| 1. |
- Blomqvist, Photjanee, et al.
(författare)
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Lesions of the locus coeruleus system aggravate ischemic damage in the rat brain
- 1985
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 58:3, s. 353-358
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Tidskriftsartikel (refereegranskat)abstract
- The possibility that the noradrenergic locus coeruleus system influences brain damage following ischemia was explored in rats. Bilateral lesions of the locus coeruleus projections to the forebrain aggravated the neuronal necrosis in the hippocampal CAI region and neocortex following complete cerebral ischemia induced by transient cardiac arrest. These findings provide evidence that the postischemic activation of the inhibitory locus coeruleus system could counteract a possible detrimental neuronal hyperexcitation, thereby limiting neuronal necrosis.
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| 2. |
- Ekström, Peter, et al.
(författare)
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The left habenular nucleus contains a discrete serotonin-immunoreactive subnucleus in the coho salmon (Oncorhynchus kisutch)
- 1988
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 91:2, s. 121-125
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Tidskriftsartikel (refereegranskat)abstract
- By use of antibodies against serotonin, a discrete subnucleus of putatively serotoninergic neurons was observed in the dorsal subdivision of the left habenular nucleus in the brain of the coho salmon. The subnucleus was observed in salmon of different life-stages: in fingerlings, during smolt transformation, after smolt transformation (in seawater), and after spawning. This finding further emphasizes the close relationship between the pineal organ and the habenular nuclei not only in terms of topographical proximity but also in terms of cytological similarities: cells of the habenular nucleus and the pineal complex have previously been shown to be immunoreactive also with antibodies directed against retinal phototransduction proteins [5]. It also underlines the asymmetric organization of the epithalamic region.
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| 3. |
- Hardebo, Jan Erik, et al.
(författare)
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Origins of substance P- and calcitonin gene-related peptide-containing nerves in the internal carotid artery of rat
- 1989
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 101:1, s. 39-45
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Tidskriftsartikel (refereegranskat)abstract
- An aggregation of substance P (SP)- and calcitonin gene-related peptide (CGRP)-containing nerve cells (internal carotid mini-ganglion) is described at the junction between the greater superficial petrosal nerve and the internal carotid nerve close to the internal carotid artery. A retrograde tracer dye technique demonstrates that this ganglion and the trigeminal and superior vagal ganglia supply the internal carotid artery with SP/CGRP fibers at, above and below this level, respectively. Implications of this finding for cranial painful syndromes in man are discussed.
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| 4. |
- Magnusson, Kerstin, et al.
(författare)
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Impairment of protein ubiquitination may cause delayed neuronal death
- 1989
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 96:3, s. 264-270
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Tidskriftsartikel (refereegranskat)abstract
- The hippocampus is a brain structure specifically vulnerable to short periods of transient cerebral ischemia, and which displays delayed neuronal necrosis. Protein ubiquitination is a posttranslational modification of proteins and an important factor in heat shock response and a regulator of ATP-dependent protein degradation. Using affinity purified antibodies against ubiquitin and ubiquitin-protein conjugates we have found that the ubiquitin immunoreactivity (UIR), normally present in all neurons of the hippocampus, disappears in the early recirculation period following cerebral ischemia from all hippocampal cells except the interneurons. Later UIR reappears in the different hippocampal regions over a 72 h period in the following order: granule cells-CA3 pyramidal cells-CA2 pyramidal cells. This is the inverse order of sensitivity of these cells to ischemia. The UIR never recovers in the CA1 pyramidal neurons where a 95% neuronal necrosis is seen following three days of recovery. We propose that the loss of UIR in the pyramidal neurons in the CA1 region signifies a persistent impairment of protein ubiquitination, and thus a change in the turnover of structural and regulatory proteins, which could be an essential part of the mechanism of slow neuronal death following cerebral ischemia.
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| 5. |
- Owman, Christer, et al.
(författare)
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Chronic nicotine treatment eliminates asymmetry in striatal glucose utilization following unilateral transection of the mesostriatal dopamine pathway in rats
- 1989
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Ingår i: Neuroscience Letters. - 0304-3940. ; 102:2-3, s. 279-283
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Tidskriftsartikel (refereegranskat)abstract
- Partial hemitransection was performed through a knife lesion at the meso-diencephalic level in rats to sever the mesostriatal dopamine system. During the subsequent 2 weeks the animals received 0.125 mg/kg/h of nicotine continuously via an osmotic minipump implanted s.c. To achieve prompt high nicotine levels, 4 i.p. injections of 0.5 mg/kg nicotine were, in addition, given during the first 2 h following the lesion. The total treatment corresponded to a mean plasma level of 50 ng/ml nicotine, measured at the end of the experiment. Control animals received corresponding volumes of 0.9% saline. Quantitative autoradiographic analysis of the glucose utilization in the caudate nucleus using Sokoloff's [14C]2-deoxyglucose method demonstrated a 16% side-to-side difference in the lesioned control animals, whereas the asymmetry was counteracted by the nicotine treatment. Although there was an overall tendency to a lower rate of glucose utilization (by 6%) in the nicotine-treated animals compared to the controls receiving saline only, the difference was not statistically significant. The eliminated asymmetry probably reflects an increased survival of the dopamine neurons and/or of striatal nerve cells on the lesioned side due to protective effects of nicotine resulting from desensitization of nicotinic-type cholinergic receptors following continuous administration of the drug.
