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PubMed1998

[Spread of spinal anesthesia with 3 different hyperbaric solutions used in Japan].

We studied the spread of spinal anesthesia with 3 different hyperbaric solutions commercially available in Japan. Percamin-S [0.3% dibucaine in 5% hyperbaric saline] (P), Neo-Percamin.S [0.24% dibucaine with 0.12% T-caine in 9.5% glucose] (N) and 0.5% Tetcaine [tetracaine] in 10% glucose (T) were studied. Two ml of each solution was administered intrathecally using a 25 gauge Quincke needle. Patients (n = 90) were allocated to one of 9 groups receiving 2 ml of P, N or T at L 2-3, L 3-4 or L 4-5 interspace. Both N and T produced significantly higher spread of analgesia than P at any of L 3-4 and L 4-5 interspaces. P and N have the same specific gravity, even though significant differences were found in spread of segmental analgesia. Local anesthesic agents and solvent solutions themselves are considered to influence the spread of spinal anesthesia as the specific gravity of hyperbaric solution does.

Adult↗
PubMed2003

Ischemia triggered by spreading neuronal activation is induced by endothelin-1 and hemoglobin in the subarachnoid space.

Delayed cerebral vasospasm has a major impact on the outcome of subarachnoid hemorrhage. Two important candidates to cause the arterial spasm are the red blood cell product oxyhemoglobin and the vasoconstrictor endothelin-1, although oxyhemoglobin alone is not sufficient to induce cerebral ischemia and endothelin-1 leads to ischemia only at relatively high concentrations. In this study, we demonstrated that the combination of oxyhemoglobin and endothelin-1 triggered spreading neuronal activation in rat cortex in vivo. In contrast with the expected transient increase of regional cerebral blood flow during spreading depression, however, cerebral blood flow decreased profoundly and was long-lasting, paralleled by delayed repolarization of the steady (direct current) potential. These changes are characteristic of cortical spreading ischemia. Replacing oxyhemoglobin for the nitric oxide synthase inhibitor Nomega-nitro-L-arginine mimicked these effects, implicating nitric oxide scavenging functions of oxyhemoglobin. Furthermore, the effect of endothelin-1 was related to a reduction of Na(+)-/K(+)-ATPase activity rather than solely to its vasoconstrictive properties. In conclusion, the threshold concentration of endothelin-1 that induces cerebral ischemia is profoundly reduced via a complex interaction between the neuronal/astroglial network and the cortical microcirculation if nitric oxide availability declines. The results may have implications for the understanding of subarachnoid hemorrhage-related cortical lesions.

Animals↗
PubMed1982

Persistent oligemia of rat cerebral cortex in the wake of spreading depression.

Cerebral blood flow during and after spreading depression (SD) was studied in rat brain by quantitative autoradiography. The rise of cortical blood flow during SD was followed by 20 to 25% reduction below normal after SD, lasting at least an hour. Blood flow in th putamen, thalamus, and hippocampus did not change at any time during or after SD. Previous measurements of cerebral blood flow in humans showed that migraine attacks may be accompanied by wavelike spreading oligemia (Olesen et al, 1981). We speculate that the spreading oligemia of migraine may be a phenomenon physiologically related to the present finding of an oligemia after SD.

Animals↗
PubMed2004

Correlation between the durations of refractory period and intrinsic optical signal of retinal spreading depression during temperature variations.

Spreading depression (SD) is a neurophysiological phenomenon which occurs in the grey substance of the central nervous system. SD is characterised by a wave-like spread of depressed neuronal activity, by large ion shifts between intra- and extracellular space, by cellular depolarization, and by altered optical properties of the tissue giving rise to an intrinsic optical signal (IOS). In the shadow of SD further waves are difficult to trigger and such waves spread at lower velocity than usual. In this paper we examine the temperature dependence of the duration of this recovery (refractory) period and the temperature dependence of the duration of the IOS in the chicken retina. It is shown that these SD accompanying events are strongly dependent on temperature and that they are likely to depend on the metabolic rate in the tissue. The observed correlation of the duration of the IOS with the duration of the refractory period suggests that the IOS is a good indicator for the duration of the tissue recovery. Such a correlation would be of great value to the experimentalist who must know about the duration of the refractory period: while the latter is laborious to determine, recording the IOS is convenient.

