Anesthetics and cerebral metabolism

Gyulai, Ferenc

doi:10.1097/00001503-200410000-00008

Cited by 10 publications

(10 citation statements)

References 34 publications

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“…Different anesthetics exert differential effects via distinct mechanisms (26). To test whether the observed phenomenon above is anesthetic specific, we examined the LFP signals with a different anesthetic in the same OB layer.…”

Section: Resultsmentioning

confidence: 99%

“…To reveal how the OB responds to odor stimulation under different brain states, we had to generate two levels of baseline activity reliably. Anesthetics, broadly used to alter global brain activity and baseline metabolism (26), are suitable for this purpose. After animal surgery and the placement of electrodes were finished, a supplementary dosage (30% of the original) was applied so both LFP and EEG recordings showed iso-electrical patterns (Fig.…”

Section: Methodsmentioning

confidence: 99%

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Brain-state–independent neural representation of peripheral stimulation in rat olfactory bulb

Gong

2011

Proc. Natl. Acad. Sci. U.S.A.

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It is critical for normal brains to perceive the external world precisely and accurately under ever-changing operational conditions, yet the mechanisms underlying this fundamental brain function in the sensory systems are poorly understood. To address this issue in the olfactory system, we investigated the responses of olfactory bulbs to odor stimulations under different brain states manipulated by anesthesia levels. Our results revealed that in two brain states, where the spontaneous baseline activities differed about twofold based on the local field potential (LFP) signals, the levels of neural activities reached after the same odor stimulation had no significant difference. This phenomenon was independent of anesthetics (pentobarbital or chloral hydrate), stimulating odorants (ethyl propionate, ethyl butyrate, ethyl valerate, amyl acetate, n-heptanal, or 2-heptanone), odor concentrations, and recording sites (the mitral or granular cell layers) for LFPs in three frequency bands and for multiunit activities. Furthermore, the activity patterns of the same stimulation under these two brain states were highly similar at both LFP and multiunit levels. These converging results argue the existence of mechanisms in the olfactory bulbs that ensure the delivery of peripheral olfactory information to higher olfactory centers with high fidelity under different brain states.T he ability to perceive the ever-changing external world accurately and precisely is a basic brain function. It is critical for daily life, survival, and higher brain functions, such as making decisions, plans, and judgments. However, the brain itself operates in ever-changing states (1, 2) or baselines (3) that are constantly modulated by external and internal factors, such as physical, physiological, psychological, clinical, and metabolic conditions. Therefore, elucidation of how sensory systems represent the same sensory information to the brain under different operational states is fundamental to understanding the related brain functions (1, 4-6).The olfactory system, as the most direct and intrinsic sensory module (1,7,8), provides a unique model to study the principles and functional mechanisms of the brain. The peripheral olfactory information takes just one synapse to enter the olfactory bulb (OB) in the brain. The OB outputs directly to the olfactory cortices that mostly belong to the limbic system. As a center to code and process the peripheral olfactory inputs and a hub to distribute the processed information to the olfactory cortices (9-11), the OB consists of laminar structures, from the outer surface to the inner core: the olfactory nerve, glomerular, external plexiform, mitral cell layer (MCL), and granular cell (GCL) layer. All peripheral olfactory input is received by a few thousand glomeruli, which generate an odor-specific spatiotemporal activity pattern across the glomerular layer (10, 12, 13). The information is mainly processed in the external plexiform layer that contains a dense dendrodendritic network formed between the secon...

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Brain-state–independent neural representation of peripheral stimulation in rat olfactory bulb

Gong

2011

Proc. Natl. Acad. Sci. U.S.A.

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“…The impact of various anaesthetics under different brain functioning conditions has been compared (for reviews: Boly et al 2004, Gyulai 2004, Heinke & Schwarzbauer 2002, showing the importance of the type of anaesthetic (volatile e.g. halothane, isoflurane, or systemic e.g.…”

Section: Pratical Issues Anaesthesia and Immobilization Of Animalsmentioning

confidence: 99%

MRI Techniques and New Animal Models for Imaging the Brain

Chaillou¹,

Tillet²,

Andersson³

2012

When Things Go Wrong - Diseases and Disorders of the Human Brain

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“…The general aim of neuroprotective strategies is to minimize damage and/or maximize recovery by influencing underlying etiology or pathogenesis [1], [2]. Evidence of the neuroprotective effect of anesthetics includes the capacity of general anesthesia to increase neuronal tolerance to hypoxic and ischemic insults [3], [4] and their protective effects in neurodegenerative diseases [5] including Alzheimer [6] and animal models of Parkinson [7]. However, limited evidence is available on the effects of anesthetic agents in terms of retinal neuroprotection.…”

Section: Introductionmentioning

confidence: 99%

Effects of Combined Ketamine/Xylazine Anesthesia on Light Induced Retinal Degeneration in Rats

et al. 2012

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ObjectivesTo explore the effect of ketamine-xylazine anesthesia on light-induced retinal degeneration in rats.MethodsRats were anesthetized with ketamine and xylazine (100 and 5 mg, respectively) for 1 h, followed by a recovery phase of 2 h before exposure to 16,000 lux of environmental illumination for 2 h. Functional assessment by electroretinography (ERG) and morphological assessment by in vivo imaging (optical coherence tomography), histology (hematoxylin/eosin staining, TUNEL assay) and immunohistochemistry (GFAP and rhodopsin staining) were performed at baseline (ERG), 36 h, 7 d and 14 d post-treatment. Non-anesthetized animals treated with light damage served as controls.ResultsKetamine-xylazine pre-treatment preserved retinal function and protected against light-induced retinal degeneration. In vivo retinal imaging demonstrated a significant increase of outer nuclear layer (ONL) thickness in the non-anesthetized group at 36 h (p<0.01) and significant reduction one week (p<0.01) after light damage. In contrast, ketamine-xylazine pre-treated animals showed no significant alteration of total retinal or ONL thickness at either time point (p>0.05), indicating a stabilizing and/or protective effect with regard to phototoxicity. Histology confirmed light-induced photoreceptor cell death and Müller cells gliosis in non-anesthetized rats, especially in the superior hemiretina, while ketamine-xylazine treated rats showed reduced photoreceptor cell death (TUNEL staining: p<0.001 after 7 d), thicker ONL and longer IS/OS. Fourteen days after light damage, a reduction of standard flash induced a-wave amplitudes and a-wave slopes (p = 0.01) and significant alterations in parameters of the scotopic sensitivity function (e.g. Vmax of the Naka Rushton fit p = 0.03) were observed in non-treated vs. ketamine-xylazine treated animals.ConclusionsOur results suggest that pre-treatment with ketamine-xylazine anesthesia protects retinas against light damage, reducing photoreceptor cell death. These data support the notion that anesthesia with ketamine-xylazine provides neuroprotective effects in light-induced cell damage.

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Anesthetics and cerebral metabolism

Cited by 10 publications

References 34 publications

Brain-state–independent neural representation of peripheral stimulation in rat olfactory bulb

Brain-state–independent neural representation of peripheral stimulation in rat olfactory bulb

MRI Techniques and New Animal Models for Imaging the Brain

Effects of Combined Ketamine/Xylazine Anesthesia on Light Induced Retinal Degeneration in Rats

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