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| 6. |
- Suzuki, Norihiro, et al.
(författare)
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Galanin-positive nerves of trigeminal origin innervate rat cerebral vessels
- 1989
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Ingår i: Neuroscience Letters. - 0304-3940. ; 100:1-3, s. 123-129
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Tidskriftsartikel (refereegranskat)abstract
- (GAL)-positive nerve fibers in rat cerebral vessels were demonstrated by immunohistochemistry, and their origin in the trigeminal ganglia and pathway in the nasociliary nerve to the vessels was shown by retrograde tracer technique and nerve transection. Some fibres in the vertebrobasilar system appear to originate in extracranial sources. With the antiserum used only few GAL fibers could be seen in the vessels, mostly in the vertebrobasilar system. In neonatally sympathectomized animals a rich network could be visualized in most pial arteries - still particularly in the vertebrobasilar system - probably as a result of a diminished competition for nerve growth factor. No vasomotor effect of GAL could be detected in isolated segments of pial arteries, neither in normal nor in sympathectomized animals, which rules out a direct postsynaptic effect on vascular tone. GAL did not display prejunctional modulatory action on the adrenergic nerves present in the vascular preparations. A sensory function of GAL is discussed.
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| 7. |
- Tossman, Ulf, et al.
(författare)
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γ-aminobutyric acid and taurine release in the striatum of the rat during hypoglycemic coma, studied by microdialysis
- 1985
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Ingår i: Neuroscience Letters. - 0304-3940. ; 62:2, s. 231-235
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Tidskriftsartikel (refereegranskat)abstract
- Extracellular levels of striatal γ-aminobutyric acid (GABA) and taurine were monitored during insulin-induced hypoglycemia using microdialysis. At the onset of isoelectricity in the electroencephalogram (EEG), a transient 5-fold increase in the levels of GABA occurred. Taurine levels increased 5 min following the onset of isoelectricity and continued to increase during the entire isoelectric period. The results demonstrate that events associated with the onset of isoelectricity during hypoglycemia trigger an increase in extracellular concentrations of GABA and taurine. The discrepancy in time-course of these changes may reflect differences in compartmentation, function and metabolism of the two amino acids.
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| 8. |
- Westerberg, Eva, et al.
(författare)
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Excitatory amino acid receptors and ischemic brain damage in the rat
- 1987
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 73:2, s. 119-124
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Tidskriftsartikel (refereegranskat)abstract
- The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [3H]AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no change was noted in the N-methyl-d-aspartate or kainic acid binding sites over this time period.
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| 9. |
- Wieloch, T., et al.
(författare)
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Lesions of the glutamatergic cortico-striatal projections in the rat ameliorate hypoglycemic brain damage in the striatum
- 1985
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 58:1, s. 25-30
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Tidskriftsartikel (refereegranskat)abstract
- Unilateral ablations of the motor cortex were performed on rats. One to two weeks following the ablation they were subjected to 30 min of reversible insulin-induced hypoglycemic coma. The levels of glutamate, aspartate, γ-aminobutyric acid (GABA), taurine, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and phosphocreatine (PCr) were determined in frozen tissue sections from the superior half of the caudate nucleus. The lesions induced a specific reduction in the levels of glutamate by approx. 10% in the dorsal caudate nucleus ipsilateral to the lesion, while no significant differences in the levels of aspartate, GABA, taurine, ATP, ADP, AMP or PCr were noted. Neuronal necrosis in the caudate nucleus in animals subjected to 30 min of insulin-induced hypoglycemic coma and one week recovery was assessed by light microscopy. Contralateral to the lesion, extensive neuronal necrosis, mainly affecting small and medium-sized neurons, was observed in the dorsal and lateral caudate nucleus. In the caudate ipsilateral to the lesion a complete amelioration of necrosis was noted in areas subjacent to the lesion. The data suggest that hypoglycemic brain damage is induced by excitotoxins such as glutamate or related compounds.
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| 10. |
- Hagberg, Henrik, 1955, et al.
(författare)
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Extracellular overflow of glutamate, aspartate, GABA and taurine in the cortex and basal ganglia of fetal lambs during hypoxia-ischemia.
- 1987
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Ingår i: Neuroscience letters. - 0304-3940. ; 78:3, s. 311-7
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Tidskriftsartikel (refereegranskat)abstract
- Extracellular levels of excitatory and inhibitory amino acids were measured in the cortex and striatum of asphyxiated fetal lambs. The fetus was exteriorized from the anesthetized ewe and dialysis probes were placed in the parietal cortex and caudate nucleus. Cerebral blood flow was measured with Xe-clearance. Cortical somatosensory-evoked potentials and electroencephalogram (EEG) were continuously recorded. Asphyxia was induced by clamping the umbilical cord or by graded compression of the maternal aorta. Asphyxia accompanied by elevated cerebral blood flow resulted in a moderate rise in extracellular amino acid levels. During extreme asphyxia, i.e. abolished evoked potentials and reduced cerebral blood flow, marked extracellular elevations of glutamate (3- to 11-fold), aspartate (3- to 7-fold), gamma-aminobutyric acid (GABA) (3- to 5-fold) and taurine (3- to 18-fold) occurred, the higher values representing striatum. Excessive levels of excitatory amino acids may exert injurious effects on immature neurons during such hypoxic-ischemic states.
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