bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE INTRAVENOUS INJECTION OF MAGNESIUM SULPHATE FOR ANESTHESIA IN ANIMALS
Authors: Auer J. , Meltzer S. J. 
Published: June 2004

These experiments justify the following general conclusions.
By the intravenous injection of M/4 magnesium sulphate into dogs at a certain rate, a stage can be reached where the abdominal walls are completely relaxed and when section of the abdomen and stimulation of sensitive parts of the parietal peritoneum do not produce pain or elicit any reaction of the animal. At the same time spontaneous respiration may still be maintained within normal limits and the lid reflex be fair or even normal. In this stage intratracheal intubation for artificial respiration can be easily accomplished. This stage may be attained in 12 to 14 minutes when the rate of injection is about 3 cc. per minute. When this stage is once attained the rate of injection should gradually be reduced, otherwise, sooner or later, spontaneous respiration will be abolished, and by a further maintenance of the rate of injection all the skeletal muscles may become paralyzed.
When the injection of magnesium is continued for a longer period, the paralytic effects of the magnesium injection will set in, even when administered at a slow rate.
The paralysis of the respiratory function is readily met by intrapharyngeal insufflation, which is easily executed even without training in this procedure, or by the method of intratracheal insufflation, if executed by one trained in its management.
When the respiration of the animal is accomplished by insufflation, the paralytic effect of the magnesium may be abolished fairly rapidly by an intravenous injection of about 10 cc. of an M/8 calcium chloride solution; or it may disappear slowly, after the infusion of the magnesium solution is discontinued for some time. The latter mode of disappearance may be favorably accelerated by an intravenous infusion of 60 to 100 cc. of an M/4 solution of sodium sulphate.
The production of anesthesia by intravenous injection of magnesium sulphate should not be undertaken unless an apparatus for intrapharyngeal insufflation is at hand, because in exceptional cases the disappearance of spontaneous respiration may be one of the earliest consequences of the magnesium injection.
The injection of calcium chloride should not be employed in cases in which the subject shows cardiac insufficiency. In such instances, moreover, injections of magnesium should not be used for the purpose of anesthesia; at least not until greater experience has been acquired in the employment of this method.
AN EXPERIMENTAL STUDY OF THE ADDITIVE AND ANTAGONISTIC ACTIONS OF SODIUM OXALATE, AND SALTS OF MAGNESIUM AND CALCIUM IN THE RABBIT
Authors: Gates F. L. , Meltzer S. J. 
Published: June 2004

The foregoing experiments establish firmly the following facts.
Subcutaneous or intramuscular injections of sodium oxalate in subtoxic doses, when administered to an animal which received a subminimal dose of magnesium sulphate, produce profound anesthesia and paralysis of long duration, although the usual effects of sodium oxalate alone are of a stimulating character. This fact is, in general, in harmony with the results reported by Starkenstein who, however, seems to have used the combination of the two salts in one solution; namely, that of magnesium oxalate.
The combined injections of subminimal doses of sodium oxalate and magnesium sulphate produce a strong reduction, or even, at times, a complete abolition of the conductivity of the motor nerve endings.
An intravenous injection of calcium salts brings on a recovery from the profound and prolonged effects of the combined action of sodium oxalate and magnesium sulphate, which is as prompt as is observed in experiments in which effective doses of magnesium alone were given. This fact is the more noteworthy, since depressions of long duration produced by prolonged continuous injections of magnesium solutions alone do not respond very promptly and effectively to calcium injections.
As will be recalled, the starting point for our investigation was the hypothesis that substances which are capable of precipitating calcium—a biological antagonist of magnesium—ought to be capable of increasing the depressive effect of magnesium. Our experiments proved that this assumption was correct. This would seem, therefore, to justify the interpretation that the augmenting action of sodium oxalate has its cause in the ability of the latter to precipitate calcium and thus increase within the body the amount of unantagonized magnesium. However, we wish to state expressly that this view is, for the present, still no more than a hypothesis and does not exclude other possible interpretations of our facts. As we pointed out it speaks against this hypothesis that oxalates do not produce phenomena of depression; the toxic symptoms produced by oxalates exhibit distinctly signs of increased and not of decreased irritability.
CHEMICAL VERSUS SERUM TREATMENT OF EPIDEMIC MENINGITIS
Authors: Flexner Simon , Amoss Harold L. 
Published: June 2004

