Further studies on the action of adrenergic drugs on cortical activity

Baust, W; Niemczyk, H.

doi:10.1016/0013-4694(64)90127-0

Cited by 22 publications

(8 citation statements)

References 16 publications

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“…Consequently, the role of the locus coeruleus and noradrenergic system in ECoG activation may be an indirect one that is mediated by the cholinergic basal forebrain system. There is ample evidence to suggest that ACh, but not noradrenaline (Baust et al 1963;Baust and Niemczyk 1964), produces LVFA by a direct action in cortex (Kanai and Szerb 1965;Cuculic et al 1968;Spehlmann and Norcross 1982;Casamenti et al 1986;Metherate and Ashe 1991;Metherate et al 1992), supporting the distinction between direct and indirect cortical activation just outlined.…”

Section: Discussionmentioning

confidence: 93%

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

1997

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The present experiments examined the central systems which mediate the electrocorticographic activation induced by electrical stimulation of forebrain and midbrain areas known to play a role in cerebral activation. In urethane-anesthetized rats, 100-Hz electrical stimulation of the amygdaloid cmplex or dorsal raphe changed neocortical electrocorticographic activity from large irregular slow activity (LISA; 1-6 Hz, up to 2 mV) to low voltage fast activity (LVFA; less than 0.5 mV, including frequencies above 10 Hz). The LVFA during amygdala stimulation, but not that during dorsal raphe stimulation, was completely abolished and replaced by LISA after administration of the anti-muscarinic agent scopolamine (5 mg/kg, i.p.), confirming previous work suggesting that neocortical LVFA is maintained by two distinct neurochemical inputs to the cortex that can be dissociated using anti-muscarinic drugs. Electrical stimulation of the locus coeruleus area or of the superior colliculus also suppressed LISA and induced LVFA. The LVFA during stimulation of the locus coeruleus area was abolished by the anti-muscarinic drug atropine (50 mg/kg, i.p.), whereas the LVFA during superior colliculus stimulation was atropine-resistant but could be abolished by the serotonergic antagonists methiothepin (5 mg/kg, i.p.) or ketanserin (5 mg/kg, i.p.). Stimulation of 44% of electrode sites in the orbitofrontal cortex produced neocortical LVFA which was reduced by atropine and completely abolished by additional administration of methiothepin. Stimulation of the entorhinal or cingulate cortex was ineffective in producing LVFA and often resulted in the appearance of epileptiform activity. Single-pulse electrical stimulation of those sites that effectively induced atropine-sensitive LVFA (amygdala, locus coeruleus area) produced excitation of over 65% of those extracellularly recorded basal forebrain neurons that fired at higher rates during the presence of neocortical LVFA relative to LISA. About 80% of basal forebrain cells that were more active during LISA relative to LVFA were inhibited by single-pulse stimulation of the amygdala or locus coeruleus area. The present results suggest that widely distributed neuronal systems can produce electrocorticographic activation by acting through mechanisms sensitive to anti-muscarinic or anti-serotonergic drugs, suggeting that these activating influences involve the release of acetylcholine and/or serotonin. Those neural systems that produce atropine-sensitive (i.e., putative cholinergic) LVFA, believed to be dependent on the cholinergic innervation of the cortex arising in the basal forebrain, may produce electrocorticographic activation by exciting basal forebrain cells that appear to contribute to neocortical LVFA, while concurrently inhibiting cells that may contribute to LISA.

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Section: Discussionmentioning

confidence: 93%

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

1997

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“…The direction of the effect obtained appears to depend upon the route of administration and the presence of an intact blood brain barrier (Key & Marley, 1962;Marley, 1966). It has been suggested (Baust & Niemczyk, 1964) that the central excitation produced by systemically injected catecholamines is due entirely to the peripheral hypertension which acts reflexly on brain stem arousal mechanisms, but there are some observations which cannot be explained by this hypothesis (Aldridge, 1965). Certainly, it appears that the effects of catecholamines, administered by the usual routes, are not the same as those of the endogenously released substances.…”

Section: Discussionmentioning

confidence: 99%

Actions of noradrenaline, other sympathomimetic amines and antagonists on neurones in the brain stem of the cat

Boakes

Bradley

Brookes

et al. 1971

British J Pharmacology

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Summary1. The effects of (-)-noradrenaline ((-)-NA) and related compounds on brain stem neurones in decerebrate unanaesthetized cats have been investigated using the technique of iontophoretic application from micropipettes. 2. Four types of response to (-)-NA have been described. These were short lasting inhibition, long lasting inhibition, excitation, and a biphasic response consisting of short lasting inhibition followed by excitation. A variable amount of desensitization of the excitatory response, but not of inhibitory responses, was observed.3. Experiments in which small currents were used to pass (-)-NA from pipettes with smaller tips did not lead to any appreciable change in the proportions of neurones excited or inhibited. 4. A variety of sympathomimetic agonists was tested. Short lasting inhibition was less sensitive than excitation to changes in molecular structure. Long lasting inhibition was more sensitive to molecular change and was not mimicked by some of the agonists which mimicked short lasting inhibition. 5. Although agonists without one ring hydroxyl had weaker effects than those with both, compounds in which both ring hydroxyl groups were absent (P-hydroxyphenylethylamine, ephedrine and amphetamine) mimicked excitation strongly. It is possible that the compounds without both ring hydroxyl groups had some effect other than simple agonistic activity. 6. A dissociation was observed between responses to dopamine and (-)-NA. p-Tyramine mimicked dopamine, rather than (-)-NA. 8. The most effective antagonist of excitation was (-)-a-methylnoradrenaline. Metaraminol and dihydroergotamine also had some antagonistic activity. None

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“…The prerequisite for any recovery, of course, is an adequate blood recirculation. However, noradrenaline which has been used to control the systemic blood pressure may have a direct effect on the cortical neurons, although such an action has been refuted in normal animals (6).…”

Section: Recovery Of Neuronal Function After Prolonged Cerebral Ischemiamentioning

confidence: 99%

“…Little is known about the relation between structure and activity in these compounds (2), but the demonstrated reactivity of unsaturated lactones toward thiols (3) and amines (4) and the presence of other reactive functional groups suggested that the cytotoxicity of these compounds may result from alkylation of nucleophilic centers in a biological system. Therefore the chemical reactivity of some of the cytotoxic lactones toward mod.l biological nucleophiles is being studied and we now describe the reactions of elephantopin (1,5), eupatundin (2,6), and vernolepin (3, 7) with aqueous solutions of L-cysteine at pH 7.4. Second-order rate constants (Table 1 ) for the reactions of the lactones with cysteine were determined spectrophotometrically with a Beckman DK-2A spectrophotometer equipped with a thermostated cell compartment.…”

Section: Recovery Of Neuronal Function After Prolonged Cerebral Ischemiamentioning

confidence: 99%

Recovery of Neuronal Function after Prolonged Cerebral Ischemia

Hossmann

Satô

1970

Science

140

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Cats were submitted to complete cerebral ischemia by clamping the innominate and subclavian arteries and simultaneously lowering the systemic blood pressure. Neuronal function was assessed by recording the electroencephalogram and the anti- and orthodromic activation of the pyramidal tract. A full recovery of the pyramidal response and even of evoked electroencephalographic activity occurred after ischemia of more than 1 hour's duration.

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Further studies on the action of adrenergic drugs on cortical activity

Cited by 22 publications

References 16 publications

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

Actions of noradrenaline, other sympathomimetic amines and antagonists on neurones in the brain stem of the cat

Recovery of Neuronal Function after Prolonged Cerebral Ischemia

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