Uncoupling of local blood flow and metabolism in the hippocampal CA3 in kainic acid-induced limbic seizure status

Tanaka, Shigeya; Sako, Kazuhiro; Tanaka, Tatsuya; Nishihara, Isao; Yonemasu, Yukichi

doi:10.1016/0306-4522(90)90430-c

Cited by 57 publications

(28 citation statements)

References 29 publications

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“…During limbic seizures and the interictal period, changes in metabolic activity and cerebral blood flow occur (Pereira de Vasconcelos et al, 2002;Tanaka et al, 1990). Therefore, differences in neuronal activations may reflect this, although 18 FDG is generally considered more sensitive to glucose transporter occupancy and blood glucose changes than blood flow itself (Schmidt et al, 1996).…”

Section: Limitations Of This Studymentioning

confidence: 99%

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

et al. 2007

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Medically-refractory seizures cause inflammation and neurodegeneration. Seizure initiation thresholds have been linked in mice to the serine protease tissue plasminogen activator (tPA); mice lacking tPA exhibit resistance to seizure induction, and the ensuing inflammation and neurodegeneration are similarly suppressed. Seizure foci in humans can be examined using PET employing 2-deoxy-2[ 18 F]fluoro-D-glucose ( 18 FDG) as a tracer to visualize metabolic dysfunction. However, there currently exist no such methods in mice to correlate measures of brain activation with behaviour. Using a novel method for small animal PET data analysis, we examine patterns of 18 FDG uptake in wild type and tPA -/-mice and find that they correlate with the severity of druginduced seizure initiation. Furthermore, we report unexpected activations that may underlie the tPA modulation of seizure susceptibility. The methods described here should be applicable to other mouse models of human neurological disease.

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Section: Limitations Of This Studymentioning

confidence: 99%

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

et al. 2007

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“…However, such uncoupling was not seen in the cerebral cortex. Considering these results, 11 disruption of the BBB is likely to have induced the moderate uptake of 14 C-ZNS in CA3 in our study, but the cortical accumulation was not caused by BBB dysfunction. We speculated that extravascular ZNS was promptly transferred to the secondarily excited zone in the cortex, maintaining a favorable extravascular/intravascular ZNS gradient for further ZNS transport from the intravascular to the extravascular space.…”

Section: Discussionmentioning

confidence: 49%

“…In KA-induced limbic status epilepticus, Tanaka et al 11 reported increases of LCGU and LCBF in the ventrobasal complex, including the ventroposteromedial nucleus of the thalamus and the ventroposterolateral nucleus of the thalamus, that most likely reflected retrograde input from the sensorimotor cortex to the ventrobasal complex. This mechanism might favor ZNS accumulation in the lateral portion of the thalamus.…”

Section: Discussionmentioning

confidence: 99%

“…According to these reports, it seems likely that distribution of 14 C-ZNS in the present study represents the accumulation of the tracer in the tissue compartment, not in the vascular space. Tanaka et al 11 demonstrated that local cerebral blood flow (LCBF) in the cerebral cortex did not increase 1-2 hours after KA injection into unilateral amygdala, whereas LCBF of the limbic system increased remarkably. Considering this, if 14 C-ZNS distribution was to represent tracer in the vascular space, high uptake should be found in the limbic system rather than the cerebral cortex.…”

Section: Discussionmentioning

confidence: 99%

“…In the present experiments, we investigated regional accumulation of ZNS in the rat brain by an autoradiographic method, and assessed the effects of ZNS on KA-induced limbic seizures [7][8][9][10][11][12][13][14] by EEG monitoring. In the present study, as soon as the seizure attenuation was recognized by 14 C-ZNS administration, 14 C-ZNS accumulation in the brain was studied.…”

Section: Discussionmentioning

confidence: 99%

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Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

Akaike

Tanaka²,

Tojo³

et al. 2001

Can. j. neurol. sci.

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Background:Zonisamide (ZNS) is an antiepileptic drug developed in Japan. Various experimental studies have investigated the effects of ZNS. However, the mechanism of action of ZNS against limbic seizures and secondary generalization is not well-known. We studied ictal regional accumulation of ZNS in the rat brain during kainic acid (KA)-induced limbic status epilepticus.Methods:Fourteen male Wistar rats underwent a stereotactic operation. For recording the electroencephalogram (EEG), electrodes were placed in the left amygdala (LA), left dorsal hippocampus, and over the left sensorimotor cortex. For microinjection, a stainless steel cannula was also inserted into the LA. Seven days after surgery, rats were anesthetized and a catheter was inserted into the femoral vein. The animals were immobilized and allowed to recover from anesthesia for at least two hours. In eight rats, 1.0μL (1.0μg) of KA was injected into the LA, and 1.0 μL of phosphate buffer solution was injected into the LA in six control rats. Sixty minutes after injection, 14C-ZNS was administered intravenously, and an autoradiographic study was done.Results:During limbic status epilepticus, only seizures in the sensorimotor cortex were markedly attenuated a few minutes after 14C-ZNS administration. Additionally, high uptake of 14C-ZNS was noted ipsilaterally in the sensorimotor cortex, parietal cortex and thalamus (lateral portion). In control rats, no EEG change was seen, and distribution of 14C-ZNS was rather homogeneous.Conclusion:These results suggested that ZNS suppresses secondary generalization of limbic seizures by a direct effect on the cerebral cortex.

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SPECT imaging in focal epilepsy

Duncan¹

1997

SPECT Imaging of the Brain

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Uncoupling of local blood flow and metabolism in the hippocampal CA3 in kainic acid-induced limbic seizure status

Cited by 57 publications

References 29 publications

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

SPECT imaging in focal epilepsy

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Uncoupling of local blood flow and metabolism in the hippocampal CA3 in kainic acid-induced limbic seizure status

Cited by 57 publications

References 29 publications

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

A novel approach for imaging brain–behavior relationships in mice reveals unexpected metabolic patterns during seizures in the absence of tissue plasminogen activator

Regional Accumulation of 14C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

SPECT imaging in focal epilepsy

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Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures