Seizure-like Activities Research Articles

Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure-Like Activities.

The corticostriatal connection plays a crucial role in cognitive, emotional, and motor control. However, the specific roles and synaptic transmissions of corticostriatal connection are less studied, especially the corticostriatal transmission from the anterior cingulate cortex (ACC). Here, a direct glutamatergic excitatory synaptic transmission in the corticostriatal projection from the ACC is found. Kainate receptors (KAR)-mediated synaptic transmission is increased in this corticostriatal connection both in vitro and in vivo seizure-like activities. GluK1 containing KARs and downstream calcium-stimulated adenylyl cyclase subtype 1 (AC1) are involved in the upregulation of KARs following seizure-like activities. Inhibiting the activities of ACC or its corticostriatal connection significantly attenuated pentylenetetrazole (PTZ)-induced seizure. Additionally, injection of GluK1 receptor antagonist UBP310 or the AC1 inhibitor NB001 both show antiepileptic effects. The studies provide direct evidence that KARs are involved in seizure activity in the corticostriatal connection and the KAR-AC1 signaling pathway is a potential novel antiepileptic strategy.

Spatial and amplitude dynamics of neurostimulation: Insights from the acute intrahippocampal kainate seizure mouse model.

Neurostimulation is an emerging treatment for patients with drug-resistant epilepsy, which is used to suppress, prevent, and terminate seizure activity. Unfortunately, after implantation and despite best clinical practice, most patients continue to have persistent seizures even after years of empirical optimization. The objective of this study is to determine optimal spatial and amplitude properties of neurostimulation in inhibiting epileptiform activity in an acute hippocampal seizure model. We performed high-throughput testing of high-frequency focal brain stimulation in the acute intrahippocampal kainic acid mouse model of status epilepticus. We evaluated combinations of six anatomic targets and three stimulus amplitudes. We found that the spike-suppressive effects of high-frequency neurostimulation are highly dependent on the stimulation amplitude and location, with higher amplitude stimulation being significantly more effective. Epileptiform spiking activity was significantly reduced with ipsilateral 250 μA stimulation of the CA1 and CA3 hippocampal regions with 21.5% and 22.2% reductions, respectively. In contrast, we found that spiking frequency and amplitude significantly increased with stimulation of the ventral hippocampal commissure. We further found spatial differences with broader effects from CA1 versus CA3 stimulation. These findings demonstrate that the effects of therapeutic neurostimulation in an acute hippocampal seizure model are highly dependent on the location of stimulation and stimulus amplitude. We provide a platform to optimize the anti-seizure effects of neurostimulation, and demonstrate that an exploration of the large electrical parameter and location space can improve current modalities for treating epilepsy. In this study, we tested how electrical pulses in the brain can help control seizures in mice. We found that the electrode's placement and the stimulation amplitude had a large effect on outcomes. Some brain regions, notably nearby CA1 and CA3, responded positively with reduced seizure-like activities, while others showed increased activity. These findings emphasize that choosing the right spot for the electrode and adjusting the strength of electrical pulses are both crucial when considering neurostimulation treatments for epilepsy.

Cannabinoid receptors involved in descending inhibition on spinal seizure-like activity in the phrenic output.

Seizure-like burst activities are induced by blockade of GABAA and/or glycine receptors in various spinal ventral roots of brainstem-spinal cord preparation from neonatal rodents. We found that this is not applicable to the phrenic nerve and that a new inhibitory descending pathway may suppress seizure-like activity in the phrenic nerve. Experiments were performed in brainstem-spinal cord preparation from newborn rats (age: 0-1 day). Left phrenic nerve and right C4 activities were recorded simultaneously. When GABAA and glycine receptors were blocked by 10 μM bicuculline and 10 μM strychnine (Bic+Str), seizure-like burst activities appeared in the fourth cervical ventral root (C4) but not the phrenic nerve. After making a transverse section at C1, the inspiratory burst activity disappeared from both C4 and the phrenic nerve, whereas seizure-like activity appeared in both nerves. We hypothesized that inhibitory descending pathways other than those via GABAA and/or glycine receptors (from the medulla to the spinal cord) work to avoid disturbance of regular respiratory-related diaphragm contraction by seizure-like activity. We found that cannabinoid receptor antagonist, AM251 was effective for the induction of seizure-like activity by Bic+Str in the phrenic nerve in brainstem-spinal cord preparation. Cannabinoid receptors may be involved in this descending inhibitory system.

