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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophoretic variants of two carbonic anhydrase enzymes CAR-1 (CA I) and Car-2 (CA II), have been found in the laboratory mouse, Mus musculus. These two loci are closely linked to each other and are located on chromosome 3 near its centromere. The close linkage of Car-1 and Car-2 supports the hypothesis that the present-day carbonic anhydrase loci are the result of tandem duplication of an earlier carbonic anhydrase locus with subsequent divergence. The red blood cells of mice of the subspecies M.m. casteneus have significantly reduced levels of CAR-1 and CAR-2.
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PMID:Evolution of mammalian carbonic anhydrase loci by tanden duplication: close linkage of Car-1 and Car-2 to the centromere region of chromosome 3 of the mouse. 82 6

Long-term potentiation is a long-lasting, use-dependent increase in the strength of synaptic connections. We investigated the role of nitric oxide (NO) in determining the duration of potentiation induced by high frequency stimulation of afferents in the CA1 region of the rat hippocampus. The calcium/calmodulin-dependent production of NO can be initiated by activation of excitatory amino acid receptors and results in increased levels of cGMP in target cells. Here we report that only a relatively short-term potentiation can be induced in the presence of nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. The effects of L-NAME on the duration of potentiation are partially reversed by coadministration of L-arginine, a precursor of neuronal NO, and by dibutyryl cGMP. Hemoglobin, which binds extracellular NO, also shortens the duration of stimulus-induced potentiation. The results suggest a role for NO in the maintenance of activity-dependent synaptic enhancements, possibly via the generation of cGMP.
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PMID:The role of nitric oxide in hippocampal long-term potentiation. 137 Dec 16

We assessed the effect of NG-Nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, on the hippocampal lesions induced either by the focal injection of N-methyl-D-aspartate (NMDA) or (s)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (s-AMPA) or by 10 min of severe forebrain ischaemia (4-vessel occlusion), in the rat. We find that L-NAME, 20 or 40 mg kg-1, selectively decreases NMDA-induced CA1 lesions while it has no effect on AMPA toxicity. L-NAME, 20 mg kg-1, does not decrease hippocampal damage induced by ischaemia. These results suggest that NO contributes to NMDA toxicity and support data indicating that NMDA receptor antagonists fail to protect against hippocampal CA1 lesions in the 4-vessel occlusion model.
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PMID:Effect of NO synthase inhibition on NMDA- and ischaemia-induced hippocampal lesions. 138 61

The neurotoxin kainic acid (KA) was iontophoretically administered to the dorsal hippocampus of female rats. Depending upon the diameter of the micropipette used to administered KA, this treatment completely depleted the dorsal hippocampus of nerve cell bodies (group LHC, N = 8) or selectively depleted CA4 (group SHC, N = 7) while sparing significant numbers of cells in CA1-CA3, and the fascia dentata. In both experimental groups, there was no apparent damage to the fimbria/fornix system, the ventral hippocampus and subiculum or neocortex adjacent to the injection site. The extensive neuron depletion (group LHC) sharply impaired the acquisition of a CAR in a shuttle box, produced a passive avoidance deficit in a step-through situation (but not in a punished-licking test), facilitated acquisition of a brightness discrimination in a T-maze, but had no significant effect on reversal learning in this situation. The more limited neuron depletions produced in group SHC produced no effect on CAR acquisition in the shuttle box but resulted in similar, though typically smaller effects in all other situations. The pronounced differences between this pattern of behavior change and that consistently reported after traditional lesions of the dorsal hippocampus indicate that damage to fibers of passage may contribute significantly to the classic hippocampal lesion syndrome.
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PMID:Spatial discrimination, reversal and active or passive avoidance learning in rats with KA-induced neuronal depletions in dorsal hippocampus. 724 6

As a known vasodilator, nitric oxide (NO) probably acts by hyperpolarizing smooth muscle by increasing K conductance (GK). Therefore NO could mediate the anoxic hyperpolarizations of brain neurons that are also mediated by GK. We investigated this question by recording from CA1 neurons in submerged hippocampal slices (from rats), kept at 33 degrees C. Incubation with the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 200 microM) had no significant effect on CA1 population spikes (delta = 2.5%, SEM +/- 3.1%, n = 7) or on the time course of their suppression by brief exposure to anoxia (2-3 min). In intracellular recordings, L-NAME did not change the resting membrane potential or input resistance (n = 10). In the presence of L-NAME, anoxic changes were not significantly different: the cells were hyperpolarized by 6.4 +/- 0.74 mV (6.3 +/- 0.82 mV for controls) and their resistance decreased by 16 +/- 3.2% (18 +/- 1.4% for controls, n = 10). In whole-cell recordings from another 15 cells (clamped at approximately -50 mV, near resting level), L-NAME also had no consistent effect on input conductase (GN) or holding current (IH); and the anoxic increased in GN were unchanged (44 +/- 12% before and 48 +/- 20% after, for n = 10). Thus NO does not appear to be a significant element in the mechanism of membrane and synaptic changes during brief anoxia in CA1 neurons in slices.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide may be a mediator of effects of prolonged but not brief anoxia in CA1 neurons in slices. 762 65