Algorithms↗
PubMed1991

Demonstration of heat production associated with spreading depression in the amphibian retina.

Using thin film of synthetic pyroelectric material, polyvinylidene fluoride, sensitive heat-sensors were constructed for the purpose of detecting heat production associated with the phenomenon of spreading depression in isolated amphibian retinae. Measurements with these sensors revealed the existence of large heat production, which closely follows the electrical sign of spreading depression. Studies of the effects of chemical agents known to affect spreading depression have demonstrated the usefulness of heat measurements.

Animals↗
PubMed1991

Glutamate release and spreading depression in the fascia dentata in response to microdialysis with high K+: role of glia.

To see electrophysiological and neurochemical events during microdialysis with high [K+], direct current (DC) and excitatory postsynaptic field potentials (fEPSPs) due to perforant path stimulation were recorded in the granule cell layer of the fascia dentata, while 3, 25, 50 or 100 mM KCl was perfused through a microdialysis probe placed 1.5 mm from the recording electrode. Glutamate and glutamine content of the dialysate was measured by high performance liquid chromatography. Raising [K+] from 3 to 25 mM reduced the efflux of glutamine, without affecting that of glutamate or the electrical activity. In about 50% of experiments, 50 mM K+ induced large (20-30 mV) negative waves of spreading depression (SD), and a suppression of fEPSPs. In the other 50%, without SD, fEPSPs did not change. Glutamate efflux increased 3-fold in both groups. SD waves were produced in all experiments with 100 mM K+ which evoked a more than 10-fold increase in glutamate release. Glutamine efflux decreased equally, by about 50%, with the 3 concentrations of K+. Microdialysis with 20 mM fluoroacetate, a glial metabolic poison, decreased the spontaneous efflux of glutamine and glutamate and increased the incidence of SD waves. Results suggest that perfusion of 50 or 100 mM K+ through a microdialysis probe causes spreading depression which blocks surrounding electrical activity. The activity of glia partly protects against spreading depression caused by high [K+].

Animals↗
PubMed1992

Current source density of sustained potential shifts associated with electrographic seizures and with spreading depression in rat hippocampus.

The membrane currents responsible for the sustained potential shifts associated with electrographic seizures and with spreading depression in hippocampus were studied in the anesthetized rat. Probes incorporating 16 sensors in a straight line, spaced at 150-microns distances, were recording the potential changes with DC-coupled amplifiers in CA1 and dentate gyrus (DG) of one hemisphere. Seizures and spreading depression were provoked by repetitive stimulation of different afferent pathways. Seizures always began in DG before CA1, regardless of the pathway stimulated. Tonic seizures were associated with a sustained negative potential shift that was largest in the cell body layers. Current source density was computed from these recordings and confirmed the presence of a current sink limited to the cell body layer throughout the duration of electrographic seizures. Spreading depression was associated with a very large sink located in the layer of apical dendrites, maximal among the proximal segment of dendrites, to which the cell body layer served as a source. We conclude that seizures are associated with an inward current in neuron cell bodies, probably flowing through membrane channels of as yet no know physiological function.

Animals↗
PubMed1984

Regional changes of blood flow, glucose, and ATP content determined on brain sections during a single passage of spreading depression in rat brain cortex.

Hemodynamic and biochemical substrate changes are associated with cortical spreading depression (CSD). Regional methods were used to measure blood flow, and glucose and ATP concentrations in intact brain sections in rats undergoing a single passage of cortical spreading depression. Changes were expressed as the percentages of the contralateral homotopic area of the unaffected cortex. A depression in tissue ATP content preceded the negative DC potential shift and ATP was reduced by 12% (P less than 0.01) despite unaltered blood flow and glucose concentration. When the negative shift of DC potential reached its maximum, glucose content decreased to 72% of control (P less than 0.01) and was accompanied by a further ATP decrease to 54%. When the cortical steady potential declined, blood flow was elevated twofold (P less than 0.01). The ATP content gradually returned to normal; however, cortical glucose concentrations remained at 55% of control values. The relationship of blood flow and glucose and ATP concentration with other known changes during spreading depression are discussed. With the advantage of higher resolution the provided techniques may be a useful tool for studies on hemodynamic and biochemical changes of other pathophysiologic conditions.

