Amygdala‐kindling induces alterations in neuronal density and in density of degenerated fibers

Halbach, Oliver von Bohlen und; Schulze, Katrin; Albrecht, Doris

doi:10.1002/hipo.10179

Cited by 15 publications

(4 citation statements)

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“…Although a significant reduction of cell density and the appearance of degenerated fibers was evident in the LA after 15 stage V seizures in BLA-kindled rats (von Bohlen und Halbach et al 2004), our pharmacological investigations in intracellular recordings showed that kindling also caused changes in GABAergic and glutamatergic transmission ).…”

Section: Effect Of Kindling Procedures On Ltp Magnitudementioning

confidence: 65%

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Schubert¹,

Siegmund²,

Pape³

et al. 2005

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Temporal lobe epilepsy (TLE) is often accompanied by interictal behavioral abnormalities, such as fear and memory impairment. To identify possible underlying substrates, we analyzed long-term synaptic plasticity in two relevant brain regions, the lateral amygdala (LA) and the CA1 region of the hippocampus, in the kindling model of epilepsy. Wistar rats were kindled through daily administration of brief electrical stimulations to the left basolateral nucleus of the amygdala. Field potential recordings were performed in slices obtained from kindled rats 48 h after the last induced seizure, and in slices from sham-implanted and nonimplanted controls. Kindling resulted in a significant impairment of long-term potentiation (LTP) in both the LA and the CA1, the magnitude of which was dependent on the number of prior stage V seizures. Saturation of CA1-LTP, assessed through repeated spaced delivery of high-frequency stimulation, occurred at lower levels in kindled compared to sham-implanted animals, consistent with the hypothesis of reduced capacity of further synaptic strengthening. Furthermore, theta pulse stimulation elicited long-term depression in the amygdala in nonimplanted and sham-implanted controls, whereas the same stimulation protocol stimulation caused LTP in kindled rats. In conclusion, kindling differentially affects the magnitude, saturation, and polarity of LTP in the CA1 and LA, respectively, most likely indicating an activity-dependent mechanism in the context of synaptic metaplasticity.Convulsive diseases in humans such as temporal lobe epilepsy (TLE) are often accompanied by impairments of learning and memory. In addition, TLE patients typically display emotional disturbances, in particular negative emotions such as fear, anxiety, and depression (Kalynchuk 2000). A wealth of data has established that the amygdala plays a critical role in neuronal activity and synaptic plasticity related to both emotionally modulated signal processing and epilepsy (Gloor 1990;Maren 1999;LeDoux 2000). Synapses in the amygdala display long-term potentiation (LTP) (Chapman and Chattarji 2000; LeDoux 2000; Maren 2001), a long-lasting increase of synaptic strength that is widely believed to be a cellular basis of learning and memory (Bliss and Collingridge 1993). The amygdala possesses the lowest threshold for the induction of kindling (Löscher 1997), an established experimental model of TLE in which daily electrical stimulation results in a gradual progression and intensification of limbic motor seizures (Goddard et al. 1969). Although kindling has been extensively investigated in the context of its clinical relevance to epilepsy and seizure-induced synaptic potentiation, only a few studies that relate to plastic synaptic changes after kindling are available. Therefore, the present study was undertaken to systematically analyze the influence of kindling 48 h after the last seizure on long-term synaptic plasticity, LTP, and long-term depression (LTD) in the lateral nucleus of the amygdala (LA) in rats. The LA was chosen ...

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Section: Effect Of Kindling Procedures On Ltp Magnitudementioning

confidence: 65%

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Schubert¹,

Siegmund²,

Pape³

et al. 2005

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“…In our protocol, direct stimulation of the amygdaloid complex acts as the epileptogenic focus from where epileptic activity spreads toward projection areas that receive amygdala inputs, including hippocampal formation, which exhibited epilepsy-related cellular changes (Lothman et al, 1985; Ikegaya et al, 1996; Aronica et al, 2000; Valentine et al, 2004; Musto et al, 2009). Moreover, the progressive increase in the ADs duration showed that the use of stimulation intensities below the ADs threshold effectively promotes the long-term plasticity described in the kindling model (Racine, 1972a; Abe, 2001; Schubert et al, 2005) minimizing the cellular damage attributable to excessive electrical charge utilized in other protocols (Lothman et al, 1985, 1989; Von Bohlen und Halbach et al, 2004; Fournier et al, 2010). …”