At room temperature (23 degrees C-25 degrees C), the induction of long-term potentiation (LTP) in area CA1 of slices from young male Sprague-Dawley rats was depressed by preincubation with the nitric oxide synthase inhibitors NG-nitro-L-arginine (L-NA, 100 microM) and NG-nitro-L-arginine methyl ester (L-NAME, 100 microM). The D isomers were ineffective under the same conditions. Hemoglobin (20 microM) reduced but did not completely block LTP. Neither L-NA (at concentrations up to 1 mM) nor hemoglobin (20 microM) had any significant effect on LTP in slices from adult rats at room temperature, or in young rats at 29 degrees C-30 degrees C. These results suggest that nitric oxide is unlikely to play a role in the induction of LTP under physiological conditions.
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PMID:The suppression of long-term potentiation in rat hippocampus by inhibitors of nitric oxide synthase is temperature and age dependent. 769 1

In whole-cell recordings from CA1 neurons, net outward currents (at ca. -20 mV, from VH ca. -50 mV) were 40-50% depressed by sodium nitroprusside (100-500 microM) or L-arginine (L-ARG; 50-200 microM), but not by D-arginine (100 microM). The NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 200 microM) restored the L-ARG-depressed current to ca. 80% of control. In naive cells, L-NAME increased outward currents by 45 +/- 12.6%; the enhanced currents were then reduced by adding L-ARG (200-400 microM). The NO-sensitive current is Ca-dependent, because L-NAME and L-ARG were ineffective in Mn/low Ca medium or when electrodes contained 2.2 mM EGTA. Since high voltage-activated Ca-currents were unaltered by L-NAME, we conclude that NO tonically enhances excitability in slices by depressing a voltage- and calcium-dependent (IK(Ca)-type) outward current.
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PMID:Nitric oxide tonically depresses a voltage- and Ca-dependent outward current in hippocampal slices. 883 Mar 13

Adult rats treated IP with domoic acid at 0, 0.22, 0.65, or 1.32 mg/kg were tested for passive avoidance (PA), auditory startle (AS), or conditioned avoidance (CAR) behaviors. Clinical signs were observed only at the 1.32 mg/kg dose level. Within 24 h of dosing, rats surviving a dose of 1.32 mg/kg exhibited transient decreased body weight and exaggerated AS responding. Startle latency and habituation, PA, and CAR were not affected. Examination of brains from six rats per group revealed a subset (2/6) of animals receiving 1.32 mg/kg domoic acid with degenerating neurons in the hippocampal CA1/CA3 subregions and gliosis. The decreased body weight and increased startle suggest a hyperreactivity syndrome possibly related to neuronal degeneration in the hippocampus. In a separate experiment, domoic acid at an IP dose of 0.93 mg/kg was found to produce hypomotility in addition to a decrease in body weight. Both effects were reduced by pretreatment with scopolamine (2 mg/kg), but not with caffeine (30 mg/kg), indicating a possible cholinergic involvement in domoate's toxicity.
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PMID:Domoic acid: neurobehavioral and neurohistological effects of low-dose exposure in adult rats. 894 43

We investigated the effects of age and nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on protein kinase C (PKC), adenylyl cyclase, calcium/calmodulin-independent cyclic-AMP phosphodiesterase (cyclic-AMP PDE) and voltage-dependent L-type calcium channels in Fischer rat brain using autoradiography. [3H]Phorbol 12,13-dibutyrate (PDBu), [3H]forskolin, [3H]rolipram and [3H]PN200-110 were used to label PKC, adenylyl cyclase, cyclic-AMP PDE and calcium channels, respectively. [3H]Forskolin binding significantly decreased in the striatum, hippocampal CA3 sector, dentate gyrus, hilus, thalamus, substantia nigra and cerebellum of 24-month-old (aged) rats, as compared with 6-month-old (adult) animals. [3H]Rolipram binding also showed an age-related reduction in the thalamus and cerebellum in rats. In contrast, no age-related changes were observed in [3H]PDBu and [3H]PN200-110 binding in the rat brain. Chronic treatment with L-NAME (5 mg/kg, once a day for 4 weeks) showed no significant changes in [3H]PDBu, [3H]rolipram and [3H]PN200-110 binding in aged rat brains. However, this treatment significantly increased age-related decreases in [3H]forskolin binding in the frontal cortex; striatum and hippocampal CA1 sector in rats. The results demonstrate that [3H]forskolin binding in the rat brain is more susceptible to aging processes than [3H]PDBu, [3H]rolipram and [3H]PN200-110 binding. Furthermore, our study shows that chronic treatment with NO inhibitor increases the age associated changes in [3H]forskolin binding in most brain areas of aged rats. These findings suggest that NO may play a key role in the regulation of adenylyl cyclase system during aging processes.
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PMID:Effect of nitric oxide synthase inhibitor on age-related changes in second messenger systems and calcium channels in rats. 910 40

The role of nitric oxide in cerebral insults remains controversial. While numerous studies have used models of ischaemia and hypoxia, few have examined nitric oxide in the kainate model of excitotoxicity. Kainate (10 mg/kg) was administered to rats via the intraperitoneal (i.p.) route to induce submaximal damage to the CA1, CA2 and CA3a regions of the hippocampus after 7 days. Systemic injections of the nitric oxide synthase (NOS) inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), both at a dose of 5 mg/kg, reduced cell death in all three regions. As 7-NI selectively inhibits the neuronal form of NOS, this study suggests that nitric oxide produced from a neuronal and not epithelial source may contribute to neuronal damage in this model.
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PMID:Nitric oxide synthase inhibitors L-NAME and 7-nitroindazole protect rat hippocampus against kainate-induced excitotoxicity. 968 20


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