Adenosine Triphosphate↗
PubMed1995

A comparison between the stimulated and paroxysmal release of endogenous amino acids from rat cerebellar, striatal and hippocampal slices: a manifestation of spreading depression?

Spreading depression, which can be evoked by a variety of stimuli both in vitro and in vivo, is associated with profound changes in extracellular ion concentrations and enhanced release of neurotransmitter amino acids. We have observed a transient spontaneous release of amino acids in slice preparations obtained from rat cerebellum, striatum and hippocampus; this phenomenon has similar properties to stimulus-evoked spreading depression. Aspartate, glutamate, glutamine, serine, glycine and gamma-aminobutyric acid (GABA) release were potentiated during these episodes in all three brain regions, with a variable effect upon taurine release. When compared to glutamate release, a consistently high release of aspartate, glycine and serine was observed. Amino acid release, evoked by whole slice depolarization using veratridine (10-25 microM) or elevated potassium (35-60 mM) consistently enhanced glutamate release, and to a lesser extent aspartate release, but had negligible effect upon the other amino acids. Thus, the release profiles for spontaneous and depolarization-evoked release are markedly different. We suggest that the spontaneous release observed in brain slices represents a spreading depression-like phenomenon; the putative roles of the amino acids are discussed.

Animals↗
PubMed1996

Protein kinase C in the rat cerebral cortex during spreading depression.

Activity and distribution of protein kinase C (PKC) in the rat cerebral cortex was correlated with the development of spreading depression. When the 'waves' of the slow potential shift, induced by topical application of concentrated KCl solutions, were allowed to spread over the cerebral cortex for 10 min, both cytosolic and particulate fractions of the enzyme were increased to 169% and 143%, respectively, of the control values obtained from the contralateral, relatively intact hemicortex. When the enzyme activities were correlated with development of a single slow potential shift, it appeared that in the cortical area fully depolarized (under the maximum of negativity), the respective values were 175% and 157%. One min after recovery of the single wave of spreading depression both cytosolic and particulate fractions continued to rise up to 218% and 239%, respectively. During 5 min of recovery both the cytosolic and particulate fractions fell to 71% and 57%, respectively, of control levels. Even at 10 min the cytosolic enzyme was still decreased to 80%. At 20 min no difference between control and experimental values was found (soluble, 111%; particulate, 96%). The results are discussed in the context of data obtained in a few studies dealing with depolarization-induced changes of PKC in vitro.

Animals↗
PubMed2004

Spreading depression induces long-lasting brain protection against infarcted lesion development via BDNF gene-dependent mechanism.

Preconditioning the rat brain with spreading depression for 48 h induces potent ischemic tolerance (infarct tolerance) after an interval of 12-15 days, consequently reducing the infarcted lesion size in the acute phase following focal cerebral ischemia. However, persistence of the morphological and functional neuroprotection has not yet been proven. We tested whether tolerance-derived neuroprotection against focal cerebral ischemia persists or merely delays the progress of cerebral infarction. Prolonged spreading depression was induced in mice by placing a depolarized focus with intracerebral microinfusion of KCl for 24 h; after intervals of 3, 6, 9 or 12 days, temporary focal ischemia was imposed. In the analysis of the infarcted lesion volume 24 h after ischemia, groups with 6 or 9 day interval demonstrated significantly smaller lesion volume compared to time-matched vehicle control group (P=0.002). Significant reduction in cerebral infarction was also observed at the chronic phase, namely 14 days after ischemia (33% reduction) (P=0.021) accompanied with less severe neurological deficits (38% reduction) (P=0.020). Using this technique, we also investigated if the mice with targeted disruption of a single BDNF allele (heterozygous BDNF-deficient mice) can gain the same potency of tolerance as the wild mice. In the result on infarcted lesion volumes following temporary focal ischemia, potent tolerance developed in the wild type (35% reduction) (P=0.007) but not in the heterozygous BDNF-deficient mice (<19% reduction) (P=0.155), indicating that BDNF expression level following spreading depression is contributing to infarct tolerance development.

Animals↗
PubMed2004

Spreading depression activates unfolded protein response.

