluoridate and soman activate the striato-pallido-nigral pathway but soman also causes spread of activity producing overt motor convulsions. Possible explanations for this difference in response to the organophosphates are differential responses in cholinergic actions within specific brain regions or some non-cholinergic action of soman.
Animals↗
Changes in extracellular amino acids during soman- and kainic acid-induced seizures.
Extracellular amino acid levels in the rat piriform cortex, an area highly susceptible to seizure-induced neuropathology, were determined by means of intracranial microdialysis. Seizures were induced by systemic administration of either soman (O-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase, or the excitotoxin kainic acid. Extracellular glutamate levels increased in animals with seizures shortly after administration of either convulsant, but this change was statistically significant only in the case of soman-treated animals. Extracellular taurine levels increased markedly, reaching two- and fourfold baseline levels during the second hour of soman- and kainic acid-induced seizures, respectively. Taurine levels did not increase in the subpopulation of soman-treated animals without seizures, a finding indicating that elevation of extracellular taurine level is seizure related. Thus, we propose that taurine efflux may be a physiological cellular response to neuronal changes produced by excitotoxic chemicals, either directly or as a consequence of seizures.
Amino Acids↗
Effects of antidotes on soman-induced brain changes.
Rats were pretreated with either diazepam, atropine or benactyzine 10 min prior to soman injection. Local cerebral glucose use (LCGU) was determined during the seizure phase (15 min post soman) or pathology phase (72 h post soman). Diazepam and benactyzine pretreatment prevented convulsive activity, whereas atropine pretreatment only reduced the duration of convulsive activity after soman exposure. Each pretreatment agent had a unique impact on LCGU pattern during the seizure phase. During the pathology phase, the marked reduction in LCGU and the conspicuous brain damage associated with soman-induced seizures was minimized by all three pretreatments.
Animals↗
Paraphysectomy-induced stimulation of parathyroid glands in mature frogs (Rana catesbeiana): evidence for telencephalic regulation of parathyroid gland function.
The relationship of the paraphyseal-choroid plexus complex to parathyroid gland function was investigated in adult frogs. Light microscopy and morphometric analysis indicated that total parathyroid gland volume, cell volume and vascular volume doubled by 7-28 days after surgical removal of the paraphyseal-choroid plexus complex (paraphysectomy). This increase correlated with the appearance of large Golgi-associated vesicles, an increase in the apparent number of cytoplasmic dense-core granules, and PTH within the parenchymal cells as monitored by immunofluorescence. Twelve months after paraphysectomy, parathyroid glands became cystic with a central fluid-filled cavity surrounded by a stratified cuboidal cell layer. The parenchymal cells of cystic glands contained numerous cytoplasmic dense-core granules and were also positive for PTH. Radioimmunoassay of cystic parathyroid fluid indicated a PTH concentration of 2 micrograms/microliter; however, analysis by SDS-PAGE indicated a wide range of proteins in cystic fluid. The results of this study indicate that paraphysectomy induces stimulation of the parathyroid glands and suggest a role for the paraphyseal-choroid plexus complex in the regulation of amphibian parathyroid gland function.
Animals↗
Health care delivery system: current trends and prospects for the future.
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Delivery of Health Care↗
Occurrence of bone fractures and parathyroid hyperplasia in paraphysectomized frogs (Rana catesbeiana).
The physiological role of the amphibian paraphysis was studied by removing the paraphysis from bullfrog tadpoles (Rana catesbeiana) and observing change in frog weight, bone development, and parathyroid glands 22 months later. Development was similar in control and paraphysectomized frogs until 6 months when the experimental frogs began to show greater weight gain which persisted for the remaining 16 months. At the time of sacrifice (22 months after paraphysectomy), the parathyroid glands of the experimental frogs were enlarged with a tenfold increase in wet weight and a sevenfold increase in dry weight. The glands from experimental frogs had numerous cysts filled with eosinophilic staining material; histologically the cell nuclei were rounded and the cytoplasm was vesiculated. At the time of sacrifice the experimental frogs had knoblike deformities along the shafts of the long bones. These deformities were due to callus formation around spontaneous bone fractures as revealed by X-rays of the tibia-fibulas and femurs. The dry weight was greater but calcium content less in femurs from experimental frogs. These findings indicate the paraphysis plays a role in calcium metabolism, possibly by producing a factor necessary for calcium action on cells.
Animals↗
Changes in local cerebral glucose utilization induced by convulsants.
With the six convulsants studied (Soman, intrahippocampal penicillin, bicuculline, pentylenetetrazol, picrotoxin and strychnine), the anatomical distribution of changes in local cerebral glucose utilization was related to the type of seizure observed. Strychnine induced a few very intense motor convulsions during the 2-deoxyglucose experimental period without having a major effect on brain local cerebral glucose utilization, in support of the view that its actions are predominantly in the spinal cord. Pentylenetetrazol and picrotoxin induced intermittent intense seizures and marked increases in local cerebral glucose utilization in the globus pallidus and substantia nigra. Soman, intrahippocampal penicillin and bicuculline all induced persistent status epilepticus associated with increases in local cerebral glucose utilization in many brain areas; those with striking increases in glucose use include: cortical areas, the limbic system, basal ganglia and substantia nigra. The glucose use changes produced by Soman, penicillin and bicuculline greatly exceeded those induced by pentylenetetrazol and picrotoxin. Activation of the substantia nigra and basal ganglia occurred with all centrally mediated convulsions and with status epilepticus there was also marked activation of cortical and limbic structures.
Animals↗
Selecting and recruiting health programs for the School Health Education Evaluation.
The School Health Curriculum Project (SHCP) and three promising health education approaches, Project Prevention, 3 Rs and High Blood Pressure (HBP), and Health Education Curriculum Guide, were the curricula used in the School Health Education Evaluation (SHEE) project. This paper contains program descriptions of each, and a brief description of the process that led to their selection. Inclusion of the School Health Curriculum Project (SHCP) was mandated by the use of government funds to support the SHEE. The three alternative curricula, Project Prevention, 3 Rs and High Blood Pressure, and Health Education Curriculum Guide, were selected on the basis of a protocol devised jointly by contractors, government project officers, and the project advisory panel.
Attitude to Health↗