ODP362 An Unexpected Finding of Adamantinomatous Type Craniopharyngioma in the Late Seventh Decade of Life: a case report

Abstract Background Craniopharyngioma is a rare solid, mixed solid, and benign cystic neoplasm derived from remnants of Rathke's pouch from the sellar region and its surroundings parasellar area. It mainly has two major histopathological subtypes, Adamantinomatous and Papillary. The adamantinomatous subtype is more common in children, and the papillary subtype is more common in adults. Clinical case: A 66-year-old male with no known endocrinological disorder presented with progressive fatigue, decreased oral intake, lightheadedness, nausea, visual changes, low libido, myalgia, nausea, vomiting, polyurea, headache, visual field defects, and seizure-like activities requiring hospital admission. The endocrinological workup revealed a deranged HPA axis (panhypopituitarism). MRI revealed 3 cm macroadenoma within the pituitary gland. An endonasal transsphenoidal resection of pituitary mass resection with abdominal fat graft was done as definitive treatment along with correction of the multiple endocrinological derangements. The surgical tissue biopsy revealed a rare with adamantinomatous type Craniopharyngioma WHO Grade I. He was discharged on testosterone supplements, hydrocortisone, levothyroxine, and Desmopressin with significant improvement in his symptoms. Conclusion Craniopharyngioma (CP) is a rare benign intracranial mass (incidence 0.5-2/100000) that can present with extensive endocrinological dysfunction. However, due to the lack of patient-level data and reporting of adult-onset craniopharyngiomas, it can be easily missed during the initial presentation. Not considering craniopharyngioma in differential diagnoses may result in delayed diagnosis and adverse outcomes. Although the papillary CP type is more common among adults, occasionally, adamantinomatous type CP may occur in this group of patients. Presentation: No date and time listed

Synaptic hyperexcitability of cytomegalic pyramidal neurons contributes to epileptogenesis in tuberous sclerosis complex.

SUMMARYTuberous sclerosis complex (TSC) is a developmental disorder associated with epilepsy, autism, and cognitive impairment. Despite inactivating mutations in the TSC1 or TSC2 genes and hyperactive mechanistic target of rapamycin (mTOR) signaling, the mechanisms underlying TSC-associated neurological symptoms remain incompletely understood. Here we generate a Tsc1 conditional knockout (CKO) mouse model in which Tsc1 inactivation in late embryonic radial glia causes social and cognitive impairment and spontaneous seizures. Tsc1 depletion occurs in a subset of layer 2/3 cortical pyramidal neurons, leading to development of cytomegalic pyramidal neurons (CPNs) that mimic dysplastic neurons in human TSC, featuring abnormal dendritic and axonal overgrowth, enhanced glutamatergic synaptic transmission, and increased susceptibility to seizure-like activities. We provide evidence that enhanced synaptic excitation in CPNs contributes to cortical hyperexcitability and epileptogenesis. In contrast, astrocytic regulation of synapse formation and synaptic transmission remains unchanged after late embryonic radial glial Tsc1 inactivation, and astrogliosis evolves secondary to seizures.

Risk Factors and Prognostic Follow-Up of Vasovagal Syncope Children With Seizure-Like Activities During Head-Up Tilt Test Induced-Syncope.

ObjectivesTo analyze the risk factors associated with seizure-like activities during head up tilt test (HUTT)-induced syncope in children with vasovagal syncope (VVS) and assess the prognosis of these patients.MethodsThis is a retrospective study. VVS children with or without seizure-like activities during HUTT-induced syncope were included in convulsive or non-convulsive group. The clinical characteristics, hemodynamic parameters during HUTT-induced syncope and follow-up data were reviewed from the HUTT case report form and analyzed.Results68 cases (25 males, mean age 11.86 ± 3.35 years) were enrolled in convulsive group and 65 cases in non-convulsive group (24 males, mean age 11.64 ± 2.11 years). There were statistical differences in history duration, response type, and asystole between the two groups (all P < 0.05). Fully adjusted logistic regression showed that the risk of seizure-like activities was increased by 37.18 folds for patients with asystole compared with those without asystole (P = 0.005), by 308.25 and 6.08 folds for patients with cardioinhibitory type or mixed type compared with vasoinhibitory type (P < 0.01). No significant difference was exhibited in negative HUTT conversion rate and the proportion of re-syncope patients between the two groups at follow-up (both P > 0.05). None of these convulsive patients underwent pacemaker implantation during follow-up.ConclusionsAsystole and response type were independent risk factors associated with seizure-like activities. Patients with asystole and mixed or cardioinhibitory responses to HUTT should be closely concerned. However, VVS children with seizure-like activities did not have a poor prognosis at follow-up.