Claims of efficiency have been made at two widely separated periods for the chemical treatment of epidemic meningitis, in the first instance for lysol and in the second for protargol. The use of lysol was long since abandoned; the recommendation for protargol is based on a single series of cases, small in number. Because of the variable severity of epidemics of meningitis, small reliance can be placed on results of treatment limited in extent to small numbers of cases and to one locality. A more uniform and accurate measure of the value of a method of treatment is provided by animals infected experimentally with pathogenic cultures of meningococci.
Young guinea pigs respond in a definite manner to intraperitoneal inoculation of virulent meningococci. Neither protargol nor lysol proved to have any curative action on the experimental infection thus produced in these animals.
Monkeys respond in a characteristic manner to the inoculation of virulent cultures into the subarachnoid space. Protargol displayed no curative action on the experimental infection thus produced in these animals.
On the contrary, both lysol and protargol exert antileukotactic and antiphagocytic effects, and are also potent protoplasmic poisons, and the leukocytes with which they come in contact are injured and made to degenerate. According to the extent to which these harmful properties are exerted, the chemicals promote the advance rather than restrain the progress of meningococcic infection.
Recovery from meningococcic infection in man and animals is accomplished chiefly through the process of phagocytosis. The specific antiserum acts curatively by increasing the emigration of leukocytes, by promoting phagocytosis directly, and by agglutinating the meningococci, and also by neutralizing endotoxin. Any means which interfere with and reduce these essential processes retard or prevent recovery. Both lysol and protargol interfere with and diminish the emigration of leukocytes and the phagocytosis of meningococci, and neither possesses antitoxic power.
The mixture of antiserum with lysol and with protargol reduces to a certain extent the antileukotactic and antiphagocytic effect of the chemicals; but this action is insufficient to set aside wholly the injurious effects which they produce.
It follows, therefore, that whatever theoretical advantages might accrue from a bactericidal activity exerted by these chemicals independently of the type of meningococcus causing epidemic meningitis, is more than offset by the harmful effects which they cause.
Hence specific antiserum seems to provide the logical therapeutic agent with which to combat epidemic meningitis, since it is itself innocuous and promotes those processes essential to recovery from the disease. The problem up to the present has been that of producing an antiserum which represents the several types of the meningococcus, and this problem is now in a fair way to being solved.
Experience‐dependent neuronal specialization and functional organization in the central auditory area of a songbird
Authors: Cousillas Hugo , Richard Jean‐Pierre , Mathelier Maryvonne , Henry Laurence , George Isabelle , Hausberger Martine 
Published: June 2004

AbstractThe effect of early experience on brain development was investigated in the central auditory area of a songbird, the field L complex, which is analogous to the mammalian auditory cortex. Multi‐unit recordings of auditory responses in the field L complex of adult starlings raised without any experience of adult song during development provide strong evidence of developmental plasticity both in the neuronal responses and in the functional organization of this area. Across the entire area, experimental birds, separated from adults from the age of 1 week old until they were 2 years old, had a much larger number of neurons that responded to all the stimuli than did control birds. The well‐known tonotopy demonstrated in adult wild birds using the same procedure was altered. This study is the first to bring evidence of developmental plasticity in the organization of the central auditory areas in songbirds. These results are discussed in relation to other reports on effects of early experience on brain development.
Allele‐dependent changes of olivocerebellar circuit properties in the absence of the voltage‐gated potassium channels Kv3.1 and Kv3.3
Authors: McMahon Anne , Fowler Stephen C. , Perney Teresa M. , Akemann Walther , Knöpfel Thomas , Joho Rolf H. 
Published: June 2004

