Small damage of brain parenchyma reliably triggers spreading depolarization

Vinogradova, Lyudmila V.; Рысакова, М. П.; Павлова, И. В.

doi:10.1080/01616412.2019.1709745

Cited by 12 publications

(25 citation statements)

References 21 publications

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“…Our study showed the highly dynamic character of CSD-induced behavioral changes – an early brief period of enhanced grooming during CSD (40–80 sec), late post-CSD behavioral activation (300–420 sec), episodes of atypical behavior such as tremor, freezing and forced circling (100–300 sec). Similar behavioral changes, including grooming during CSD, episodes of freezing, circling and locomotor activation after CSD, have been described in other studies in awake rodents (10,29,30). The only change in spontaneous behavior, observed during CSD traveling over the neocortex in our study, was increased grooming, which is known to be associated with facial pain in rodents (31) and is produced by CGRP administration (32).…”

Section: Discussionsupporting

confidence: 83%

“…Comparison of spontaneous behavior after sham stimulation (n = 14) and a single unilateral CSD (n = 13) has shown significant enhancement of grooming during CSD (40–80 sec) and remote post-CSD (300–420 sec) behavioral activation (Figure 6). In addition to these changes in general behavior, atypical behavioral patterns were observed following CSD (Figure 6): Behavioral arrest (freezing-like episodes) with or without tremor (100–280 sec) and forced circling to the side contralateral to CSD (140–280 sec) heralded CSD penetration into the striatum, as we reported previously (10). The abnormal behavioral patterns were time-locked with the observed post-CSD hemispheric disconnection (Figure 6).…”

Section: Resultssupporting

confidence: 69%

“…The post-CSD drop of hemispheric communication coincides with the occurrence of freezing episodes (10,29,30) and development of mild neurological deficits (contralateral sensory neglect and motor impairment) described after CSD in experimental animals, including models of familial hemiplegic migraine (4,30,33). Impaired perception of sensory stimuli received by the contralateral side of the body is thought to underlie the neurological deficits induced by CSD (4).…”

Section: Discussionmentioning

confidence: 63%

“…The cortical hyperactivation following CSD may have detrimental effects and carry the risk of producing abnormal excitation (seizures) (10,18,19). Long-range excitatory trans-hemispheric connections may easily transfer the seizure-like activity to the unaffected contralateral cortex, but we found no signs of its abnormal activation.…”

Section: Discussionmentioning

confidence: 99%

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Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

2020

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Objective Growing evidence shows a critical role of network disturbances in the pathogenesis of migraine. Unilateral pattern of neurological symptoms of aura suggests disruption of interhemispheric interactions during the early phase of a migraine attack. Using local field potentials data from the visual and motor cortices, this study explored effects of unilateral cortical spreading depression, the likely pathophysiological mechanism of migraine aura, on interhemispheric functional connectivity in freely behaving rats. Methods Temporal evolution of the functional connectivity was evaluated using mutual information and phase synchronization measures applied to local field potentials recordings obtained in homotopic points of the motor and visual cortices of the two hemispheres in freely behaving rats after induction of a single unilateral cortical spreading depression in the somatosensory S1 cortex and sham cortical stimulation. Results Cortical spreading depression was followed by a dramatic broadband loss of interhemispheric functional connectivity in the visual and motor regions of the cortex. The hemispheric disconnection started after the end of the depolarization phase of cortical spreading depression, progressed gradually, and terminated by 5 min after initiation of cortical spreading depression. The network impairment had region- and frequency-specific characteristics and was more pronounced in the visual cortex than in the motor cortex. The period of impaired neural synchrony coincided with post-cortical spreading depression electrographic aberrant activation of the ipsilateral cortex and abnormal behavior. Conclusion The study provides the first evidence that unilateral cortical spreading depression induces a reversible loss of functional hemispheric connectivity in the cortex of awake animals. Given a critical role of long-distance cortical synchronization in sensory processing and sensorimotor integration, the post-cortical spreading depression breakdown of functional connectivity may contribute to neuropathological mechanisms of aura generation.

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Section: Discussionsupporting

confidence: 83%

Section: Resultssupporting

confidence: 69%

Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

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Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

2020

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“…The mere presence of the cannulas might lead to inflammatory reactions of the surrounding tissue, which might even be exaggerated by the mechanical and psychological stress of daily injections. Recently it was shown that the insertion of an injection needle through a guide cannula into the BLA was sufficient to trigger the occurrence of an acute spreading depolarization that in turn caused freezing behavior and lasted for 1.5 min after the initial insult 58 . In addition, BLA lesions have been specifically associated with decreased mutual-reward choices in the PCT 14 and do interfere with general reward learning in multiple ways (reviewed in Wassum and Izquierdo 59 ).…”

Section: Discussionmentioning

confidence: 99%

5-HT1A receptor agonism in the basolateral amygdala increases mutual-reward choices in rats

Schönfeld

Schäble

Zech

et al. 2020

Sci Rep

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Rats show mutual-reward preferences, i.e., they prefer options that result in a reward for both themselves and a conspecific partner to options that result in a reward for themselves, but not for the partner. In a previous study, we have shown that lesions of the basolateral amygdala (BLA) reduced choices for mutual rewards. Here, we aimed to explore the role of 5-HT1A receptors within the BLA in mutual-reward choices. Rats received daily injections of either 50 or 25 ng of the 5-HT1A receptor agonist 8-OH-DPAT or a vehicle solution into the BLA and mutual-reward choices were measured in a rodent prosocial choice task. Compared to vehicle injections, 8-OH-DPAT significantly increased mutual-reward choices when a conspecific was present. By contrast, mutual-reward choices were significantly reduced by 8-OH-DPAT injections in the presence of a toy rat. The effect of 8-OH-DPAT injections was statistically significant during the expression, but not during learning of mutual-reward behavior, although an influence of 8-OH-DPAT injections on learning could not be excluded. There were no differences between 8-OH-DPAT-treated and vehicle-treated rats in general reward learning, behavioral flexibility, locomotion or anxiety. In this study, we have shown that repeated injections of the 5-HT1A receptor agonist 8-OH-DPAT have the potential to increase mutual-reward choices in a social setting without affecting other behavioral parameters.

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Spreading depolarization induced by amygdala micro-injury prevents disruption of fear memory extinction in rats

Рысакова

Павлова

Vinogradova

2022

Behavioural Brain Research

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Small damage of brain parenchyma reliably triggers spreading depolarization

Cited by 12 publications

References 21 publications

Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

5-HT1A receptor agonism in the basolateral amygdala increases mutual-reward choices in rats

Spreading depolarization induced by amygdala micro-injury prevents disruption of fear memory extinction in rats

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