Cytoarchitectonics and afferent/efferent reorganization of neurons in layers II and III of the lateral entorhinal cortex in the mouse pilocarpine model of temporal lobe epilepsy

Dong, Liang; Tang, Yong; Tang, Feng Ru

doi:10.1002/jnr.21583

Cited by 8 publications

(6 citation statements)

References 65 publications

(81 reference statements)

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“…All animal experiments were approved by the Institutional Animal Care and Use Committee at the Tan Tock Seng Hospital/National Neuroscience Institute. Male Swiss mice (25–30 g) used for all experiments in this study were treated as described previously (Ma et al, 2006 , 2008 ; Tang et al, 2006 ). In brief, mice were given a single subcutaneous injection of methyl-scopolamine nitrate (1 mg/kg) 30 min before the injection of either saline or pilocarpine to limit the peripheral toxic effects.…”

Section: Methodsmentioning

confidence: 99%

“…These epileptic mice share similar neuropathological mechanisms and seizure states with human TLE; animals experiencing status epilepticus (SE) for several hours showed histopathological alterations throughout the limbic system (Coulter, 1999 ; Curia et al, 2008 ; Tang and Loke, 2010 ; Reddy and Kuruba, 2013 ). The affected areas involve not only the hippocampus but also the amygdala, the entorhinal cortex (Du et al, 1995 ; Biagini et al, 2005 ; Wozny et al, 2005 ; Ma et al, 2008 ), the piriform cortex, the thalamus (Mathieson, 1975 ; Mello and Covolan, 1996 ), and specifically the midline thalamic nuclei (including the medial dorsal nucleus; Ben-Ari et al, 1980 ; Lothman and Collins, 1981 ; Cavalheiro et al, 1991 ). Although these affected areas are directly connected to the hippocampus and are similar to those found in human TLE, it is still unclear if there are any lesions in other regions not observed in human TLE.…”

Section: Introductionmentioning

confidence: 99%

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Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Goh

et al. 2016

Front. Neuroanat.

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In this study, we investigated the reorganized basolateral amygdala (BLA)-subiculum pathway in a status epilepticus (SE) mouse model with epileptic episodes induced by pilocarpine. We have previously observed a dramatic loss of neurons in the CA1–3 fields of the hippocampus in epileptic mice. Herein, we observed a 43–57% reduction in the number of neurons in the BLA of epileptic mice. However, injection of an anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA-L) into the BLA indicated 25.63% increase in the number of PHA-L-immunopositive terminal-like structures in the ventral subiculum (v-Sub) of epileptic mice as compared to control mice. These data suggest that the projections from the basal nucleus at BLA to the vSub in epileptic mice are resistant to epilepsy-induced damage. Consequently, these epileptic mice exhibit partially impairment but not total loss of context-dependent fear memory. Epileptic mice also show increased c-Fos expression in the BLA and vSub when subjected to contextual memory test, suggesting the participation of these two brain areas in foot shock-dependent fear conditioning. These results indicate the presence of functional neural connections between the BLA-vSub regions that participate in learning and memory in epileptic mice.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Goh

et al. 2016

Front. Neuroanat.

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“…This unbalance may be stronger in some regions. For example, in the mouse model of TLE, significant loss of the total neurons (both principal and interneurons) in layers II-III of entorhinal cortex, and drastic loss of interneurons in layer IV-VI of entorhinal cortex, may result in a marked unbalance between excitatory and inhibitory components [166]. In addition, an excess excitation is provided by the sprouted CA1 pyramidal cell axons [117, 167, 168], as well as by the sprouting of afferents from the dentate gyrus, CA3, and/or the CA2 region [169-172], and/or from extrahippocampal pathways [168].…”

Section: Neuronal Loss and Plasticitymentioning

confidence: 99%

Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

Curia

Lucchi²,

Vinet³

et al. 2014

CMC

183

135

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Temporal lobe epilepsy (TLE) is frequently associated with hippocampal sclerosis, possibly caused by a primary brain injury that occurred a long time before the appearance of neurological symptoms. This type of epilepsy is characterized by refractoriness to drug treatment, so to require surgical resection of mesial temporal regions involved in seizure onset. Even this last therapeutic approach may fail in giving relief to patients. Although prevention of hippocampal damage and epileptogenesis after a primary event could be a key innovative approach to TLE, the lack of clear data on the pathophysiological mechanisms leading to TLE does not allow any rational therapy. Here we address the current knowledge on mechanisms supposed to be involved in epileptogenesis, as well as on the possible innovative treatments that may lead to a preventive approach. Besides loss of principal neurons and of specific interneurons, network rearrangement caused by axonal sprouting and neurogenesis are well known phenomena that are integrated by changes in receptor and channel functioning and modifications in other cellular components. In particular, a growing body of evidence from the study of animal models suggests that disruption of vascular and astrocytic components of the blood-brain barrier takes place in injured brain regions such as the hippocampus and piriform cortex. These events may be counteracted by drugs able to prevent damage to the vascular component, as in the case of the growth hormone secretagogue ghrelin and its analogues. A thoroughly investigation on these new pharmacological tools may lead to design effective preventive therapies.

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“…The infralimbic PFC modulates amygdala‐dependent fear memories and has become a central element of extinction models (Quirk et al., 2006), but the role of the PFC in temporal lobe epilepsy is only rarely understood. One study described changes of efferent projections of the entorhinal cortex to the PFC after pilocarpine treatment in mice (Ma et al., 2008). We cannot exclude changes on the neural and network levels of the prefrontal cortex that are responsible for the observed impaired extinction of fear in SRS mice.…”

Section: Discussionmentioning

confidence: 99%

Impaired extinction of fear and maintained amygdala‐hippocampal theta synchrony in a mouse model of temporal lobe epilepsy

Lesting¹,

Geiger²,

Narayanan

et al. 2010

Epilepsia

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SUMMARYPurpose: The relationship between epilepsy and fear has received much attention. However, seizure-modulated fear and physiologic or structural correlates have not been examined systematically, and the underlying basics of network levels remain unclear to date. Therefore, this project was set up to characterize the neurophysiologic basis of seizure-related fear and the contribution of the amygdala-hippocampus system. Methods: The experimental strategy was composed of the following steps: (1) use of the mouse pilocarpine model of temporal lobe epilepsy (TLE); (2) behavioral analyses of anxiety states in the elevated plus maze test, light-dark avoidance test, and Pavlovian fear conditioning; and (3) probing neurophysiologic activity patterns in amygdala-hippocampal circuits in freely behaving mice.Results: Our results displayed no significant differences in basic anxiety levels comparing mice that developed spontaneous recurrent seizures (SRS) and controls. Furthermore, conditioned fear memory retrieval was not influenced in SRS mice. However, during fear memory extinction, SRS mice showed an extended freezing behavior and a maintained amygdala-hippocampal theta frequency synchronization compared to controls. Discussion: These results indicate specific alterations in conditioned fear behavior and related neurophysiologic activities in the amygdala-hippocampal network contributing to impaired fear memory extinction in mice with TLE. Clinically, the nonextinguished fear memories may well contribute to the experience of fear in patients with TLE.

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Cytoarchitectonics and afferent/efferent reorganization of neurons in layers II and III of the lateral entorhinal cortex in the mouse pilocarpine model of temporal lobe epilepsy

Cited by 8 publications

References 65 publications

Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

Impaired extinction of fear and maintained amygdala‐hippocampal theta synchrony in a mouse model of temporal lobe epilepsy

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