Section: Discussionmentioning

confidence: 99%

“…Classical kindling protocols require a long period of stimulation (up to 30 days) applied directly to the amygdaloid complex (Behr et al, 2000; Von Bohlen und Halbach et al, 2004). Several variants of the classic protocol have been developed (Gersch and Goddard, 1970; Racine, 1972b; Lothman et al, 1985; Fournier et al, 2010) by changing the stimulation site and/or by adjusting stimulation parameters (i.e., intensity, pulse duration, phase, frequency, stimuli train duration and inter-stimulus interval).…”

Section: Introductionmentioning

confidence: 99%

A new rapid kindling variant for induction of cortical epileptogenesis in freely moving rats

Morales

Álvarez-Ferradas

Roncagliolo

et al. 2014

Front. Cell. Neurosci.

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Kindling, one of the most used models of experimental epilepsy is based on daily electrical stimulation in several brain structures. Unlike the classic or slow kindling protocols (SK), the rapid kindling types (RK) described until now require continuous stimulation at suprathreshold intensities applied directly to the same brain structure used for subsequent electrophysiological and immunohistochemical studies, usually the hippocampus. However, the cellular changes observed in these rapid protocols, such as astrogliosis and neuronal loss, could be due to experimental manipulation more than to epileptogenesis-related alterations. Here, we developed a new RK protocol in order to generate an improved model of temporal lobe epilepsy (TLE) which allows gradual progression of the epilepsy as well as obtaining an epileptic hippocampus, thus avoiding direct surgical manipulation and electric stimulation over this structure. This new protocol consists of basolateral amygdala (BLA) stimulation with 10 trains of biphasic pulses (10 s; 50 Hz) per day with 20 min-intervals, during 3 consecutive days, using a subconvulsive and subthreshold intensity, which guarantees tissue integrity. The progression of epileptic activity was evaluated in freely moving rats through electroencephalographic (EEG) recordings from cortex and amygdala, accompanied with synchronized video recordings. Moreover, we assessed the effectiveness of RK protocol and the establishment of epilepsy by evaluating cellular alterations of hippocampal slices from kindled rats. RK protocol induced convulsive states similar to SK protocols but in 3 days, with persistently lowered threshold to seizure induction and epileptogenic-dependent cellular changes in amygdala projection areas. We concluded that this novel RK protocol introduces a new variant of the chronic epileptogenesis models in freely moving rats, which is faster, highly reproducible and causes minimum cell damage with respect to that observed in other experimental models of epilepsy.

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“…In order to avoid the counting of all stained fibres within a brain region, the determination of the relative fibre densities allows a quick and reliable measurement of fibre densities. This method for analysing fibre densities is also suitable for quantifying degenerating axons, e.g., in animal models of epilepsy (von Bohlen und Halbach et al 2004). In most cases, images are taken at high magnification by using a digital camera and are analysed off-line as follows:

a sampling line of 100 μm is randomly placed over the image and the number of positive fibres crossing the line is counted in different sections of each brain region and animal (Greferath et al 2012)

a frame with a defined region of interest is randomly placed over the image.

…”

Section: Fibre Densitiesmentioning

confidence: 99%

Analysis of morphological changes as a key method in studying psychiatric animal models

Halbach

2013

Cell Tissue Res

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A major interest in the analysis of animal models of psychiatric diseases is their underlying cellular pathology and to gain information regarding whether pharmacological treatments, genetic differences or an altered environment exert an impact upon the brain morphology or on the morphology or activity of single neurones. In this review, several key methods will be introduced that allow the analysis of morphological changes that are frequently observed in psychiatric animal models. An overview of the techniques that enable dendritic arborisation, alterations in dendritic spines and changes in fibre densities to be analysed are described. Moreover, methods for the analysis of adult neurogenesis and neurodegeneration and for the analysis of neuronal activity in fixed brain tissue are described. An important step during the analysis of morphological changes is the estimation of the number of stained cells. Since conventional cell counting methods have several limitations, two different approaches that permit an estimate of the number of stained cells within three-dimensional tissue are also discussed.

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Amygdala‐kindling induces alterations in neuronal density and in density of degenerated fibers

Cited by 15 publications

References 51 publications

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

A new rapid kindling variant for induction of cortical epileptogenesis in freely moving rats

Analysis of morphological changes as a key method in studying psychiatric animal models

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