Insights into the role astrocytes and microglia play in normal and diseased brain functioning has expanded drastically over the last decade. Recently, chemogenetic tools have emerged as cutting-edge techniques, allowing targeted and spatiotemporal precise manipulation of a specific glial cell type. As a result, significant advances in astrocyte and microglial cell function have been made, showing how glial cells can intervene in central nervous system (CNS) functions such as cognition, reward and feeding behavior in addition to their established contribution in brain diseases, pain, and CNS inflammation. Here, we discuss the latest insights in glial functions in health and disease that have been made through the application of chemogenetics. We will focus on the manipulation of intracellular signaling pathways induced by activation of the designer receptors exclusively activated by designer drugs (DREADDs) in astrocytes and microglia. We will also elaborate on some of the potential pitfalls and the translational potential of the DREADD technology.

Microglia, the innate immune cells of the central nervous system, actively participate in brain development by supporting neuronal maturation and refining synaptic connections. These cells are emerging as highly metabolically flexible, able to oxidize different energetic substrates to meet their energy demand. Lactate is particularly abundant in the brain, but whether microglia use it as a metabolic fuel has been poorly explored. Here we show that microglia can import lactate, and this is coupled with increased lysosomal acidification. In vitro, loss of the monocarboxylate transporter MCT4 in microglia prevents lactate-induced lysosomal modulation and leads to defective cargo degradation. Microglial depletion of MCT4 in vivo leads to impaired synaptic pruning, associated with increased excitation in hippocampal neurons, enhanced AMPA/GABA ratio, vulnerability to seizures and anxiety-like phenotype. Overall, these findings show that selective disruption of the MCT4 transporter in microglia is sufficient to alter synapse refinement and to induce defects in mouse brain development and adult behavior.

Microglia, the resident macrophages of the central nervous system (CNS), play important functions in the healthy and diseased brain. In the emerging field of immunometabolism, progress has been made in understanding how cellular metabolism can orchestrate the key responses of tissue macrophages, such as phagocytosis and inflammation. However, very little is known about the metabolic control of microglia. Lactate, now recognized as a crucial metabolite and a central substrate in metabolic flexibility, is emerging not only as a novel bioenergetic fuel for microglial metabolism but also as a potential modulator of cellular function. Parallels with macrophages will help in understanding how microglial lactate metabolism is implicated in brain physiology and pathology, and how it could be targeted for therapeutic purposes.

Epilepsy is a neurological disease affecting more than 50 million individuals worldwide. Notwithstanding the availability of a broad array of antiseizure drugs (ASDs), 30% of patients suffer from pharmacoresistant epilepsy. This highlights the urgent need for novel therapeutic options, preferably with an emphasis on new targets, since "me too" drugs have been shown to be of no avail. One of the appealing novel targets for ASDs is the ghrelin receptor (ghrelin-R). In epilepsy patients, alterations in the plasma levels of its endogenous ligand, ghrelin, have been described, and various ghrelin-R ligands are anticonvulsant in preclinical seizure and epilepsy models. Up until now, the exact mechanism-of-action of ghrelin-R-mediated anticonvulsant effects has remained poorly understood and is further complicated by multiple downstream signaling pathways and the heteromerization properties of the receptor. This review compiles current knowledge, and discusses the potential mechanisms-of-action of the anticonvulsant effects mediated by the ghrelin-R.

Serotoninergic psychedelics such as psilocybin have been reported to elicit a long-lasting reduction in depressive symptoms. Although the main target for serotoninergic psychedelics, serotonin type 2A receptor (5-HT2A), has been established, the possible mechanism of the antidepressant action of psychedelics remains unknown. Using the mouse forced swim test model, we examined whether the administration of the synthetic serotoninergic psychedelic 2,5-dimethoxy-4-iodoamphetamine (DOI) would modulate 5-HT2A receptor levels in the medial prefrontal cortex (mPFC) and revert stress-induced changes in behavior. Mice subjected to swim stress developed a passive stress-coping strategy when tested in the forced swim test 6 days later. This change in behavior was not associated with the hypothesized increase in 5-HT2A receptor-dependent head twitch behaviors or consistent changes in 5-HT2A receptor levels in the mPFC. When DOI was administered 1 day before the forced swim test, a low dose (0.2 mg/kg i.p.) unexpectedly increased immobility while a high dose (2 mg/kg i.p.) had no significant effect on immobility. Nevertheless, DOI evoked a dose-dependent decrease in 5-HT2A levels in the mPFC of mice previously exposed to swim stress. Our findings do not support the hypothesis that the downregulation of 5-HT2A receptors in the mPFC contributes to the antidepressant-like properties of serotoninergic psychedelics.

