Anesthesia-induced hypothermia mediates decreased ARC gene and protein expression through ERK/MAPK inactivation

Whittington, Robert A.; Bretteville, Alexis; Virág, László; Emala, Charles W.; Maurin, Thomas; Marcouiller, François; Julien, Carl; Petry, Franck R.; El-Khoury, Noura B.; Morin, Françoise; Charron, Jean; Planel, Emmanuel

doi:10.1038/srep01388

Cited by 29 publications

(25 citation statements)

References 46 publications

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“…Anesthesia is an effective method for inducing hypothermia, and hypothermia induced by isoflurane-anesthesia has been shown to alter hippocampal protein expression and brain function independently of other anesthesia-related effects [38]. Moreover, neurobiological changes induced by isoflurane-anesthesia can be achieved at doses that do not significantly alter blood gas and blood pressure [25, 26].…”

Section: Discussionmentioning

confidence: 99%

Anesthesia-Induced Hypothermia Attenuates Early-Phase Blood-Brain Barrier Disruption but Not Infarct Volume following Cerebral Ischemia

et al. 2017

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Blood-brain barrier (BBB) disruption is thought to facilitate the development of cerebral infarction after a stroke. In a typical stroke model (such as the one used in this study), the early phase of BBB disruption reaches a peak 6 h post-ischemia and largely recovers after 8–24 h, whereas the late phase of BBB disruption begins 48–58 h post-ischemia. Because cerebral infarct develops within 24 h after the onset of ischemia, and several therapeutic agents have been shown to reduce the infarct volume when administered at 6 h post-ischemia, we hypothesized that attenuating BBB disruption at its peak (6 h post-ischemia) can also decrease the infarct volume measured at 24 h. We used a mouse stroke model obtained by combining 120 min of distal middle cerebral arterial occlusion (dMCAo) with ipsilateral common carotid arterial occlusion (CCAo). This model produced the most reliable BBB disruption and cerebral infarction compared to other models characterized by a shorter duration of ischemia or obtained with dMCAO or CCAo alone. The BBB permeability was measured by quantifying Evans blue dye (EBD) extravasation, as this tracer has been shown to be more sensitive for the detection of early-phase BBB disruption compared to other intravascular tracers that are more appropriate for detecting late-phase BBB disruption. We showed that a 1 h-long treatment with isoflurane-anesthesia induced marked hypothermia and attenuated the peak of BBB disruption when administered 6 h after the onset of dMCAo/CCAo-induced ischemia. We also demonstrated that the inhibitory effect of isoflurane was hypothermia-dependent because the same treatment had no effect on ischemic BBB disruption when the mouse body temperature was maintained at 37°C. Importantly, inhibiting the peak of BBB disruption by hypothermia had no effect on the volume of brain infarct 24 h post-ischemia. In conclusion, inhibiting the peak of BBB disruption is not an effective neuroprotective strategy, especially in comparison to the inhibitors of the neuronal death signaling cascade; these, in fact, can attenuate the infarct volume measured at 24 h post-ischemia when administered at 6 h in our same stroke model.

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Section: Discussionmentioning

confidence: 99%

Anesthesia-Induced Hypothermia Attenuates Early-Phase Blood-Brain Barrier Disruption but Not Infarct Volume following Cerebral Ischemia

et al. 2017

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“…Anesthetics have been previously shown to induce tau hyperphosphorylation through a mechanism involving hypothermia-induced inhibition of protein phosphatase 2A activity [36,37]. However, the effect of propofol on tau phosphorylation under normothermic conditions has also been recently demonstrated in the mouse [38], and brief exposure to different anesthetics in human surgery procedures has resulted in t-tau increase [39]. These lines of evidence support the urgent need for studies to assess the role of anesthetics in a severe brain disorder as status epilepticus.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid tau proteins in status epilepticus

Monti

Tondelli

Giovannini

et al. 2015

Epilepsy & Behavior

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“…On completion of behavioral training (2e4 hours following the last probe test), LE and LOU non-fasted non-anesthetized rats were quickly sacrificed by rapid decapitation for ex vivo biochemical analyses (Menard and Quirion, 2012b;Menard et al, 2014b;Whittington et al, 2013).…”

Section: Lou Ratsmentioning

confidence: 99%

Glutamate presynaptic vesicular transporter and postsynaptic receptor levels correlate with spatial memory status in aging rat models

Ménard

Quirion

Vigneault

et al. 2015

Neurobiology of Aging

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In humans, memory capacities are generally affected with aging, even without any reported neurologic disorders. The mechanisms behind cognitive decline are not well understood. We studied here whether postsynaptic glutamate receptor and presynaptic vesicular glutamate transporters (VGLUTs) levels may change in the course of aging and be related to cognitive abilities using various age-impaired (AI) or age-unimpaired rat strains. Twenty-four-month-old Long-Evans (LE) rats with intact spatial memory maintained postsynaptic ionotropic glutamate receptor levels in the hippocampal-adjacent cortex similar to those of young animals. In contrast, AI rats showed significantly reduced expression of ionotropic glutamate receptor GluR2, NR2A and NR2B subunits. In AI LE rats, VGLUT1 and VGLUT2 levels were increased and negatively correlated with receptor levels as shown by principal component analysis and correlation matrices. We also investigated whether glutamatergic receptors and VGLUT levels were altered in the obesity-resistant LOU/C/Jall (LOU) rat strain which is characterized by intact memory despite aging. No difference was observed between 24-month-old LOU rats and their young counterparts. Taken together, the unaltered spatial memory performance of 24-month-old age-unimpaired LE and LOU rats suggests that intact coordination of the presynaptic and postsynaptic hippocampal-adjacent cortex glutamatergic networks may be important for successful cognitive aging. Accordingly, altered expression of presynaptic and postsynaptic glutamatergic components, such as in AI LE rats, could be considered a marker of age-related cognitive deficits.

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Anesthesia-induced hypothermia mediates decreased ARC gene and protein expression through ERK/MAPK inactivation

Cited by 29 publications

References 46 publications

Anesthesia-Induced Hypothermia Attenuates Early-Phase Blood-Brain Barrier Disruption but Not Infarct Volume following Cerebral Ischemia

Anesthesia-Induced Hypothermia Attenuates Early-Phase Blood-Brain Barrier Disruption but Not Infarct Volume following Cerebral Ischemia

Cerebrospinal fluid tau proteins in status epilepticus

Glutamate presynaptic vesicular transporter and postsynaptic receptor levels correlate with spatial memory status in aging rat models

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