Preconditioning is a process where a preceding non-lethal form of stress activates a stress response that protects cells against an otherwise lethal form of stress. Preconditioning can be induced in various ways including short-term ischemia or spreading depression. Here we investigated the effect of 1 h repetitive spreading depression on the unfolded protein response (UPR), a stress response activated under conditions associated with endoplasmic reticulum (ER) dysfunction. Spreading depression induced processing of xbp1 mRNA, indicative of an activation of UPR. Processing of xbp1 was paralleled by a rise in grp78 mRNA levels resulting from an activation of a signal transduction pathway that depends on protein synthesis. Preconditioning-induced activation of UPR may preserve ER functioning under pathological conditions interfering with ER functions.

Animals↗
PubMed2006

Effect of eugenol on spreading depression and epileptiform discharges in rat neocortical and hippocampal tissues.

Eugenol, an aromatic molecule derived from several plants, has been receiving examination for clinical relevance in epilepsy and headache. To investigate the neurophysiologic properties of the action of eugenol, its effects on epileptiform field potentials elicited by omission of extracellular Mg2+, spreading depression induced by KCl microinjection, electrically evoked field potentials, and long-term potentiation were tested in rat neocortical and hippocampal tissues. Eugenol (10-100 micromol/l) dose-dependently and reversibly suppressed both epileptiform field potentials and spreading depression Eugenol also reversibly decreased the amplitude of the field postsynaptic potentials evoked in CA1 area of hippocampus and the third layer of neocortex. Eugenol significantly reduced the long-term potentiation by approximately 30% compared with controls. Thus, eugenol can suppress epileptiform field potentials and spreading depression, likely via inhibition of synaptic plasticity. The results indicate the potential for eugenol to use in the treatment of epilepsy and cephalic pain.

Action Potentials↗
PubMed2005

Audiogenic seizures associated with a cortical spreading depression wave suppress spike-wave discharges in rats.

To study the role of the cortex and sub-cortical structures in the generation of epileptic spike-wave discharges in more detail, cortical and striatal activity was eliminated by the induction of spreading depression in a non-invasive way. EEG and DC potentials were recorded from the cortex and striatum of WAG/Rij rats. Several of these rats show two forms of generalised epilepsy: spontaneously occurring non-convulsive absence seizures, together with convulsive audiogenic seizures. The latter can be evoked by a brief sound stimulation, provoking a fit of wild running, which is regarded as the first phase of an audiogenic seizure. In a majority of fits the cortical DC potential does not show main changes, while the spontaneously occurring spike-wave discharges are briefly suppressed for some minutes. In a minority of fits, however, audiogenic seizures are associated with a spreading depression wave, clearly expressed in the cortical DC potential. This wave is bilaterally initiated in the cortex and propagates to the caudate nucleus of the striatum. In these cases spontaneously occurring spike-wave discharges are fully suppressed for about 1 h. It is suggested that cortical spreading depression, triggered by a short audiogenic seizure, induces a long-lasting suppression of spike-wave discharges. These results are in line with the concept that spike-wave discharges are originally initiated in the cortex, as proposed by the 'cortical focus' theory. The precise role of the striatum remains less clear, although this structure seems not to play a pivotal role in spike-wave generation.

Acoustic Stimulation↗
PubMed2000

CP-101,606, an NR2B subunit selective NMDA receptor antagonist, inhibits NMDA and injury induced c-fos expression and cortical spreading depression in rodents.

(1S, 2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol (CP-101,606) is a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptors containing the NR2B subunit. This compound was used to investigate the role of NR2B containing receptors in three responses to NMDA receptor activation in vivo. In mouse, CP-101,606 completely inhibited increases in fos-like immunoreactivity in dentate gyrus caused by a subconvulsant intraperitoneal dose of NMDA. In rat, the compound completely blocked cortical c-fos mRNA induction following focal injury in parietal cortex and the initiation and propagation of electrically induced cortical spreading depression. Inhibition of these responses by CP-101,606 indicates that c-fos induction and cortical spreading depression are dependent on activation of NMDA receptors containing the NR2B subunit. Since NMDA receptor dependent c-fos induction and cortical spreading depression may contribute to neuron loss after focal CNS injury, inhibition of these responses by CP-101,606 may contribute to the neuroprotective efficacy of the compound.

Animals↗
PubMed2003

Functional imaging of the retinal layers by laser scattering: an approach for the study of Leão's spreading depression in intact tissue.