Introduction: Single housing of laboratory mice is a common practice to meet experimental needs, or to avoid intermale aggression. However, single housing is considered to negatively affect animal welfare and may compromise the scientific validity of experiments. The aim of this study was to investigate whether the use of a cage with a cage divider, which avoids physical contact between mice while maintaining sensory contact, may be a potential refinement strategy for experiments in which group housing of mice is not possible. Methods: Eight-week-old male C57BL/6JRj mice were single housed, pair housed or pair housed with a cage divider for four (experiment 1) or ten (experiment 2) weeks, after which we performed an open field test, Y-maze spontaneous alternation test, elevated plus maze test, an auditory fear conditioning task, and assessed responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis. Results: Housing conditions did not affect body weight, exploratory activity, anxiety, working memory, fear memory processing or markers for HPA-axis functioning in either experiment 1 or experiment 2. There was an increased distance traveled in mice housed with a cage divider compared to pair housed mice after 4 weeks, and after 10 weeks mice housed with a cage divider made significantly more arm entries in the Y-maze spontaneous alternation test. Conclusion: Taken together, our study did not provide evidence for robust differences in exploratory activity, anxiety, working memory and fear memory processing in male C57BL/6JRj mice that were single housed, pair housed or pair housed with a cage divider.

BACKGROUND:Current drugs for epilepsy affect seizures, but no antiepileptogenic or disease-modifying drugs are available that prevent or slow down epileptogenesis, which is characterized by neuronal cell loss, inflammation and aberrant network formation. Ghrelin and ghrelin receptor (ghrelin-R) agonists were previously found to exert anticonvulsant, neuroprotective and anti-inflammatory effects in seizure models and immediately after status epilepticus (SE). Therefore, the aim of this study was to assess whether the ghrelin-R agonist macimorelin is antiepileptogenic in the pharmacoresistant intrahippocampal kainic acid (IHKA) mouse model.METHODS:SE was induced in C57BL/6 mice by unilateral IHKA injection. Starting 24 h after SE, mice were treated intraperitoneally with macimorelin (5 mg/kg) or saline twice daily for 2 weeks, followed by a 2-week wash-out. Mice were continuously electroencephalogram-monitored, and at the end of the experiment neuroprotection and gliosis were assessed.RESULTS:Macimorelin significantly decreased the number and duration of seizures during the treatment period, but had no antiepileptogenic or disease-modifying effect in this dose regimen. While macimorelin did not significantly affect food intake or body weight over a 2-week treatment period, its acute orexigenic effect was preserved in epileptic mice but not in sham mice.CONCLUSIONS:While the full ghrelin-R agonist macimorelin was not significantly antiepileptogenic nor disease-modifying, this is the first study to demonstrate its anticonvulsant effects in the IHKA model of drug-refractory temporal lobe epilepsy. These findings highlight the potential use of macimorelin as a novel treatment option for seizure suppression in pharmacoresistant epilepsy.