Hippocampal orexin-1 and endocannabinoid-1 receptors underlie the kainate-induced occlusion in theta-burst long- term potentiation

IntroductionSeizures may result from the hyperexcitable neuronal activity of the brain. Multiple neurotransmitter receptors, including orexin (OX) and endocannabinoids interfere with forming the synaptic responses linked to the seizures. Therefore, this study investigates the involvement of OX-1 (OX1R) and endocannbinoid-1 (CB1R) receptors in the kainate- induced excitability in the synaptic field responses. Material and methodsTheta pattern used to stimulate Schaffer collaterals and then metal microelectrodes to record the CA1 field excitatory postsynaptic potentials (fEPSPs). Input/ output stimulation and responses and paired- pulse (PP) stimuli employed to measure the state of synaptic activity in normal and kainate- induced seizure-like hyperexcitable activities and the slope of fEPSPs used as a measure of the change in the synaptic activity. Furthermore, agonists and antagonists of OX and endocannabinoids infused to investigate the involvement of their receptors. ResultThe results showed that kainate application increased the fEPSP slope either in input stimuli with different intensities/output synaptic responses (I/O), or test pulse stimulated baseline synaptic responses (BSR) and, hence, increased the excitability of field responses in the CA1 region. However, neither kainate nor theta burst stimulation (TBS) could alter the PP stimuli -induced synaptic responses. TBS increased the fEPSP slope of the kainate-applied I/O and BSR, however, the increase was not high enough in BSR to be classified as long-term potentiation (LTP). The single-antagonist OX1R and CB1R administration prevented TBS- induced potentiation and partially recovered the effect by adding eCB or OX agonists in kainate-injected animals. In contrast, OX or combined eCB-OX antagonist application group demonstrated nearly full recovery of LTP induction. ConclusionOur study concludes that blockade of OX1 or CB1 prevents the induction of LTP, and OX infusion or both receptor blockade recovers the LTP.

QT Prolongation-induced Seizures Masquerading as Depression with Mixed Features

IntroductionSevere mental disorders experience premature mortality mostly from physical causes. When a patient with a history of bipolar disorder is admitted to the emergency room (ER) for psychiatric symptoms, these are routinely interpreted as a psychiatric disturbance. However, a careful history should be performed to correctly interpret key clinical information to rule out somatic etiology and establish adequate diagnosis.ObjectivesTo describe a patient whose presenting symptoms were misdiagnosed as psychiatric relapse, rather than serious somatic comorbidity debut.MethodsA 70-year-old man, with a history of type I bipolar disorder and multiple cardiovascular conditions, was admitted to the ER for self-referred nervousness, depressed mood, insomnia, and suicidal thoughts. Symptoms had greatly worsened the previous week to his consultation with paroxysmal episodes of severe anxiety, feelings of strangeness, and sensations of unpleasant odors.ResultsDuring observation, the patient was found lying down with loss of consciousness, urinary incontinence, and amnesia of the event. Generalized tonic-clonic seizures were observed by neurologists while mental status examination was being performed. After symptoms were oriented as having a neurological etiology, the patient suffered cardiac arrest and defibrillation was required. After admittance to the intensive care unit and inpatient cardiology care, the patient was discharged from the hospital with the diagnosis of ventricular fibrillation due to drug-induced QT prolongation. There was no evidence of mixed depression or seizures once the cardiac dysfunction was identified and treated.ConclusionsThe psychiatric symptoms were the clinical manifestation of a generalized seizure-like activities that were attributed to transient cerebral hypoperfusion secondary to ventricular fibrillation.DisclosureNo significant relationships.

GABA receptor inhibition and severe hypoxia induce a paroxysmal depolarization shift in goldfish neurons.

Mammalian neurons undergo rapid excitotoxic cell death when deprived of oxygen; however, the common goldfish (Carassius auratus) has the unique ability of surviving in oxygen-free waters, under anoxia. This organism utilizes γ-amino butyric acid (GABA) signaling to suppress excitatory glutamatergic activity during anoxic periods. Although GABAA receptor antagonists are not deleterious to the cellular survival, coinhibition of GABAA and GABAB receptors is detrimental by abolishing anoxia-induced neuroprotective mechanisms. Here we show that blocking the anoxic GABAergic neurotransmission induces seizure-like activity (SLA) analogous to a paroxysmal depolarization shift (PDS), with hyperpolarization of action potential (AP) threshold and elevation of threshold currents. The observed PDS was attributed to an increase in excitatory postsynaptic currents (EPSCs) that are normally attenuated with decreasing oxygen levels. Furthermore, for the first time, we show that in addition to PDS, some neurons undergo depolarization block and do not generate AP despite a suprathreshold membrane potential. In conclusion, our results indicate that with severe hypoxia and absence of GABA receptor activity, telencephalic neurons of C. auratus manifest a paroxysmal depolarization shift, a key feature of epileptic discharge.NEW & NOTEWORTHY This work shows that the combination of anoxia and inhibition of GABA receptors induces seizure-like activities in goldfish telencephalic pyramidal and stellate neurons. Importantly, to prevent seizure-like activity, an intact GABA-mediated inhibitory pathway is required.

EpilepsyGAN: Synthetic Epileptic Brain Activities With Privacy Preservation.

Epilepsy is a chronic neurological disorder affecting more than 65 million people worldwide and manifested by recurrent unprovoked seizures. The unpredictability of seizures not only degrades the quality of life of the patients, but it can also be life-threatening. Modern systems monitoring electroencephalography (EEG) signals are being currently developed with the view to detect epileptic seizures in order to alert caregivers and reduce the impact of seizures on patients' quality of life. Such seizure detection systems employ state-of-the-art machine learning algorithms that require a large amount of labeled personal data for training. However, acquiring EEG signals during epileptic seizures is a costly and time-consuming process for medical experts and patients. Furthermore, this data often contains sensitive personal information, presenting privacy concerns. In this work, we generate synthetic seizure-like brain electrical activities, i.e., EEG signals, that can be used to train seizure detection algorithms, alleviating the need for sensitive recorded data. Our experiments show that the synthetic seizure data generated with our GAN model succeeds at preserving the privacy of the patients without producing any degradation in performance during seizure monitoring.

Evaluation methods for drug-induced seizure by microelectrode array recording using human iPS cell-derived neurons

In the drug development in pharmaceuticals, development of drugs may be discontinued due to the toxicity and clinical side effect, therefore, safety assessment is one of the important factors in drug development. Consortium for Safety Assessment using Human Cells (CSAHi) has been launched for developing and standardizing a toxicity evaluation system for development of drug using human iPS cell differentiated cells. CSAHi focuses on hepato-, cardio-, and neuro-toxicities as important toxicity organs which are attributed to the causes of discontinuation of drug development. In neurotoxicity, seizure is an important finding because of high frequency expression in nonclinical. Multi-electrode array (MEA) systems have recently attracted attention as useful for evaluating seizure risk because they can non-invasively measure the electrophysiological activities of neural networks. We are evaluating the electrophysiological responses to several seizure compounds using MEA in cultured hiPSC-derived neurons. It is important to establish an analytical method to detecting seizure-like activities. We have focused the establish of the effective analysis parameters for detecting seizure risk. We identify to be separate the responses between seizure-positive and seizure-negative compounds using principal component analysis of 10 analysis parameters. In addition, we could separate the mechanism of action of the seizure-positive compounds by principal component analysis and cluster analysis using 10 parameters. It is considered that principal component analysis or cluster analysis could not only assess the seizure risk but also classify mechanism of action by in vitro MEA system using human iPS cell-derived neurons.

Paroxysmal Seizure-Like Activities Caused by Unrecognized Acute Myocarditis Masquerading as Febrile Seizures in Children

Paroxysmal Seizure-Like Activities Caused by Unrecognized Acute Myocarditis Masquerading as Febrile Seizures in Children

CSAHi study: Detection of drug-induced seizure-like activities of three convulsants at five facilities using micro-electrode arrays in combination with human iPS cell-derived neurons

CSAHi study: Detection of drug-induced seizure-like activities of three convulsants at five facilities using micro-electrode arrays in combination with human iPS cell-derived neurons

Detection of drug-induced seizure-like activities using MEA system in cultured human iPSC-derived neurons: Report from multi-site pilot study of the HESI NeuTox committee in collaboration with CSAHi and iNCENS

Detection of drug-induced seizure-like activities using MEA system in cultured human iPSC-derived neurons: Report from multi-site pilot study of the HESI NeuTox committee in collaboration with CSAHi and iNCENS

Role of estradiol in mediation of etomidate-caused seizure-like activity in neonatal rats

BackgroundThe goal of this study was to investigate the effect of estradiol in mediation of electroencephalogram (EEG) abnormality induced by etomidate in neonatal rats. MethodsSprague-Dawley rats were anesthetized using intraperitoneal etomidate for 2 h on postnatal days (P) 4, 5, or 6 and recorded electroencephalogram in two ways. First, pups were recorded EEG two and a half hours under etomidate anesthesia, in subgroups, estradiol receptor antagonist ICI182780 and estradiol synthase inhibitor formestane were given subcutaneously in male rats 15 min prior to etomidate. Second, pups were anesthetized with etomidate for 2 h on P4,5 or 6 and then recovered from anesthesia, EEG were recorded for one hour in two postnatal periods of P9-P11 and P14-P16. Subgroup rats that received bumetanide, NKCC1 inhibitor, to test the NKCC1-GABAAR signaling effect on neonatal brain development, negative control groups and maternally separated for 2 h on P4, 5, or 6 were studied in 16 groups. Each group’s n was = 8. ResultsMale pups showed more severe seizure-like activities than female pups in P4-P6 under etomidate anesthesia. Pups pretreated with ICI182780 and formestane showed a less abnormalities of EEG in male rats. Etomidate caused seizure-like activity in P4-P6 could extend to P9-P11, but not seen in P14-P16, Pretreated with bumetanide only alleviated abnormalities in male pups other than female in P9-P11. ConclusionsEstradiol involves in the NKCC1-GABAAR mediated seizure-like activity caused by etomidte in neonatal rats and these the abnormality lasts near two weeks.

Seizure-like activities in patients with head-up tilt test-induced syncope

The purpose of this study was to assess the prevalence and the characteristics of seizure-like activities during head-up tilt test (HUT)-induced syncope, in patients with suspected vasovagal syncope (VVS). We also evaluated the differences in hemodynamic parameters between patients with and without seizure-like activities.A total of 71 patients with suspected VVS, who showed syncope during HUT between October 2010 and May 2013, were analyzed. Electrocardiogram and hemodynamic parameters were continuously monitored during HUT. We also performed video recording of patients during HUT to identify eyeball deviation or seizure-like limb movements.In all, 47 patients (66.2%) showed seizure-like activities at the time of syncope during HUT, 14 patients presented eyeball deviation, without abnormal limb movements, and 33 patients showed abnormal limb movements, such as myoclonic or tonic-clonic activities, as well as eyeball deviation. Upon comparison of the 2 groups with or without seizure-like activities, patients showing seizure-like activities presented a significantly lower heart rate at the time of syncope in HUT (38.51 ± 16.81 vs 49.67 ± 20.12, P < .05). Also, upon comparison within patients showing seizure-like activities, the patients who showed abnormal limb movements with eyeball deviation demonstrated a significantly lower systolic blood pressure and cardiac output at the time of syncope (34.30 ± 12.24 vs 49.00 ± 14.14, P < .05; 0.58 ± 0.40 vs 1.32 ± 0.97, P < .05).Seizure-like activities were observed in high percentage in about 66% of patients during HUT-induced syncope. The occurrence of seizure-like activities was associated with more severe transient hemodynamic changes, such as lower heart rate, systolic blood pressure, and cardiac output at the time of the HUT-induced syncope.

Inhibitory Thoracic Interneurons are not Essential to Generate the Rostro-caudal Gradient of the Thoracic Inspiratory Motor Activity in Neonatal Rat

The inspiratory motor activities are greater in the intercostal muscles positioned at more rostral thoracic segments. This rostro-caudal gradient of the thoracic inspiratory motor activity is thought to be generated by the spinal interneurons. To clarify the involvement of the inhibitory thoracic interneurons in this rostro-caudal gradient, we examined the effects of 10 μM strychnine, an antagonist of glycine and GABAA receptors, applied to the neonatal rat thoracic spinal cord. The respiratory-related interneuron activities were optically recorded from thoracic segments in the isolated neonatal rat brainstem-spinal cord preparations stained with voltage-sensitive dye, and the electrical inspiratory motor activities were obtained from the third and eleventh thoracic ventral roots (T3VR, T11VR). Although strychnine caused seizure-like activities in all of the ventral roots recorded, the inspiratory motor activities continued. The inspiratory optical signals in the rostral thoracic segments (T2–T5) were significantly larger than those in the caudal thoracic segments (T9–T11) regardless of the existence of strychnine. Similarly, the percent ratio of the amplitude of the inspiratory electrical activity in the T3VR under control and strychnine was significantly larger than that in the T11VR regardless of the existence of strychnine. Strychnine significantly increased the inspiratory activity in both the T3VR and T11VR. These results suggest that the glycinergic and GABAergic inhibitory interneurons are not essential to generate the rostro-caudal gradient in the neonatal rat thoracic inspiratory motor outputs, but these interneurons are likely to play a role in the inhibitory control of inspiratory motor output.

