24 research outputs found
Neuropeptide Y (18–36) modulates chromaffin cell catecholamine secretion by blocking the nicotinic receptor ion
or Poiuu.cowcy AND ExP iuME rr.u. THERAPEuTIC
Nuclear energy in the public sphere: Anti-nuclear movements vs. industrial lobbies in Spain (1962-1979)
The final publication is available at Springer via http://dx.doi.org/10.1007/s11024-014-9263-0This article examines the role of the Spanish Atomic Forum as the
representative of the nuclear sector in the public arena during the golden years of the
nuclear power industry from the 1960s to 1970s. It focuses on the public image
concerns of the Spanish nuclear lobby and the subsequent information campaigns
launched during the late 1970s to counteract demonstrations by the growing and
heterogeneous anti-nuclear movement. The role of advocacy of nuclear energy by
the Atomic Forum was similar to that in other countries, but the situation in Spain
had some distinguishing features. Anti-nuclear protest in Spain peaked in 1978
paralleling the debates of a new National Energy Plan in Congress, whose first draft
had envisaged a massive nuclearization of the country. We show how the approval
of the Plan in July 1979, with a significant reduction in the nuclear energy component,
was influenced by the anti-nuclear protest movements in Spain. Despite the
efforts of the Spanish Atomic Forum to counter its message, the anti-nuclear
movement was strengthened by reactions to the Three Mile Island accident in March
1979
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Neurochemical consequences of status epilepticus induced in rats by coadministration of lithium and pilocarpine
Status epilepticus was produced in rats by administering pilocarpine (30 mg/kg, s.c.) 16 h after treatment with LiCl (3 meq/kg, i.p.). After 35 min of status epilepticus, several parameters of cholinergic activity were measured. Seizures had no effect on the
in vivo concentration of acetylcholine or choline in cerebellum, cortex, hippocampus, or striatum. Synaptosomal high-affinity choline transport was also not changed by seizures in hippocampus, cortex, or striatum. Cortical slices from seizing rats had elevated concentrations of acetylcholine and released acetylcholine at a greater rate than did controls, but these effects seemed to be due to a reduction in the postmortem hydrolysis of acetylcholine. Synaptosomal
45calcium uptake during 2 to 60 s of incubation was no different from control rates in tissue prepared from seizing rats. These results indicate that presynaptic cholinergic activity is not markedly altered by 35 min of continuous seizure activity induced by lithium and pilocarpine. In contrast, the
in vivo concentration of cyclic guanosine 5′-monophosphate was elevated above control values in seizing rats by 57 to 170% in cerebellum, cortex, hippocampus, and striatum
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Effects of drugs on the initiation and maintenance of status epilepticus induced by administration of pilocarpine to lithium-pretreated rats
The ability of various drugs to prevent the onset of status epilepticus induced by administration of the muscarinic agonist, pilocarpine, to lithium-pretreated rats was determined. Motor limbic seizures and status epilepticus occurred in 100% of rats administered pilocarpine (30 mg/kg, s.c.) 20 h after pretreatment with lithium (3 meq/kg, i.p.). The latency to spike activity and to status epilepticus was 20 ± 1 min and 24 ± 1 min, respectively. Atropine, diazepam, phenytoin, carbamazepine, phenobarbital, paraldehyde, and
l-phenylisopropyladenosine (
l-PIA) prevented all phases of seizure activity induced by lithium/pilocarpine treatment. The initiation of status epilepticus was significantly prolonged by pretreatment with sodium valproate. These findings indicate that the seizures induced by administration of lithium and pilocarpine accurately model generalized tonic-clonic epilepsy. The anticonvulsant activity of
l-PIA was prevented by prior treatment with the adenosine antagonist, theophylline. The latency to spike and seizure activity was decreased by theophylline, indicating that endogenous adenosine may have a tonic inhibitory influence on cholinergic neurons. Atropine, diazepam, phenobarbital, phenytoin, sodium valproate,
l-PIA, and carbamazepine did not interrupt seizure activity when administered 60 min after pilocarpine (approximately 35 min after initiation of status epilepticus). When rats were administered paraldehyde at this time, status epilepticus was rapidly terminated and all rats survived. Thus, status epilepticus induced by lithium and pilocarpine provides a seizure model that is not responsive to conventional anticonvulsants
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Characterization of lithium potentiation of pilocarpine-induced status epilepticus in rats
Subcutaneous administration of pilocarpine to rats that were pretreated with a small dose of lithium chloride results in the evolution of generalized convulsive status epilepticus. The production of status epilepticus is absolutely reproducible, has a very consistent time to onset (22 min), has a duration of several hours, and is extremely severe with a high mortality rate. Experimental results show that this animal model of status epilepticus: (i) requires activation of muscarinic receptors because the initiation of seizures is blocked by atropine; (ii) requires presynaptic cholinergic activity because it is attenuated by hemicholinium-3; (iii) recruits noncholinergic cells because when status epilepticus is established it is not altered by atropine administration; and (iv) is blocked by pretreatment with diazepam and ongoing seizures are terminated by administration of diazepam, similar to certain forms of status epilepticus in humans. The reproducibility, prolonged nature, and involvement of a clearly defined neurochemical system as the triggering mechanism, i.e., cholinergic activation, makes this a potentially valuable animal model of generalized convulsive status epilepticus
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Status epilepticus is produced by administration of cholinergic agonists to lithium-treated rats: Comparison with kainic acid
Electroencephalographic techniques were used to study generalized convulsive status epilepticus induced by administration of subconvulsive doses of cholinomimetics (e.g., pilocarpine) to rats pretreated with lithium chloride. Status epilepticus induced by this treatment was compared with status epilepticus induced by kainic acid. Lithium/pilocarpine-induced status epilepticus developed within 10 min of initial paroxysmal spike activity, 24 ± 1 min (
N = 20) after administration of pilocarpine, and continued uninterrupted for more than 3 h. Kainic acid (10 mg/kg)-induced status epilepticus developed approximately 60 min after initial spike activity, 96 ± 3 min (
N = 7) after kainate administration, and continued for 0.5 h. Thus, the interval of intermittent seizure activity and the duration of status epilepticus differed markedly between these two models. The potentiation by lithium (3 meq/kg) of the convulsant effect of cholinergic agonists was found to be 10 to 13-fold for two direct-acting cholinomimetics, pilocarpine and arecoline, whereas the convulsant effect of the indirectacting agonist, physostigmine, was potentiated by 50%. The full proconvulsant effect of lithium lasted from 2 to 24 h after a single acute treatment (3 meq/kg). The dose response of the proconvulsant effect of lithium was determined and the EC
50 of lithium was approximately 1.5 meq/kg when pilocarpine (30 mg/kg) was administered 20 h later. Chronic treatment with lithium for 4 weeks potentiated the convulsant effect of pilocarpine by more than 26-fold. These results demonstrated that both acute and chronic administration of lithium enhance cholinergic function
in vivo. Potentiation of cholinergic function by lithium may play a role in the therapeutic action of lithium in affective disorders