Tectal induction of cortical arousal: Evidence implicating multiple output pathways

Dean, Paul; Simkins, M.; Hetherington, L; Mitchell, Ian; Redgrave, Peter

doi:10.1016/0361-9230(91)90184-l

Cited by 30 publications

(20 citation statements)

References 42 publications

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“…Thus, our findings confirm previous work showing that stimulation of the amygdala, the dorsal raphe, locus coeruleus region, superior colliculus, and orbitofrontal cortex can produce neocortical activation (Kaada 1951;Segundo et al 1955;Berridge and Foote 1991;Dean et al 1991;Peck and Vanderwolf 1991;Kapp et al 1994). …”

Section: Discussionsupporting

confidence: 81%

“…The fact that LVFA to colliculus stimulation could be abolished by the 5-HT receptor antagonists methiothepin or ketanserin may suggest that this activating effect depends on the release of 5-HT and, therefore, may be mediated by the 5-HT-raphe activating system described above. To our knowledge, these are the first data to suggest that the 5-HT system may be involved in mediating the cortical activation to stimulation of the superior colliculus (Dean et al 1991). The projections from the superior colliculus to areas of the reticular formation such as the cuneiform nucleus Redgrave et al 1988), which in turn has inputs to the raphe nuclei (Edwards 1975), could be involved in mediating the stimulation of the 5-HT input to the cortex and subsequent LVFA generation during colliculus stimulation.…”

Section: Discussionmentioning

confidence: 94%

“…However, when cholinergic and serotonergic pathways are functional, stimulation of brain areas outside those containing cortically projecting serotonergic and cholinergic neurons can be very effective in inducing neocortical LVFA. In several species, stimulation of the amygdala, locus coeruleus, cingulate cortex, orbitofrontal cortex, entorhinal cortex, and superior colliculus has been shown to produce neocortical LVFA (Kaada 1951;Gloor 1960;Segundo et al 1955;French 1958;Kaada and Johannessen 1960;Neuman 1986a;Berridge and Foote 1991;Dean et al 1991) and, consequently, the possibility has been raised that noradrenergic or glutamergic pathways or other non-cholinergic and non-serotonergic systems may also have an activating influence on the ECoG (Bernardi 1982;Neuman 1986a;Berridge and Foote 1991).…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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

1997

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“…536–537). These global deficits appear to indicate, he suggested, that the tectum is the “primary driver of the mesencephalic reticulum” (which fits with the evidence for a collicular role in cerebral activation cited above, Jefferson, 1958; Dean et al, 1991; Dringenberg et al, 2003). …”

Section: The Key To Collicular Functionmentioning

confidence: 63%

“…The canonical form of this re-orienting is the swift and seamlessly integrated joint action of eyes, ears (in many animals), head, and postural adjustments that make up what its pioneering students called the orienting reflex (Sokolov, 1963) 3 . Collicular involvement in this central pivot of behavior extends even to its autonomic and cerebral activation aspects (Jefferson, 1958; Dean et al, 1991; Dringenberg et al, 2003). …”

Section: The Key To Collicular Functionmentioning

confidence: 99%

The efference cascade, consciousness, and its self: naturalizing the first person pivot of action control

Merker¹

2013

Front. Psychol.

108

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The 20 billion neurons of the neocortex have a mere hundred thousand motor neurons by which to express cortical contents in overt behavior. Implemented through a staggered cortical “efference cascade” originating in the descending axons of layer five pyramidal cells throughout the neocortical expanse, this steep convergence accomplishes final integration for action of cortical information through a system of interconnected subcortical way stations. Coherent and effective action control requires the inclusion of a continually updated joint “global best estimate” of current sensory, motivational, and motor circumstances in this process. I have previously proposed that this running best estimate is extracted from cortical probabilistic preliminaries by a subcortical neural “reality model” implementing our conscious sensory phenomenology. As such it must exhibit first person perspectival organization, suggested to derive from formating requirements of the brain's subsystem for gaze control, with the superior colliculus at its base. Gaze movements provide the leading edge of behavior by capturing targets of engagement prior to contact. The rotation-based geometry of directional gaze movements places their implicit origin inside the head, a location recoverable by cortical probabilistic source reconstruction from the rampant primary sensory variance generated by the incessant play of collicularly triggered gaze movements. At the interface between cortex and colliculus lies the dorsal pulvinar. Its unique long-range inhibitory circuitry may precipitate the brain's global best estimate of its momentary circumstances through multiple constraint satisfaction across its afferents from numerous cortical areas and colliculus. As phenomenal content of our sensory awareness, such a global best estimate would exhibit perspectival organization centered on a purely implicit first person origin, inherently incapable of appearing as a phenomenal content of the sensory space it serves.

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Cholinergic activation of the electrocorticogram: an amygdaloid activating system

Dringenberg

Vanderwolf

1996

Exp Brain Res

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In urethane-anesthetized rats, electrical 100-Hz stimulation of the basal amygdala changed neocortical electrical activity from 6-Hz or less large-amplitude, irregular slow activity to low-voltage fast activity (LVFA) including frequencies of above 10 Hz. A similar activating effect was seen in the hippocampus, where amygdala stimulation induced the appearance of rhythmical slow activity in the 2- to 6-Hz range. This activation of neocortical and hippocampal activity by amygdala stimulation was blocked by the cholinergic-muscarinic receptor antagonist scopolamine (0.5-5.0 mg/kg i.p.), but not by the peripheral antagonist methylscopolamine, in a concentration-dependent manner. In contrast, a blockade of ascending inputs from the midbrain to the neocortex by treatment with the serotonin-depletor p-chlorophenylalanine or cauterization of the rostral midbrain did not block neocortical LVFA to amygdala stimulation, even though the lesions abolished all LVFA to strong noxious stimuli such as tail pinches. Unilateral infusions of the local anesthetic lidocaine (1%) into the basal forebrain selectively blocked LVFA in the neocortex ipsilateral to the infusion. However, intracerebral or systemic administration of various excitatory amino acid antagonists (2-amino-5-phosphonovaleric acid, kynurenic acid, NPC 12626) was not effective in blocking LVFA to amygdala stimulation. An input from the amygdala to the basal forebrain cholinergic system appears to be one of multiple systems involved in the cholinergic activation of neocortical and hippocampal activity. Further, basal forebrain-cholinergic inputs to the cerebrum alone are sufficient to activate the electrocorticogram, as they sustain activation even in the absence of inputs from the mesencephalon.

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Tectal induction of cortical arousal: Evidence implicating multiple output pathways

Cited by 30 publications

References 42 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

The efference cascade, consciousness, and its self: naturalizing the first person pivot of action control

Cholinergic activation of the electrocorticogram: an amygdaloid activating system

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