Psychogenic Nonepileptic Seizures in a Mother and Her Son–Fate or Chance?

Psychogenic Nonepileptic Seizures (PNES) are defined as typical seizure-like activities or behaviors without cortical epileptiform discharges. The diagnosis of PNES remains a challenge and continuous video electroencephalography (cEEG) remains the gold standard to differentiate between epileptic seizures and PNES. Despite advances made in our understanding of PNES, diagnosing and treating this well-known entity remains a challenge. 25% of patients with seizures will be misdiagnosed as having PNES or epileptic seizures even by certified Neurologists. Do patient characteristics and demographics increase our accuracy to diagnose PNES? We present a case of a mother and her son, both diagnosed with PNES by cEEG monitoring in our epilepsy monitoring unit. While familial prevalence of conversion disorders is reported in the literature, this will be the first case report describing the incidence of PNES in two members of the same family. Do psychogenic epilepsies run in families? Will the diagnosis of PNES in one family member increase the probability of PNES in their relatives with seizures? Larger patient pools need to be studied to draw a definite conclusion regarding our observation.

Beneficial Effects of Selective Orexin-A Receptor Antagonist in 4-aminopyridine-induced Seizures in Male Rats.

Background:Orexins are excitatory neuropeptides which stimulate the central regulatory pathways. Orexins increase the penicillin-induced epileptic activity in rats. Orexin-A increases in different types of seizures and its elevated level is the characteristic feature in the epileptic children during polysomnography. Recently, the orexin receptor blockage has been reported to increase seizure threshold in mice; however, effect of the selective orexin-A receptor antagonist (SB-334867) on 4-aminopyridine (4-AP)-induced seizures has not been investigated.Materials and Methods:We used the intraperitoneal injection of 4-AP to induce seizure in male rats. Under urethane anesthesia, SB-334867 (50 and 100 nmol) was injected stereotaxically into the ventral hippocampal commissure. Using video recording, the effects of SB-334867 on electroencephalogram and tonic–clonic convulsions were compared to those that received diazepam or dimethyl sulfoxide (DMSO).Results:SB-334867 significantly decreased the duration of spike trains compared to DMSO-treated rats (P < 0.001) and reduced the duration of convulsive seizures (P < 0.05). Seizure onset was increased significantly by SB-334867, 50 nmol, compared to DMSO (P < 0.05) and diazepam (P < 0.01) treated rats.Conclusion:Antagonism of orexin-A receptor by a low-dose SB-334867 showed protective effects in 4-AP-induced seizure-like activities in anesthetized rats.

Direct-current Stimulation and Multi-electrode Array Recording of Seizure-like Activity in Mice Brain Slice Preparation.

Cathodal transcranial direct-current stimulation (tDCS) induces suppressive effects on drug-resistant seizures. To perform effective actions, the stimulation parameters (e.g., orientation, field strength, and stimulation duration) need to be examined in mice brain slice preparations. Testing and arranging the orientation of the electrode relative to the position of the mice brain slice are feasible. The present method preserves the thalamocingulate pathway to evaluate the effect of DCS on anterior cingulate cortex seizure-like activities. The results of the multichannel array recordings indicated that cathodal DCS significantly decreased the amplitude of the stimulation-evoked responses and duration of 4-aminopyridine and bicuculline-induced seizure-like activity. This study also found that cathodal DCS applications at 15 min caused long-term depression in the thalamocingulate pathway. The present study investigates the effects of DCS on thalamocingulate synaptic plasticity and acute seizure-like activities. The current procedure can test the optimal stimulation parameters including orientation, field strength, and stimulation duration in an in vitro mouse model. Also, the method can evaluate the effects of DCS on cortical seizure-like activities at both the cellular and network levels.