Influence of cooling rate on activity of ionotropic glutamate receptors in brain slices at hypothermia

Mokrushin, A. A.; Pavlinova, L. I.; Borovikov, Sergey E.

doi:10.1016/j.jtherbio.2014.05.005

Cited by 16 publications

(11 citation statements)

References 55 publications

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“…Efflux of K + ions from neurons beginning at 27 ºC does not end further and can lead to a significant decrease of membrane potential level under further cooling or just in a certain time course (Aihara et al 2001). Against depolarization shift, the drop of spike amplitude takes place (Fig.2), which is confirmed by earlier investigations (Mednikova et al,2002;Mokrushin et al, 2014;Volgushev et al,2004) and the destructive intracellular processes are triggered (Hochachka, 1986;Ivanov, 2004). But even a small depolarization for potential-dependent K + channels is quite enough to open ever more (Adams et al 1982), causing further increase of K + efflux from the cell and further depolarization shift (Aslanidi, 1997).…”

Section: Discussionsupporting

confidence: 78%

On the Regulator of Spike Activity in Cortical Neurons Under Hypothermic Conditions

Mednikova

Zakharova

Pasikova

et al. 2016

Preprint

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In sensorimotor cortical slices of guinea pig in the course of cooling incubating fluid from 34 to 21-22ºC it was shown that hypothermia exerted both increase and decrease of spontaneous activity in different neurons. On hypothermic increase of firing level spike responses of soma to iontophoretic application of glutamate to dendritic locus appeared with shorter latencies and with longer latencies -on hypothermic decrease of spontaneous activity. At the same time hypothermia did not influence on the evoked spike reactions to iontophoretic application of glutamate straight to the soma. It means that hypothermic disorders of neuronal activity are not connected with changes in sensitivity to glutamate but determined by changes of amplitude of glutamatergic excitation while propagating along dendritic branches. The changes in spontaneous activity began at 30ºC along with the decreased spike reactions to iontophoretic applications of acetylcholine and efficacy of dendro-somatic propagation. At the same temperature the fall of spike amplitude was initiated and increased with further hypothermia. It is proposed that the basis for hypothermic changes of neuronal activity is the decreased rate of M-cholinergic process at 27-29ºC which leads both to attenuation of conductive function of dendrites and imbalance of K + ion homeostasis.Peculiarities of hypothermic regulation of neuronal spike activity depend on individual functional properties of cortical neurons.

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Section: Discussionsupporting

confidence: 78%

On the Regulator of Spike Activity in Cortical Neurons Under Hypothermic Conditions

Mednikova

Zakharova

Pasikova

et al. 2016

Preprint

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“…The cortical temperature was changed before each recording. The change in cortical temperature, the interval, and the average rate of temperature change between two recordings were 3.7 ± 1.5 • C, 4.2 ± 2.9 min, and 1.6 ± 1.6 • C/min, respectively, in Experiments 1 and 3, 3.0 ± 0.2 • C, 6.1 ± 3.7 min, and 0.6 ± 0.2 • C/min, respectively, in Experiments 2 and 4, and 9.0 ± 0.3 • C, 10.7 ± 8.6 min, and 1.1 ± 0.4 • C /min, respectively, in Experiments 5-7 (Mokrushin et al, 2014).…”

Section: Thermal Control Devicementioning

confidence: 83%

Brain Temperature Alters Contributions of Excitatory and Inhibitory Inputs to Evoked Field Potentials in the Rat Frontal Cortex

Gotoh

Nagasaka

Nakata

et al. 2020

Front. Cell. Neurosci.

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Changes in brain temperature have been reported to affect various brain functions. However, little is known about the effects of temperature on the neural activity at the network level, where multiple inputs are integrated. In this study, we recorded cortical evoked potentials while altering the local brain temperature in anesthetized rats. We delivered electrical stimulations to the midbrain dopamine area and measured the evoked potentials in the frontal cortex, the temperature of which was locally altered using a thermal control device. We focused on the maximum negative peaks, which was presumed to result mainly from polysynaptic responses, to examine the effect of local temperature on network activity. We showed that focal cortical cooling increased the amplitude of evoked potentials (negative correlation, >17°C); further cooling decreased their amplitude. This relationship would be graphically represented as an inverted-U-shaped curve. The pharmacological blockade of GABAergic inhibitory inputs eliminated the negative correlation (>17°C) and even showed a positive correlation when the concentration of GABAA receptor antagonist was sufficiently high. Blocking the glutamatergic excitatory inputs decreased the amplitude but did not cause such inversion. Our results suggest that the negative correlation between the amplitude of evoked potentials and the near-physiological local temperature is caused by the alteration of the balance of contribution between excitatory and inhibitory inputs to the evoked potentials, possibly due to higher temperature sensitivity of inhibitory inputs.

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“…However, deep hypothermia (below 18°C) results in suppression of long-term potentiation (LTP), the neuroplastic process by which efficiency of synaptic transmission is upregulated via coincident bursts of high-frequency stimulation between neurons. [13,27] Taken with the behavioral data, this suggests that mild TH for long durations is not inherently harmful to natural plastic processes; however, given the risk of impairing LTP, caution should be taken when cooling to greater depths or durations. In addition, these limited studies are in naïve animals, and they do not include the study of other pharmacological agents that are often given concurrently with TH, which may potentially impact plastic processes.…”

Section: Effects Of Hypothermia In Naïve Animalsmentioning

confidence: 87%

“…Thus, TH may directly impact repair by impeding such processes (e.g., glutamatergic neurotransmission). [13] Indirect effects are also expected. For example, a highly neuroprotective cooling protocol would likely diminish the need for repair.…”

Section: Hypothermia and Neuroprotectionmentioning

confidence: 98%

Hypothermia: Impact on plasticity following brain injury

Kalisvaart¹,

Prokop²,

Colbourne³

2019

Brain Circ

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Therapeutic hypothermia (TH) is a potent neuroprotectant against multiple forms of brain injury, but in some cases, prolonged cooling is needed. Such cooling protocols raise the risk that TH will directly or indirectly impact neuroplasticity, such as after global and focal cerebral ischemia or traumatic brain injury. TH, depending on the depth and duration, has the potential to broadly affect brain plasticity, especially given the spatial, temporal, and mechanistic overlap with the injury processes that cooling is used to treat. Here, we review the current experimental and clinical evidence to evaluate whether application of TH has any adverse or positive effects on postinjury plasticity. The limited available data suggest that mild TH does not appear to have any deleterious effect on neuroplasticity; however, we emphasize the need for additional high-quality preclinical and clinical work in this area.

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Influence of cooling rate on activity of ionotropic glutamate receptors in brain slices at hypothermia

Cited by 16 publications

References 55 publications

On the Regulator of Spike Activity in Cortical Neurons Under Hypothermic Conditions

On the Regulator of Spike Activity in Cortical Neurons Under Hypothermic Conditions

Brain Temperature Alters Contributions of Excitatory and Inhibitory Inputs to Evoked Field Potentials in the Rat Frontal Cortex

Hypothermia: Impact on plasticity following brain injury

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