Event Abstract Back to Event CHEMOGENETIC MODULATION OF ASTROCYTES IN A MODEL FOR TEMPORAL LOBE EPILEPSY Yana Van Den Herrewegen1*, An Buckinx1, Ann Van Eeckhaut1, Dimitri De Bundel1 and Ilse Smolders1 1 Vrije University Brussel, Belgium Temporal lobe epilepsy (TLE) is an acquired form of focal epilepsy, in which patients suffer from unprovoked, devastating seizures. In one-third of the patients the available anti-seizure drugs, which are mainly focused on neuronal targets, do not adequately control seizures, emphasizing the need for novel treatment strategies. More recently, the crucial role of astrocytes, the most abundant cell-type in the central nervous system, in TLE has been acknowledged. Reactive astrogliosis, characterized by morphological and molecular changes in astrocyte phenotype, is one of the hallmarks of TLE. They exhibit multiple changes in transporter- and enzyme expression, underlying epileptic hyperexcitability. For instance, during epileptiform activity, significant elevations in the frequency of Ca2+ oscillations have been observed in brain slices as well as in vivo. These Ca2+-waves lead to astrocytic glutamate release, which in turn favor synchronized neuronal activation. Moreover, astrocytes play a key role in cognition, which is often severely affected TLE-patients. We use a clinically relevant mouse model for TLE, the intrahippocampal kainic acid mouse model, achieved by unilateral kainic acid injection in the hippocampus of the mouse brain. The mice immediately enter a status epilepticus and develop spontaneous limbic seizures after a latency period of 2 weeks. First, we validated the mouse model for TLE and the related cognitive comorbidity. To this end we use in vivo EEG-monitoring and a test for spatial learning and memory, the Barnes maze test. On average, we have found that 36 ± 5,643 epileptic discharges per hour occurred (n = 7). In the Barnes maze test we demonstrated that the epileptic mice understand the paradigm context, but perform significantly worse compared to naive and sham control mice. Moreover, epileptic mice did not adopt the efficient, hippocampus-dependent spatial search strategy, but used a less-efficient serial search strategy, resulting in poorer task performance (i.e. longer escape-latencies and higher amounts of errors). As a next step, we will use a chemogenetic approach to selectively address the role of astrocyte signalling in TLE. To obtain astrocyte-specific modulation, hippocampal astrocytes are transfected with designer receptors exclusively activated by designer drugs (DREADDs), allowing us to evaluate the effect of astrocyte-specific modulation on the recurrence of spontaneous seizures and the associated comorbidities. To assure DREADD-functionality, we will perform ex vivo slice electrophysiology, ex vivo calcium imaging and immunohistochemistry experiments. As a final step, the effect of DREADD-transfected astrocytes on seizures and comorbidities will be determined. Acknowledgements Yana Van Den Herrewegen is a research fellow of the Fund for Scientific Research Flanders (FWO). An Buckinx is a research fellow of the Fund for Strategic Basic Research (SB-FWO). We would like to thank Gino De Smet for his technical assistance. This study was supported by the Scientific Fund Willy Gepts of UZ Brussel, the Queen Elizabeth Medical Foundation (ING prize) and the Vrije Universiteit Brussel. Keywords: Temporal lobe epilepcy, Intrahippocampal kainic acid mouse model, Barnes maze test, Astrocytes, Chemogenetic Conference: 13th National Congress of the Belgian Society for Neuroscience , Brussels, Belgium, 24 May - 24 May, 2019. Presentation Type: Poster presentation Topic: Behavioral/Systems Neuroscience Citation: Van Den Herrewegen Y, Buckinx A, Van Eeckhaut A, De Bundel D and Smolders I (2019). CHEMOGENETIC MODULATION OF ASTROCYTES IN A MODEL FOR TEMPORAL LOBE EPILEPSY. Front. Neurosci. Conference Abstract: 13th National Congress of the Belgian Society for Neuroscience . doi: 10.3389/conf.fnins.2019.96.00021 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 29 Apr 2019; Published Online: 27 Sep 2019. * Correspondence: Mx. Yana Van Den Herrewegen, Vrije University Brussel, Brussels, Belgium, yana.van.den.herrewegen@vub.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Yana Van Den Herrewegen An Buckinx Ann Van Eeckhaut Dimitri De Bundel Ilse Smolders Google Yana Van Den Herrewegen An Buckinx Ann Van Eeckhaut Dimitri De Bundel Ilse Smolders Google Scholar Yana Van Den Herrewegen An Buckinx Ann Van Eeckhaut Dimitri De Bundel Ilse Smolders PubMed Yana Van Den Herrewegen An Buckinx Ann Van Eeckhaut Dimitri De Bundel Ilse Smolders Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. 