AbstractDouble‐mutant mice (DKO) lacking the two voltage‐gated K+ channels Kv3.1 and Kv3.3 display a series of phenotypic alterations that include ataxia, myoclonus, tremor and alcohol hypersensitivity. The prominent cerebellar expression of mRNAs encoding Kv3.1 and Kv3.3 subunits raised the question as to whether altered electrical activity resulting from the lack of these K+ channels might be related to the dramatic motor changes. We used the tremorogenic agent harmaline to probe mutant mice lacking different K+ channel alleles for altered olivocerebellar circuit properties. Harmaline induced the characteristic 13‐Hz tremor in wildtype mice (WT); however, no tremor was observed in DKO suggesting that the ensemble properties of the olivocerebellar circuitry are altered in the absence of Kv3.1 and Kv3.3 subunits. Harmaline induced tremor in Kv3.1‐single mutants, but it was of smaller amplitude and at a lower frequency indicating the participation of Kv3.1 subunits in normal olivocerebellar system function. In contrast, harmaline tremor was virtually absent in Kv3.3‐single mutants indicating an essential role for Kv3.3 subunits in tremor induction by harmaline. Immunohistochemical staining for Kv3.3 showed clear expression in the somata and proximal dendrites of Purkinje cells and in their axonal projections to the deep cerebellar nuclei (DCN). In DCN, both Kv3.1 and Kv3.3 subunits are expressed. Action potential duration is increased by ≈ 100% in Purkinje cells from Kv3.3‐single mutants compared to WT or Kv3.1‐single mutants. We conclude that Kv3.3 channel subunits are essential for the olivocerebellar system to generate and sustain normal harmaline tremor whereas Kv3.1 subunits influence tremor amplitude and frequency.
Neonatal methamphetamine administration induces region‐specific long‐term neuronal morphological changes in the rat hippocampus, nucleus accumbens and parietal cortex
Authors: Williams Michael T. , Brown Russell W. , Vorhees Charles V. 
Published: June 2004

AbstractPrevious studies have demonstrated that rats exposed to methamphetamine (MA) during the neonatal period display deficits in spatial learning and memory. The underlying correlates are unknown; therefore, this study was devised to determine whether neuronal changes occur in the dentate gyrus (DG), nucleus accumbens (NAcc) and cortex of adult rats exposed to 10 mg/kg MA administered four times daily from P11–20 using Golgi–Cox staining [Gibb, R. & Kolb, B. (1998) J. Neurosci. Meth., 79, 1–4]. The DG and NAcc demonstrated a decrease in the number of spines per neuron and the NAcc showed an associated decrease in dendritic length. Selective changes in cortex were observed because increased dendritic length in the parietal cortex occurred with no change in the number of spines, and no differences were noted for either dendritic length or spines in the medial frontal cortex. The data suggest a potential cause for the learning and memory deficits induced by neonatal MA exposure; however, the underlying mechanism that produces these neuronal changes is unknown.
Status epilepticus in immature rats leads to behavioural and cognitive impairment and epileptogenesis
Authors: Kubová Hana , Mareš Pavel , Suchomelová Lucie , Brožek Gustav , Druga Rastislav , Pitkänen Asla 
Published: June 2004

AbstractIt remains under dispute whether status epilepticus (SE) in the perinatal period or early childhood or the underlying neuropathology is the cause of functional impairment later in life. The present study examined whether SE induced by LiCl–pilocarpine in normal immature brain (at the age of 12 or 25 days; P12 or P25) causes cognitive decline and epileptogenesis, and the data were compared to those of rats undergoing SE as adults. Rats in the P12 group had impaired memory (repeated exposure to open‐field paradigm) and emotional behaviour (lower proportion of open‐arm entries and higher incidence of risk assessment period in elevated plus‐maze) when assessed 3 months after SE, although not as severe as in the older age groups. Importantly, video‐electroencephalography monitoring 3 months after SE demonstrated that 25% of rats in the P12 and 50% in P25 group developed spontaneous seizures. Only nonconvulsive seizures (ictal activity in hippocampus accompanied by automatisms) were recorded in the P12 group whereas rats in the P25 group exhibited clonic convulsions. The present findings indicate that SE is harmful to the immature brain as early as P12, which might be compared with early infancy in humans.
Continuous cytosine‐b‐D‐arabinofuranoside infusion reduces ectopic granule cells in adult rat hippocampus with attenuation of spontaneous recurrent seizures following pilocarpine‐induced status epilepticus
Authors: Jung Keun‐Hwa , Chu Kon , Kim Manho , Jeong Sang‐Wuk , Song Young‐Mok , Lee Soon‐Tae , Kim Jin‐Young , Lee Sang Kun , Roh Jae‐Kyu 
Published: June 2004

