Transient hyperemia succeeds oligemia in the wake of cortical spreading depression

doi:10.1016/0006-8993(93)90701-N

Brain Research

Volume 602, Issue 2, 5 February 1993, Pages 350-353

https://doi.org/10.1016/0006-8993(93)90701-N Get rights and content

Abstract

Regional cerebral blood flow (rCBF) was examined following single episodes of cortical spreading depression (CSD) in rat brain after an intravenous bolus injection of [¹⁴C]iodoantipyrine. Cortical rCBF decreased to approximately 75% of control values during the first 60 min after CSD. This change was suceeded at 90–105 min by a small, transient flow increase. rCBF returned to normal at 120 min after CSD, and remained normal for the following 2 h. The same sequence of rCBF changes has been recorded in patients during migraine attacks. This study therefore supports the notion that CSD may serve as an animal model of migraine.

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Dynamic interactions between GABAergic and astrocytic networks
2019, Neuroscience Letters
Citation Excerpt :
Experimental results showed that the oscillatory Ca2+ activity in astrocytes did not require synaptic transmission, since it persisted in the presence of TTX or AMPA receptor antagonists, and it was independent on purinergic and glutamatergic receptors. Interestingly, during SD an increase in extracellular GABA has been reported [62,63] and, as previously described, long-lasting Ca2+ oscillations can be induced in astrocytes by activation of GABABRs [30]. Accordingly, by using GABABR antagonists the authors succeeded in abolishing both the oscillatory Ca2+ activity in astrocytes and the enhancement of SICs in neurons.
Brain network activity derives from the concerted action of different cell populations. Together with interneurons, astrocytes play fundamental roles in shaping the inhibition in brain circuitries and modulating neuronal transmission. In this review, we summarize past and recent findings that reveal in neural networks the importance of the interaction between GABAergic signaling and astrocytes and discuss its physiological and pathological relevance.
Mechanisms involved in the cerebrovascular dilator effects of cortical spreading depression
2008, Progress in Neurobiology
Cortical spreading depression (CSD) leads to dramatic changes in cerebral hemodynamics. However, mechanisms involved in promoting and counteracting cerebral vasodilator responses are unclear. Here we review the development and current status of this important field of research especially with respect to the role of perivascular nerves and nitric oxide (NO). It appears that neurotransmitters released from the sensory and the parasympathetic nerves associated with cerebral arteries, and NO released from perivascular nerves and/or parenchyma, promote cerebral hyperemia during CSD. However, the relative contributions of each of these factors vary according to species studied. Related to CSD, axonal and reflex responses involving trigeminal afferents on the pial surface lead to increased blood flow and inflammation of the overlying dura mater. Counteracting the cerebral vascular dilation is the production and release of constrictor prostaglandins, at least in some species, and other possibly yet unknown agents from the vascular wall. The cerebral blood flow response in healthy human cortex has not been determined, and thus it is unclear whether the cerebral oligemia associated with migraines represents the normal physiological response to a CSD-like event or represents a pathological response. In addition to promoting cerebral hyperemia, NO produced during CSD appears to initiate signaling events which lead to protection of the brain against subsequent ischemic insults. In summary, the cerebrovascular response to CSD involves multiple dilator and constrictor factors produced and released by diverse cells within the neurovascular unit, with the contribution of each of these factors varying according to the species examined.
Phosphate-related energy compounds are not exhausted in chronically hypoperfused rat brain cortex after cortical spreading depression
2004, Journal of Stroke and Cerebrovascular Diseases
Long-term bilateral common carotid occlusion (BCCAO) in rats induces brain hypoperfusion and structural injury, and could have relevance as a model of vascular dementia in which cortical metabolism is reduced. The present study was designed to assess whether phosphate-related energy compounds and blood supplies are markedly affected by KCI-induced cortical spreading depression (CSD), which leads to metabolic and cerebral blood flow changes in rats with chronic BCCAO, by means of near-infrared spectroscopy and phosphorus magnetic resonance spectroscopy. Male Wistar rats were divided into 4 groups: BCCAO for 1 week (n = 6) and 4 weeks (n = 15), and sham operation for 1 week (n = 7) and 4 weeks (n = 7). The phosphocreatine (Pcr) index (PCr/PCr+Pi) and intracellular pH (pHi) were measured pre-CSD, just after KCl application, and at 20 and 40 minutes after CSD. Brains were evaluated by histology with hematoxylin and eosin and immunohistochemical reaction for glial fibrillary acidic protein (GFAP). Rapid signal changes of oxy-, deoxy-, and total hemoglobin were observed in all KCl-applied brains. The PCr index and pHi values in BCCAO were not different than those in control rats. The percentage of vacuolated area in the optic tract and percentage values of GFAP-positive area in the frontoparietal cortex were significantly increased in BCCAO. The generation of CSD was seen in regions of cortical gliosis induced by BCCAO, and severe energy exhaustion did not occur during or after CSD. Our results may suggest that the functional interaction of neurons and glia is sustained even in brain tissue where the metabolic state of neurons is impaired and astrocytes are proliferated.
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: This study was supported by the Friis Foundation. The Danish Medical Research Council, the COOL Sorption Foundation, and the Danish Migraine Society. The expert technical assistance of Ms. Lillian Grøndahl is gratefully acknowledged.

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Transient hyperemia succeeds oligemia in the wake of cortical spreading depression

Abstract

Brain Res.

Trends Neurosci.

Brain Res.

EEG Clin. Neurophysiol.

Brain Res.

Dealyed hyperemia following hypoperfusion in classic migraine

Arch. Neurol.

The mechanisms and applications of Leao's spreading depression of electroencephalographic activity

Regional cerebral blood flow during spreading cortical depression in conscious rats

J. Cereb. Blood Flow Metab.

Changes in brain extracellular ions during spreading depression

Acta Physiol. Scand.

Metabolic and hemodynamic activation of postischemic rat brain by cortical spreading depression

J. Cereb. Blood Flow Metab.

Some metabolic changes accompanying cortical spreading depression in the rat

J. Neurochem.