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Event Abstract Back to Event The effect of housing conditions on working memory and anxiety in male C57BL/6 mice An Buckinx1*, Andries Van Schuerbeek1*, Yana Van Den Herrewegen1, Ilse Smolders1 and Dimitri De Bundel1* 1 Experimental Pharmacology (EFAR/FASC), Vrije Universiteit Brussel, Belgium Laboratory mice are often single housed during experiments due to protocol requirements or in case of aggression towards cage mates. Several conflicting studies exist regarding behavioral consequences of individual housing of mice. However, the overall suggestion is that individual housing of mice is associated with increased anxiety and memory impairments (1, 2), and may affect scientific endpoints of experiments. In an attempt to reduce negative effects associated with single housing, we wanted to explore the potential use of a new type of cage that could improve animal welfare. This cage includes a cage divider that separates mice, as such avoiding physical contact while maintaining olfactory contact. The aim of this study is therefore to investigate anxiety and memory processing in mice housed in this new cage set-up compared to mice that are paired housed and single housed. 8-week-old male C57BL/6 mice were paired housed, single housed, or housed in a cage with a cage divider for a duration of four weeks, after which we performed behavioral tests, fear conditioning and the dexamethasone suppression test to assess plasma corticosterone levels. First, we performed the Y maze spontaneous alternation test, a test that is used to assess working memory, locomotor activity and exploratory drive in mice (2). The total number of arm entries and the spontaneous alternation percentage did not differ between the three groups. The open field test revealed no difference between the three experimental groups regarding locomotor activity nor anxiety-like behavior. An elevated plus maze test was performed to evaluate anxiety-like behavior. The total time spent in the open arms and the total distance travelled did not differ between groups, confirming the results obtained in the previous test. We performed a discriminative fear conditioning protocol (3), in which no significant differences were observed between experimental groups. The dexamethasone suppression test was performed at the end of the experiment to evaluate the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis (4, 5). Dexamethasone-treated mice had significantly lower corticosterone plasma levels compared to vehicle-treated mice, while basal corticosterone levels did not differ between groups. We dissected the adrenal glands and pituitary gland for further analysis, as the weight of the adrenal glands is associated with anxiety and stress (6). The weight of the pituitary gland and adrenal gland normalized against body weight did not significantly differ between experimental groups. Our results suggest that four weeks of single housing did not affect anxiety nor working memory in single housed mice, a much-debated topic in view of animal welfare. Behavioral observations were consistent with serum corticosterone levels, as the dexamethasone suppression test suggested no HPA axis dysregulation in neither of the experimental conditions. These results are possibly due to the short duration of housing conditions as previous studies were able to demonstrate differences in anxiety-like behavior, memory impairments and an increase in locomotor activity after eight weeks of single housing (1, 2). Therefore, future perspectives are to evaluate anxiety-like behavior and working memory after a housing duration of ten weeks. This will enable us to more effectively study the potential use of the cage with a cage divider that could improve animal welfare. * These authors contributed equally to this work. References 1. Kalliokoski, O., Teilmann, A.C., Jacobsen, K.R., Abelson, K.S., Hau, J. The lonely mouse - single housing affects serotonergic signaling integrity measured by 8-OH-DPAT-induced hypothermia in male mice. PLoS One. 2014; 9(12): e111065. 2. Võikar, V., Polus, A., Vasar, E., Rauvala H. Long-term individual housing in C57BL/6J and DBA/2 mice: assessment of behavioral consequences. Genes Brain Behav. 