Interactions between limbic, thalamo-striatal-cortical, and central autonomic pathways during epileptic seizure progression

Mraovitch, Sima; Calando, Yolande

doi:10.1002/(sici)1096-9861(19990816)411:1<145::aid-cne11>3.0.co;2-1

Cited by 48 publications

(20 citation statements)

References 75 publications

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“…The GABAergic thalamic reticular nucleus (TRN), a key component of thalamocortical circuits, has been implicated by other work as being associated with the progression of limbic epileptogenesis [18]. Consistent with this, the administration of carbachol, a muscarinic receptor agonist, into lateral thalamic regions including the ventrobasal complex of thalamus and TRN was able to stimulate limbic and generalized convulsive seizures [19], [20].…”

Section: Introductionmentioning

confidence: 67%

Enduring Effects of Early Life Stress on Firing Patterns of Hippocampal and Thalamocortical Neurons in Rats: Implications for Limbic Epilepsy

et al. 2013

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Early life stress results in an enduring vulnerability to kindling-induced epileptogenesis in rats, but the underlying mechanisms are not well understood. Recent studies indicate the involvement of thalamocortical neuronal circuits in the progression of kindling epileptogenesis. Therefore, we sought to determine in vivo the effects of early life stress and amygdala kindling on the firing pattern of hippocampus as well as thalamic and cortical neurons. Eight week old male Wistar rats, previously exposed to maternal separation (MS) early life stress or early handling (EH), underwent amygdala kindling (or sham kindling). Once fully kindled, in vivo juxtacellular recordings in hippocampal, thalamic and cortical regions were performed under neuroleptic analgesia. In the thalamic reticular nucleus cells both kindling and MS independently lowered firing frequency and enhanced burst firing. Further, burst firing in the thalamic reticular nucleus was significantly increased in kindled MS rats compared to kindled EH rats (p<0.05). In addition, MS enhanced burst firing of hippocampal pyramidal neurons. Following a stimulation-induced seizure, somatosensory cortical neurons exhibited a more pronounced increase in burst firing in MS rats than in EH rats. These data demonstrate changes in firing patterns in thalamocortical and hippocampal regions resulting from both MS and amygdala kindling, which may reflect cellular changes underlying the enhanced vulnerability to kindling in rats that have been exposed to early life stress.

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Section: Introductionmentioning

confidence: 67%

Enduring Effects of Early Life Stress on Firing Patterns of Hippocampal and Thalamocortical Neurons in Rats: Implications for Limbic Epilepsy

et al. 2013

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“…Mraovitch and Calando [73] used immunocytochemistry to determine the regional and temporal distribution of Fos protein expression in awake and unrestrained rats after a unilateral stereotaxic microinjection of the cholinergic agonist carbachol in the thalamic ventroposterolateral and reticular nuclei, previously shown to cause limbic and generalized seizures [73]. They found that paraventricular thalamus activation occurred after 15 min after administration of epileptic agents.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Reduces Cocaine-Induced Seizures and Mortality in Mice

Chen

Ivanic

Chuang

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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The aims of this study were to characterize the protective profile of electroacupuncture (EA) on cocaine-induced seizures and mortality in mice. Mice were treated with EA (2 Hz, 50 Hz, and 100 Hz), or they underwent needle insertion without anesthesia at the Dazhui (GV14) and Baihui (GV20) acupoints before cocaine administration. EA at 50 Hz applied to GV14 and GV20 significantly reduced the seizure severity induced by a single dose of cocaine (75 mg/kg; i.p.). Furthermore, needle insertion into GV14 and GV20 and EA at 2 Hz and 50 Hz at both acupoints significantly reduced the mortality rate induced by a single lethal dose of cocaine (125 mg/kg; i.p.). In the sham control group, EA at 50 Hz applied to bilateral Tianzong (SI11) acupoints had no protective effects against cocaine. In addition, EA at 50 Hz applied to GV14 and GV20 failed to reduce the incidence of seizures and mortality induced by the local anesthetic procaine. In an immunohistochemistry study, EA (50 Hz) pretreatment at GV14 and GV20 decreased cocaine (75 mg/kg; i.p.)-induced c-Fos expression in the paraventricular thalamus. While the dopamine D3 receptor antagonist, SB-277011-A (30 mg/kg; s.c), did not by itself affect cocaine-induced seizure severity, it prevented the effects of EA on cocaine-induced seizures. These results suggest that EA alleviates cocaine-induced seizures and mortality and that the dopamine D3 receptor is involved, at least in part, in the anticonvulsant effects of EA in mice.