AbstractBrief or prolonged seizures induce various patterns of plasticity. Axonal or dendritic remodelling and development of ectopic granule cells have been described in the hilus and molecular layer of the adult rodent hippocampus. Hippocampal cell proliferation also occurs after seizures. However, whether the seizure‐induced cell proliferation plays a pathological or reparative role in the epileptic brain is unknown. In this study, we attempted to suppress the seizure‐induced cell proliferation with the antimitotic agent cytosine‐b‐D‐arabinofuranoside (Ara‐C) and to examine the development of spontaneous recurrent seizures (SRS). Experimental status epilepticus was induced with pilocarpine, and Ara‐C or vehicle alone was infused continuously with an osmotic minipump. SRS were video‐monitored. BrdU immunohistochemistry was used for the spatial and temporal analysis of hippocampal cell proliferation, and double labelling with NeuN, calbindin and GFAP antibodies was performed for the differentiation of BrdU‐positive cells. Timm staining was also performed for evaluation of mossy fibre sprouting (MFS). With continuous Ara‐C infusion, the likelihood of developing SRS was decreased and, during the latent period, the development of ectopic granule cells in the hilus and new glia in the CA1 area was reduced when compared with the vehicle‐infused group, while MFS was not altered. The results suggest that the hippocampal cell proliferation plays a pro‐epileptogenic role rather than a compensatory role, and that the epileptogenic process may be associated with the generation of new glia in the CA1 area and/or new neurons in the dentate gyrus, particularly the ectopically located hilar granule cells.
The LIM homeobox gene, L3/Lhx8, is necessary for proper development of basal forebrain cholinergic neurons
Authors: Mori Tetsuji , Yuxing Zhang , Takaki Hiromi , Takeuchi Mayumi , Iseki Ken , Hagino Seita , Kitanaka Jun‐ichi , Takemura Motohiko , Misawa Hidemi , Ikawa Masahito , Okabe Masaru , Wanaka Akio 
Published: June 2004

AbstractBasal forebrain cholinergic neurons (BFCNs) are involved in cognitive functions such as learning and memory, and are affected in several neurodegenerative diseases (e.g. Alzheimer's disease). Despite their importance, the molecular mechanisms of their development are not fully elucidated. A recent report demonstrated that some BFCNs in adult rat are positive for L3/Lhx8, a LIM homeobox transcription factor. To examine the function of L3/Lhx8 in the development of BFCNs, we generated L3/Lhx8 gene‐disrupted mice. In these mice, cells expressing cholinergic neuron markers, such as choline acetyltransferase, vesicular acetylcholine transporter and p75 low‐affinity NGF receptor, were markedly reduced in the basal forebrain, whereas other cholinergic neurons including brain stem and spinal motor neurons expressed the markers. Neurotransmitter phenotypes other than cholinergic in the basal forebrain appeared intact. From these results, we suggested that L3/Lhx8 has a pivotal and specific role in the development and/or maintenance of BFCNs.
β‐Endorphin elevations in the ventral tegmental area regulate the discriminative effects of Δ‐9‐tetrahydrocannabinol
Authors: Solinas M. , Zangen A. , Thiriet N. , Goldberg S. R. 
Published: June 2004

Abstractβ‐Endorphin is an endogenous opioid that produces behavioral effects similar to heroin and morphine and is released in the nucleus accumbens by cocaine, amphetamine and ethanol, suggesting a general involvement in the reinforcing effects of abused drugs. Here we show that, in rats, Δ‐9‐tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, produces large increases in extracellular levels of β‐endorphin in the ventral tegmental area and lesser increases in the shell of the nucleus accumbens. We then used a two‐lever choice THC‐discrimination procedure to investigate whether THC‐induced changes in endogenous levels of β‐endorphin regulate the discriminative effects of THC. In rats that had learned to discriminate injections of THC from injections of vehicle, the opioid agonist morphine did not produce THC‐like discriminative effects but markedly potentiated discrimination of THC. Conversely, the opioid antagonist naloxone reduced the discriminative effects of THC. Bilateral microinjections of β‐endorphin directly into the ventral tegmental area, but not into the shell of the nucleus accumbens, markedly potentiated the discriminative effects of ineffective threshold doses of THC but had no effect when given alone. This potentiation was blocked by naloxone. Together these results indicate that certain psychotropic effects of THC related to drug abuse liability are regulated by THC‐induced elevations in extracellular β‐endorphin levels in brain areas involved in opiate reward and reinforcement processes.
S1P and LPA trigger Schwann cell actin changes and migration
Authors: Barber Siân C. , Mellor Harry , Gampel Alex , Scolding Neil J. 
Published: June 2004

AbstractThe processes by which a Schwann cell (SC) migrates towards, wraps around and, in some cases, myelinates an axon are incompletely understood. The complex morphological rearrangements involved in these events require fundamental changes in the actin cytoskeleton. Sphingosine 1‐phosphate (S1P) and lysophosphatidic acid (LPA) are two modulators of the actin cytoskeleton, and receptors for these signalling lipids are expressed on SCs at the time of differentiation. Previous work has revealed a role for LPA in SC survival, morphology and differentiation, but the effects of S1P have received less attention. Here we show that S1P and LPA both cause major rearrangements to the actin cytoskeleton in primary rat SCs and the SCL4.1/F7 rat SC line. S1P and LPA caused formation of lamellipodia and a circular geodesic actin network. We also show that S1P and LPA increased cell migration. The small GTPases RhoA and Rac1 were both activated by S1P/LPA treatment, but the actin rearrangements were dependent on Rac1 and not RhoA. These effects of S1P/LPA could be mimicked by SCL4.1/F7 cell‐conditioned medium, which was found to contain S1P. Reduction in cellular synthesis of S1P by adding the sphingosine kinase inhibitor dimethyl sphingosine during medium conditioning reduced the ability of conditioned medium to cause actin rearrangements. These results support a role for S1P as an autocrine signal regulating the actin cytoskeleton during Schwann cell development.
Brain‐derived neurotrophic factor signaling modifies hippocampal gene expression during epileptogenesis in transgenic mice
Authors: Lähteinen Sari , Pitkänen Asla , Knuuttila Juha , Törönen Petri , Castrén Eero 
Published: June 2004

AbstractBrain‐derived neurotrophic factor (BDNF) regulates neuronal survival, differentiation and plasticity. It has been shown to promote epileptogenesis and transgenic mice with decreased and increased BDNF signaling show opposite alterations in epileptogenesis. However, the mechanisms of BDNF action are largely unknown. We studied the gene expression changes 12 days after kainic acid‐induced status epilepticus in transgenic mice overexpressing either the functional BDNF receptor trkB or a dominant‐negative truncated trkB. Epileptogenesis produced marked changes in expression of 27 of 1090 genes. Cluster analysis revealed BDNF signalling‐mediated regulation of functional gene classes involved in cellular transport, DNA repair and cell death, including kinesin motor kinesin family member 3A involved in cellular transport. Furthermore, the expression of cytoskeletal and extracellular matrix components, such as tissue inhibitor of metalloproteinase 2 was altered, emphasizing the importance of intracellular transport and interplay between neurons and glia during epileptogenesis. Finally, mice overexpressing the dominant‐negative trkB, which were previously shown to have reduced epileptogenesis, showed a decrease in mRNAs of several growth‐associated genes, including growth‐associated protein 43. Our data suggest that BDNF signaling may partly mediate the development of epilepsy and propose that regrowth or repair processes initiated by status epilepticus and promoted by BDNF signaling may not be as advantageous as previously thought.
Clock gene mRNA and protein rhythms in the pineal gland of mice
Authors: Karolczak Magdalena , Burbach Guido J. , Sties Gabriele , Korf Horst‐Werner , Stehle Jörg H. 
Published: June 2004

AbstractIn vertebrates, the rhythmic transcription of clock genes, regulated by their own gene products, provides the basis for self‐sustaining circadian clockworks. These endogenous clocks are lost in most mammalian tissues, but not in the central pacemaker of the hypothalamic suprachiasmatic nucleus (SCN). An interesting model system to understand this phylogenetic shift in function of clock gene products is the rodent pineal gland, as its intrinsic clockwork was replaced during evolution by an input‐dependent oscillator. By means of immunohistochemistry, immunoblotting and real time PCR, we investigated the day/night expression profiles of all major clock genes and their products in the pineal gland of one melatonin‐proficient and one melatonin‐deficient mouse strain. All clockwork elements known to be indispensable for a sustained rhythm generation in the SCN were also found in the pineal organ of both mouse strains. Only mPer1 mRNA and PER1 protein accumulation coincides with timecourses of many other pineal genes and their products, which are cyclicAMP inducible. Here, presented data together with the known mechanisms for regulation of the mPer1 gene in the rodent pineal gland forward the idea that in this tissue PER1 may have a trigger function for initiating the cycles of the clockwork's transcriptional/translational feedback loops.