2005 Jun;4(4):240-52. 3. De Bundel, D., Zussy, C., Espallergues, J., Gerfen, C.R., Girault, J.A., Valjent, E. Dopamine D2 receptors gate generalization of conditioned threat responses through mTORC1 signaling in the extended amygdala. Mol Psychiatry. 2016 Nov;21(11):1545-1553. 4. Lee, R. and Sawa, A. Environmental stressors and epigenetic control of the hypothalamic-pituitary-adrenal-axis (HPA-axis). Neuroendocrinology. 2014; 100(4): 278–287. 5. Jankord, R., Solomon, M.B., Albertz, J., Flak, J.N., Zhang, R., Herman, J.P. Stress vulnerability during adolescent development in rats. Endocrinology. 2010;152(2):629–638. 6. Ieraci, A., Mallei, A., Popoli, M. Social Isolation Stress Induces Anxious-Depressive-Like Behavior and Alterations of Neuroplasticity-Related Genes in Adult Male Mice. Neural Plast. 2016;2016:6212983. Keywords: Anxiety, Single housing, C57BL/6, Fear conditioning, Behavior Conference: 13th National Congress of the Belgian Society for Neuroscience , Brussels, Belgium, 24 May - 24 May, 2019. Presentation Type: Poster presentation Topic: Behavioral/Systems Neuroscience Citation: Buckinx A, Van Schuerbeek A, Van Den Herrewegen Y, Smolders I and De Bundel D (2019). The effect of housing conditions on working memory and anxiety in male C57BL/6 mice. Front. Neurosci. Conference Abstract: 13th National Congress of the Belgian Society for Neuroscience . doi: 10.3389/conf.fnins.2019.96.00004 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 May 2019; Published Online: 27 Sep 2019. * Correspondence: Miss. An Buckinx, Experimental Pharmacology (EFAR/FASC), Vrije Universiteit Brussel, Brussels, Belgium, an.buckinx@vub.be Mr. Andries Van Schuerbeek, Experimental Pharmacology (EFAR/FASC), Vrije Universiteit Brussel, Brussels, Belgium, andries.van.schuerbeek@vub.be Mx. Dimitri De Bundel, Experimental Pharmacology (EFAR/FASC), Vrije Universiteit Brussel, Brussels, Belgium, dimitri.de.bundel@vub.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers An Buckinx Andries Van Schuerbeek Yana Van Den Herrewegen Ilse Smolders Dimitri De Bundel Google An Buckinx Andries Van Schuerbeek Yana Van Den Herrewegen Ilse Smolders Dimitri De Bundel Google Scholar An Buckinx Andries Van Schuerbeek Yana Van Den Herrewegen Ilse Smolders Dimitri De Bundel PubMed An Buckinx Andries Van Schuerbeek Yana Van Den Herrewegen Ilse Smolders Dimitri De Bundel Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gαq/11, Gαi/o, Gα12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1843), a Gαq and Gα12 biased ligand unable to recruit β-arrestin (YIL781), a ghrelin-R antagonist (JMV-2959), or saline. Mice treated with JMV-1843 had fewer and less severe seizures compared to saline-treated controls, while mice treated with YIL781 experienced longer and more severe seizures. JMV-2959 treatment did not lead to differences in seizure severity and number. Altogether, these results indicate that the Gαq or Gα12 signaling pathways are not responsible for mediating JMV-1843′s anticonvulsive effects and suggest a possible involvement of β-arrestin signaling in the anticonvulsive effects mediated by ghrelin-R modulation.

Temporal lobe epilepsy (TLE) is an acquired form of focal epilepsy, in which patients not only suffer from unprovoked, devastating seizures, but also from severe comorbidities, such as cognitive dysfunction. Correspondingly, several animal models of TLE exhibit memory dysfunction, especially spatial memory. The Morris water maze test is the most commonly used test for assessing spatial learning and memory in rodents. However, high stress and poor swimming abilities are common confounders and may contribute to misinterpretation. Particularly epileptic mice show altered behaviour during the test as they fail to understand the paradigm context. In the Barnes maze test, a dry-land maze test for spatial learning and memory that uses milder aversive stimuli, these drawbacks have not yet been reported. In the present study, we use this task to evaluate spatial learning and memory in the intrahippocampal kainic acid mouse model of TLE. We demonstrate that the epileptic mice understand the Barnes maze paradigm context, as they learn the location of the escape-chamber by using a serial search strategy but fail to develop the more efficient spatial search strategy. Our data indicate that the Barnes maze may be a better alternative to the Morris water maze for assessing search strategies and impairment of learning and memory in epileptic mice.