This paper presents a novel optical approach for the study of spreading depression in isolated retina. The method makes it possible to register the laser light scattered from each layer of the tissue, yielding a functional image of the retina during spreading depression. The tissue is kept intact, since histological cuts are not necessary. Measurements of other variables, such as extracellular potential, are also allowed by the described method. This is done simultaneously with the functional image in a high spatial resolution, with the positioning of the microelectrode tip being easily monitored. The information about temporal and spatial evolution of light was compacted in a single image. The image-processing technique used here enables the visualization of the light scattered by the inner plexiform layer (IPL), which is the most prominent scatter layer during spreading depression. The wavefront velocity and its increase as two wavefronts approach each other can then be determined, and it is also possible to observe the thickness variation of the tissue during the wave travel. The relationship between two peaks of light-scattering sequence during the phenomenon was studied at two wavelengths (632.8 and 543.5 nm). This relationship is shown to be dependent on the wavelength.

Animals↗
PubMed1997

Possible mechanism of c-fos expression in trigeminal nucleus caudalis following cortical spreading depression.

Cortical spreading depression (CSD) is characterized by a transient, reversible depression of EEG activity which advances across the cortical surface at a velocity of 2-5 mm/min. CSD was originally linked to the aura phase of migraine, but recently also to migraine headache. The theory is that CSD activates meningeal trigeminal C-fibers causing neurogenic inflammation and pain (Moskowitz, M.A., Nozaki, K. and Kraig, R.P., Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms, J. Neurosci., 13 (1993) 1167-1177). The present study is an examination of the proposed link between CSD elicited in rats and activation of trigeminal nerve fibers. Multiple CSDs were elicited unilaterally for 1 h by KCl injections (1 M, 5 microliters) into the right hemisphere, while NaCl (1 M, 5 microliters) was injected into the left as control. After an additional 1 h the animals were sacrificed and trigeminal activation assessed by the expression of c-fos in trigeminal nucleus caudalis (TNC) using immunohistochemistry. The correlation between the number of CSDs and the extent of c-fos expression was determined. In addition the effect of sumatriptan (0.3 mg/kg) and morphine (3 mg/kg) given i.v. 30 min before elicitation of CSD was evaluated. CSD caused increased c-fos expression in lamina I and II of TNC where C-fibers, end, the response being greater ipsilaterally. Morphine, but not sumatriptan, reduced c-fos expression in both the ipsilateral and contralateral TNC by 71% (P < 0.05 and P = 0.19, respectively), confirming that nociceptors have been activated. No positive correlation was seen between the number of CSDs and the extent of c-fos expression in TNC. Instead we observed a positive, linear correlation between the number of KCl injections and the extent of c-fos expression in TNC (correlation coefficient r = 0.709, P < 0.05). We suggest that the C-fiber activation observed is caused by hyperosmolar KCl/NaCl and not CSD. Hence, our results do not support the hypothesis of Moskowitz et al. (Moskowitz, M.A., Nozaki, K. and Kraig, R.P., Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms, J. Neurosci., 13 (1993) 1167-1177) which links CSD with migraine headache.

Animals↗
PubMed1999

Cortical spreading depression reversibly disrupts convulsive motor seizure expression in amygdala-kindled rats.

To determine the role of the frontal cortex in the generalization of limbic seizures, we first produced unilateral cortical spreading depression to reversibly suppress neuronal activity in the motor cortex and then triggered an amygdala-kindled seizure. Three minutes following induction of unilateral spreading depression, stimulation of the ipsilateral kindled amygdala produced only a brief electrographic seizure, and completely failed to produce the bilateral electrographic and clonic convulsive seizures that were normally present during control trials. A very different outcome occurred when unilateral spreading depression was induced in the cortex contralateral to the kindled amygdala. In these cases, the electrographic amygdala seizures were normal and bilateral like control trials, yet the clonic convulsive seizures were lateralized and appeared to be controlled by the non-depressed, kindled hemisphere. These lateralized convulsions were identical to those observed following forebrain commissurotomy, when direct communication between the frontal cortices was permanently severed. The results of the present study further define the pathways of temporal lobe seizure propagation, and highlight the important contribution frontal cortical regions provide to both the electrographic and convulsive expression of amygdala-kindled seizures by amplifying local seizures and projecting them into downstream brainstem and spinal cord circuits.

Amygdala↗