1967
DOI: 10.1016/0013-4694(67)90019-3
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Alterations in the non-specific cortical afference during hyperventilation

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Cited by 17 publications
(16 citation statements)
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“…Because cortical rhythmic activity arises from an interplay between thalamic relay cells with cells in the reticular nuclei and cortico-cortical reverberant loops [30, 31], the VEP changes we recorded after deep-breathing-induced HV could plausibly depend on thalamic neuronal hyperpolarization. This neural mechanism accords perfectly with early evidence that lesions involving the anterior pole of the thalamus (nucleus centralis lateralis) abolish the cortical response to HV [32, 33]. Another major brain nervous structure involved in HV-induced EEG changes is the reticular formation.…”
Section: Discussionsupporting
confidence: 87%
“…Because cortical rhythmic activity arises from an interplay between thalamic relay cells with cells in the reticular nuclei and cortico-cortical reverberant loops [30, 31], the VEP changes we recorded after deep-breathing-induced HV could plausibly depend on thalamic neuronal hyperpolarization. This neural mechanism accords perfectly with early evidence that lesions involving the anterior pole of the thalamus (nucleus centralis lateralis) abolish the cortical response to HV [32, 33]. Another major brain nervous structure involved in HV-induced EEG changes is the reticular formation.…”
Section: Discussionsupporting
confidence: 87%
“…Experiments performed by Ira Sherwin in the 1960s represent some of the few attempts to do so. Sherwin posed two key questions in his experiments: (1) what brain structures are recruited by hyperventilation to increase the occurrence of SWDs (Sherwin, 1965, 1967), and (2) do these structures possess a specific, element that is responsive to respiratory-induced changes in pH?…”
Section: A Basic Modulation Of the Thalamusmentioning
confidence: 99%
“…In 1967, Sherwin presented a study that demonstrated a critical role for the NSTPS in modulating cortical excitability (Sherwin, 1967). Sherwin specifically examined the contribution of the central lateral (CL) nucleus, a member of the NSTPS, to hyperventilation-induced changes in cortical excitability and HIHARS.…”
Section: A Basic Modulation Of the Thalamusmentioning
confidence: 99%
“…The study of regional cerebral blood flow (rCBF) by the subtraction technique of brain images with single-photon emission computed tomography directly demonstrates a close correlation between the hyperventilation-induced EEG and rCBF changes [36]. Bonvallet and Dell [37] suggested that hypocapnia produces depression of the ascending reticular activating system and causes synchronous slowing, while clinical [38] and experimental [39] studies implicated increased activity in the non-specific thalamocortical projecting systems during hyperventilation as the cause of slowing.…”
Section: Discussionmentioning
confidence: 99%