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Section: Discussionmentioning

confidence: 99%

“…Connections between these regions primarily use glutamate as a neurotransmitter, whereas GABAergic interneurons modulate this circuitry (Mraovitch and Calando, 1999). The prelimbic cortex, which also showed genotype-dependent activation in ethanol withdrawn mice, sends glutamatergic projections to the hippocampus and basolateral amygdala (Mraovitch and Calando, 1999; Watson et al, 1985). Furthermore, the basolateral amygdala and the hippocampus both have excitatory glutamatergic projections (Nieuwenhuys, 1996), while the lateral septum sends inhibitory GABAergic projections (Nieuwenhuys, 1996), to the central nucleus of the amygdala.…”

Section: Discussionmentioning

confidence: 99%

Differential activation of limbic circuitry associated with chronic ethanol withdrawal in DBA/2J and C57BL/6J mice

Chen

Reilly

Kozell

et al. 2009

Alcohol

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Although no animal model exactly duplicates clinically defined alcoholism, models for specific factors, such as the withdrawal syndrome, are useful for identifying potential neural determinants of liability in humans. The well-documented difference in withdrawal severity following chronic ethanol exposure, between the DBA/2J and C57BL/6J mouse strains, provides an excellent starting point for dissecting the neural circuitry affecting predisposition to physical dependence on ethanol. To induce physical dependence, we used a paradigm in which mice were continuously exposed to ethanol vapor for 72 hr. Ethanol-exposed and air-exposed (control) mice received daily injections of pyrazole hydrochloride, an alcohol dehydrogenase inhibitor, to stabilize blood ethanol levels. Ethanol-dependent and air-exposed mice were killed seven hours after removal from the inhalation chambers. This time point corresponds to the time of peak ethanol withdrawal severity. The brains were processed to assess neural activation associated with ethanol withdrawal indexed by c-Fos immunostaining. Ethanol-withdrawn DBA/2J mice showed significantly (p<0.05) greater neural activation than ethanol-withdrawn C57BL/6J mice in the dentate gyrus, hippocampus CA3, lateral septum, basolateral and central nuclei of the amygdala, and prelimbic cortex. Taken together with results using an acute model, our data suggest that progression from acute ethanol withdrawal to the more severe withdrawal associated with physical dependence following chronic ethanol exposure involves recruitment of neurons in the hippocampal formation, amygdala and prelimbic cortex. To our knowledge, these are the first studies to use c-Fos to identify the brain regions and neurocircuitry that distinguish between chronic and acute ethanol withdrawal severity using informative animal models.

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Interactions between limbic, thalamo-striatal-cortical, and central autonomic pathways during epileptic seizure progression

Cited by 48 publications

References 75 publications

Enduring Effects of Early Life Stress on Firing Patterns of Hippocampal and Thalamocortical Neurons in Rats: Implications for Limbic Epilepsy

Enduring Effects of Early Life Stress on Firing Patterns of Hippocampal and Thalamocortical Neurons in Rats: Implications for Limbic Epilepsy

Electroacupuncture Reduces Cocaine-Induced Seizures and Mortality in Mice

Differential activation of limbic circuitry associated with chronic ethanol withdrawal in DBA/2J and C57BL/6J mice

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