The effect of atropine on cortical potentials

Funderburk, William H.; Case, Theodore J.

doi:10.1016/0013-4694(51)90013-2

Cited by 102 publications

(7 citation statements)

References 23 publications

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“…produce no clear change in the normal patterns of neocortical activity but a larger dose (5.0 mg/kg) results in occasional bursts of large amplitude slow wave activity; these occur only during behavioral immobility. Such large slow waves occur in a pattern similar to the one observed during natural slow wave sleep, as originally noted by Funderburk & Case (1951; cf. Montplaisir 1975).…”

Section: Neocortical Activation and Behavior: Cholinergic Influencessupporting

confidence: 73%

“…It is interesting that volatile anaesthetics, which permit the occurrence of a good deal of LVFA, also permit higher rates of ACh release than such anaesthetics as chloralose and barbiturates, which modify or abolish LVFA (Phillis 1968). Lastly, there is an extensive literature claiming that cholinergic antagonists, such as atropine and scopolamine, abolish LVFA, resulting in an animal that emits continuous slow waves (Bradley & Elkes 1953Funderburk & Case 1951;Montplaisir 1975;Rinaldi & Himwich 1955;Torii & Wikler 1966;Wikler 1952).…”

Section: Neocortical Activation and Behavior: Cholinergic Influencesmentioning

confidence: 99%

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Reticulo-cortical activity and behavior: A critique of the arousal theory and a new synthesis

1981

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It is traditionally believed that cerebral activation (the presence of low voltage fast electrical activity in the neocortex and rhythmical slow activity in the hippocampus) is correlated with arousal, while deactivation (the presence of large amplitude irregular slow waves or spindles in both the neocortex and the hippocampus) is correlated with sleep or coma. However, since there are many exceptions, these generalizations have only limited validity. Activated patterns occur in normal sleep (active or paradoxical sleep) and during states of anesthesia and coma. Deactivated patterns occur, at times, during normal waking, or during behavior in awake animals treated with atropinic drugs. Also, the fact that patterns characteristic of sleep, arousal, and waking behavior continue in decorticate animals indicates that reticulo-cortical mechanisms are not essential for these aspects of behavior.These puzzles have been largely resolved by recent research indicating that there are two different kinds of input from the reticular activating system to the hippocampus and neocortex. One input is probably cholinergic; it may play a role in stimulus control of behavior. The second input is noncholinergic and appears to be related to motor activity; movement-related input to the neocortex may be dependent on a trace amine.Reticulo-cortical systems are not related to arousal in the traditional sense, but may play a role in the control of adaptive behavior by influencing the activity of the cerebral cortex, which in turn exerts control over subcortical circuits that co-ordinate muscle activity to produce behavior.

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Section: Neocortical Activation and Behavior: Cholinergic Influencessupporting

confidence: 73%

Section: Neocortical Activation and Behavior: Cholinergic Influencesmentioning

confidence: 99%

Reticulo-cortical activity and behavior: A critique of the arousal theory and a new synthesis

1981

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“…Experimental manipulations of the cholinergic system in a number of species (e.g., cat, dog, rabbit) have shown that a blockade of the cholinergic input to cortex by administration of anti-muscarinic drugs, either systemically or locally in the neocortex, reduces LVFA (Funderburk and Case 1951;Wikler 1952;Cuculic et al 1968;Spehlmann and Norcross 1982). Similarly, in rats, lesions of the cholinergic cell groups of the basal forebrain reduce both cortical markers of ACh activity (e.g., staining for acetylcholinesterase) and cortical LVFA (Stewart et al 1984;Buzsaki et al 1988;Ray and Jackson 1991).…”

Section: Introductionmentioning

confidence: 99%

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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“…A similar kind of excitatory effect (Baglioni & Magnini, 1909;Funderburk & Case, 1951;Chang, 1953;Morlock & Ward, 1961) may account for the actions of tubocurarine (cf. Purpura & Grundfest, 1957).…”

Section: Strychninementioning

confidence: 99%

Pharmacology of cortical inhibition

Krnjević¹,

Randić²,

Straughan³

1966

The Journal of Physiology

167

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SUMMARY1. We have studied the effects of various pharmacological agents on the cortical inhibitory process described in the previous two papers (Krnjevid, Randic & Straughan, 1966a, b); the drugs were mostly administered directly by iontophoresis from micropipettes and by systemic injection (i.v.).2. Strychnine given by iontophoresis or by the application of a strong solution to the cortical surface potentiated excitatory effects, but very large iontophoretic doses also depressed neuronal firing. Subconvulsive and even convulsive systemic doses had little or no effect at the cortical level. There was no evidence, with any method of application, that strychnine directly interferes with the inhibitory process.3. Tetanus toxin, obtained from two different sources and injected into the cortex 12-48 hr previously, also failed to block cortical inhibition selectively. As with strychnine, there was some evidence of increased responses to excitatory inputs. 4. Other convulsant drugs which failed to block cortical inhibition included picrotoxin, pentamethylene tetrazole, thiosemicarbazide, longchain w-amino acids and morphine.5. The inhibition was not obviously affected by cholinomimetic agents or by antagonists of ACh.6. a-and fl-antagonists of adrenergic transmission were also ineffective.

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The effect of atropine on cortical potentials

Cited by 102 publications

References 23 publications

Reticulo-cortical activity and behavior: A critique of the arousal theory and a new synthesis

Reticulo-cortical activity and behavior: A critique of the arousal theory and a new synthesis

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

Pharmacology of cortical inhibition

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