Hadron production in e+e- annihilation at sqrt s =29 GeV.
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Biomedical subjects
Publications and source records attributed to H Neal.
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An automated technique for the continuous analysis of different frequency bands of the electrocorticogram (ECoG) of the rat has been used to quantify the actions of phencyclidine (PCP) and various other stimulant drugs. It has been demonstrated that phencyclidine, etoxadrol and LY154045 produced similar changes in the individual frequency bands whereas amphetamine and apomorphine had different profiles of activity. The phencyclidine-like compounds exhibited extremely strong stimulation of the ECoG with very large increases recorded in high frequency (15-50 Hz) activity and reductions in all other frequency bands. Various compounds have been used in an attempt to antagonise the changes in the ECoG. Chlorpromazine caused a slight shift in the dose-response curves as did chlordiazepoxide when used with phencyclidine. The GABA agonists, THIP and muscimol, had no effect on the stimulation of the ECoG. In contrast another presumed GABA agonist, baclofen, proved to be the most effective agent for blocking the stimulation induced by phencyclidine. The role of the GABAB receptor in the action of phencyclidine is discussed.
The effects of drugs modifying GABAergic neurotransmission have been examined on ponto-geniculo-occipital (PGO) waves induced in the encéphale isolé cat by reserpine (PGOres), Ro4-1284 (PGO1284) or PCPA (PGOPCPA). The GABA agonists muscimol and THIP both caused large increases in density of PGOPCPA. The PGO1284 and PGOres were less affected although, of these, a larger increase in PGO1284 density was recorded. None of the increases could be reversed by subsequent injection of bicuculline. Chlordiazepoxide brought about large increases in PGOPCPA density but was ineffective in altering PGOres or PGO1284. The GABA transaminase inhibitor gamma-acetylenic GABA increased the density of all PGO waves but was not effective in the case of PGOPCPA. These results confirm a role for GABA in modulating PGO activity. The pathways involved in this GABA modulation are discussed.
Electrocortical activity was recorded in encéphale isolé rats during injection of various dopaminergic compounds into the caudate nucleus. Slow waves and spindles were observed following injection of compounds with different mechanisms of action in stimulating the dopamine receptor. Some arylalkylamine analogues also induced similar electrocortical changes, whereas others were inactive. The possible dopamine agonist activities of these compounds are discussed. The results support an involvement of dopamine in the production of electrocortical slow waves and spindles.
The effects of electrical and chemical stimulation of brain areas known to contain dopaminergic cell bodies or terminals on electrocortical activity have been studied in the encéphale isolé rat. Electrical stimulation of medial basal midbrain areas with single stimuli resulted in a single evoked spindle but stimulation of more lateral areas resulted in the appearance of slow waves and spindling. These effects were blocked or reduced by prior treatment with 6-hydroxydopamine. Electrical stimulation of the caudate nucleus also produced a single evoked spindle. Local injection of dopamine into the caudate nucleus induced spindling, with higher doses also resulting in slow waves. Electrical stimulation of the basal forebrain brought about slow waves, an effect which was also seen following injection of dopamine into this area. It appears that electrical stimulation of certain brain areas produces similar effects to those produced by the injection of dopamine. This suggests the involvement of dopaminergic pathways in the production of cortical spindling and slow waves and also the involvement of neurones of both limbic and striatal systems.
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The effects of various opiate compounds have been studied on the electrocorticogram (ECoG) of the rat following local injection into various brain areas. Injections of all compounds studied into both the caudate-putamen and the basal forebrain, in particular the olfactory tubercles, induced changes in the ECoG. Injections of saline vehicle into these areas were ineffective as were injections of morphine into the corpus callosum. Potency was etorphine greater than morphine = codeine greater than thebaine. Naloxone alone was inactive following injection but if combined with morphine markedly attenuated the normal morphine response and reversed the morphine response if injected following morphine. The endogenous opiate compound enkephalin and the synthetic analogue D-ala2-met5-encamide also induced electrocortical changes which were naloxone sensitive. The results are similar to those following systemic administration of opiates. It is possible that the areas studied represent the site of action of systemically applied opiates. It is suggested that the opiates and enkephalins produce their actions by acting at the same site. Since the areas studied are rich in dopaminergic terminals an interaction may exist between dopaminergic and opiate mechanism to bring about the observed changes.