Event Abstract Back to Event Wireless telemetry as an ideal tool for continuous intrahippocampal EEG recording in chronic epilepsy mouse models Yana Van Den Herrewegen1*, An Buckinx1*, Gino De Smet1, Ilse J. Smolders1 and Dimitri De Bundel1 1 Vrije Universiteit Brussel, Experimental Pharmacology (EFAR), cluster Neurosciences, Belgium Tethered recording systems are routinely used as a method for long-term continuous EEG monitoring in animal models of epilepsy. Nevertheless, tethered systems display some disadvantages when chronically used in mice, in some cases even compromising experiments and behavioral follow-up of the mice. Therefore, wireless telemetry systems are increasingly being used as an alternative method to precisely measure biopotentials in the rodent brain. As EEG recordings are the most powerful read-outs in animal models of epilepsy, we evaluated the use of wireless radio-telemetry in the intrahippocampal post-status epilepticus kainic acid model, an established mouse model for studying temporal lobe epilepsy and epileptogenesis. Via intraperitoneal implantation of a radiofrequency transmitter (ETA-F10, DSI) and electrodes positioned in the hippocampus, we were able to record intrahippocampal signals for up to two months. We could clearly monitor the epileptic activity during the status epilepticus, followed by a short latent period and the subsequent occurrence of the typical spontaneous epileptic discharges. This study discusses the advantages of telemetric EEG recordings and strategies to maximize the signal-to-noise ratio in order to obtain high-quality deep-brain EEG recordings. In conclusion, wireless telemetry systems are a valuable EEG monitoring method in the intrahippocampal kainic acid mouse model and other models of chronic epilepsy in mice. References Bouilleret V, Ridoux V, Depaulis A, et al. Recurrent seizures and hippocampal sclerosis following intrahippocampal kainate injection in adult mice: electroencephalography, histopathology and synaptic reorganization similar to mesial temporal lobe epilepsy. Neuroscience. 1999; Mar;89(3):717-29. Duveau V, Pouyatos B, Bressand K, et al. Differential Effects of Antiepileptic Drugs on Focal Seizures in the Intrahippocampal Kainate Mouse Model of Mesial Temporal Lobe Epilepsy. CNS Neuroscience & Therapeutics: CNS Neurosci Ther. 2016;(22):497-50. doi: 10.1111/cns.12523 Lundt A, Wormuth C, Siwek ME, et al. EEG Radiotelemetry in Small Laboratory Rodents: A Powerful State-of-the Art Approach in Neuropsychiatric, Neurodegenerative, and Epilepsy Research. Neural Plasticity. 2016;2016:8213878. doi:10.1155/2016/8213878. Twele F, Tollner K, Bankstahl M, Loscher W, et al. The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain. Epilepsia Open, 2016; 1(1):45–60,. doi: 10.1002/epi4.2 Zayachkivsky A, Lehmkuhle MJ, Dudek FE. Long-term Continuous EEG Monitoring in Small Rodent Models of Human Disease Using the Epoch Wireless Transmitter System. Journal of Visualized Experiments : JoVE. 2015;(101):52554. doi:10.3791/52554. Keywords: wireless radio-telemetry, EEG, Epilepsy, Temporal Lobe, mouse models, Seizures Conference: 12th National Congress of the Belgian Society for Neuroscience, Gent, Belgium, 22 May - 22 May, 2017. Presentation Type: Poster Presentation Topic: Novel Methods and Technology Development Citation: Van Den Herrewegen Y, Buckinx A, De Smet G, Smolders IJ and De Bundel D (2019). Wireless telemetry as an ideal tool for continuous intrahippocampal EEG recording in chronic epilepsy mouse models. Front. Neurosci. Conference Abstract: 12th National Congress of the Belgian Society for Neuroscience. doi: 10.3389/conf.fnins.2017.94.00001 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 May 2017; Published Online: 25 Jan 2019. * Correspondence: Miss. Yana Van Den Herrewegen, Vrije Universiteit Brussel, Experimental Pharmacology (EFAR), cluster Neurosciences, Brussels, 1090, Belgium, yana.van.den.herrewegen@vub.ac.be Miss. An Buckinx, Vrije Universiteit Brussel, Experimental Pharmacology (EFAR), cluster Neurosciences, Brussels, 1090, Belgium, an.buckinx@vub.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Yana Van Den Herrewegen An Buckinx Gino De Smet Ilse J Smolders Dimitri De Bundel Google Yana Van Den Herrewegen An Buckinx Gino De Smet Ilse J Smolders Dimitri De Bundel Google Scholar Yana Van Den Herrewegen An Buckinx Gino De Smet Ilse J Smolders Dimitri De Bundel PubMed Yana Van Den Herrewegen An Buckinx Gino De Smet Ilse J Smolders Dimitri De Bundel Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.