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chemogenetics seizure

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https://www.readbyqxmd.com/read/30233328/chemogenetic-recruitment-of-specific-interneurons-suppresses-seizure-activity
#1
Alexandru Cǎlin, Mihai Stancu, Ana-Maria Zagrean, John G R Jefferys, Andrei S Ilie, Colin J Akerman
Current anti-epileptic medications that boost synaptic inhibition are effective in reducing several types of epileptic seizure activity. Nevertheless, these drugs can generate significant side-effects and even paradoxical responses due to the broad nature of their action. Recently developed chemogenetic techniques provide the opportunity to pharmacologically recruit endogenous inhibitory mechanisms in a selective and circuit-specific manner. Here, we use chemogenetics to assess the potential of suppressing epileptiform activity by enhancing the synaptic output from three major interneuron populations in the rodent hippocampus: parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (VIP) expressing interneurons...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29618778/dynamic-interaction-of-local-and-transhemispheric-networks-is-necessary-for-progressive-intensification-of-hippocampal-seizures
#2
Fredrik Berglind, My Andersson, Merab Kokaia
The detailed mechanisms of progressive intensification of seizures often occurring in epilepsy are not well understood. Animal models of kindling, with progressive intensification of stimulation-induced seizures, have been previously used to investigate alterations in neuronal networks, but has been obscured by limited recording capabilities during electrical stimulations. Remote networks in kindling have been studied by physical deletions of the connected structures or pathways, inevitably leading to structural reorganisations and related adverse effects...
April 4, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29536948/optogenetic-dissection-of-ictogenesis-in-search-of-a-targeted-anti-epileptic-therapy
#3
K P Lillis, K J Staley
For over a century, epileptic seizures have been characterized as a state of pathological, hypersynchronous brain activity. Anti-epileptic therapies have been developed largely based on the dogma that the altered brain rhythms result from an overabundance of glutamatergic activity or insufficient GABAergic inhibition. The most effective drugs in use today act to globally decrease excitation, increase inhibition, or decrease all activity. Unfortunately, such broad alterations to brain activity often lead to impactful side effects such as drowsiness, cognitive impairment, and sleep disruption...
August 2018: Journal of Neural Engineering
https://www.readbyqxmd.com/read/29186699/seizure-induced-activation-of-the-hpa-axis-increases-seizure-frequency-and-comorbid-depression-like-behaviors
#4
Andrew Hooper, Rumzah Paracha, Jamie Maguire
Our laboratory recently demonstrated that seizures activate the hypothalamic-pituitary-adrenal (HPA) axis, increasing circulating levels of corticosterone (O'Toole et al., 2013). Given the well-established proconvulsant actions of corticosterone, we hypothesized that seizure-induced activation of the HPA axis may contribute to future seizure susceptibility. Further, since hypercortisolism is associated with depression, we propose that seizure-induced activation of the HPA axis may contribute to comorbid depression and epilepsy...
January 2018: Epilepsy & Behavior: E&B
https://www.readbyqxmd.com/read/29114861/kappa-opioid-receptors-regulate-hippocampal-synaptic-homeostasis-and-epileptogenesis
#5
Bridget N Queenan, Raymond L Dunn, Victor R Santos, Yang Feng, Megan N Huizenga, Robert J Hammack, Stefano Vicini, Patrick A Forcelli, Daniel T S Pak
OBJECTIVE: Homeostatic synaptic plasticity (HSP) serves as a gain control mechanism at central nervous system (CNS) synapses, including those between the dentate gyrus (DG) and CA3. Improper circuit control of DG-CA3 synapses is hypothesized to underlie epileptogenesis. Here, we sought to (1) identify compounds that preferentially modulate DG-CA3 synapses in primary neuronal culture and (2) determine if these compounds would delay or prevent epileptogenesis in vivo. METHODS: We previously developed and validated an in vitro assay to visualize the behavior of DG-CA3 synapses and predict functional changes...
January 2018: Epilepsia
https://www.readbyqxmd.com/read/28791729/applications-of-optogenetic-and-chemogenetic-methods-to-seizure-circuits-where-to-go-next
#6
REVIEW
Patrick A Forcelli
Epilepsy is the quintessential circuit disorder, with seizure activity propagating through anatomically constrained pathways. These pathways, necessary for normal sensory, motor, and cognitive function, are hijacked during seizures. Understanding the network architecture at the level of both local microcircuits and distributed macrocircuits may provide new therapeutic avenues for the treatment of epilepsy. Over the past decade, optogenetic and chemogenetic tools have enabled previously impossible levels of functional circuit mapping in neuroscience...
December 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28297715/autism-gene-ube3a-and-seizures-impair-sociability-by-repressing-vta-cbln1
#7
Vaishnav Krishnan, David C Stoppel, Yi Nong, Mark A Johnson, Monica J S Nadler, Ekim Ozkaynak, Brian L Teng, Ikue Nagakura, Fahim Mohammad, Michael A Silva, Sally Peterson, Tristan J Cruz, Ekkehard M Kasper, Ramy Arnaout, Matthew P Anderson
Maternally inherited 15q11-13 chromosomal triplications cause a frequent and highly penetrant type of autism linked to increased gene dosages of UBE3A, which encodes a ubiquitin ligase with transcriptional co-regulatory functions. Here, using in vivo mouse genetics, we show that increasing UBE3A in the nucleus downregulates the glutamatergic synapse organizer Cbln1, which is needed for sociability in mice. Epileptic seizures also repress Cbln1 and are found to expose sociability impairments in mice with asymptomatic increases in UBE3A...
March 23, 2017: Nature
https://www.readbyqxmd.com/read/28113165/controlling-seizures-through-chemogenetics-a-new-technique-may-provide-a-more-precise-way-of-targeting-faulty-circuitry-in-the-brain
#8
Michele Solis
Electricity is the currency of our nervous systems. Thinking and planning, walking and talking, eating and sleeping-all our mental and physical activities are driven by electrical signals moving through the brain. This electrical traffic ebbs and flows in consistent patterns across different brain regions, carrying information from one neuron to the next.
September 2016: IEEE Pulse
https://www.readbyqxmd.com/read/27416078/dreadds-suppress-seizure-like-activity-in-a-mouse-model-of-pharmacoresistant-epileptic-brain-tissue
#9
N Avaliani, M Andersson, A H Runegaard, D Woldbye, M Kokaia
Epilepsy is a neurological disorder with a prevalence of ≈1% of general population. Available antiepileptic drugs (AEDs) have multiple side effects and are ineffective in 30% of patients. Therefore, development of effective treatment strategies is highly needed, requiring drug-screening models that are relevant and reliable. We investigated novel chemogenetic approach, using DREADDs (designer receptors exclusively activated by designer drugs) as possible inhibitor of epileptiform activity in organotypic hippocampal slice cultures (OHSCs)...
October 2016: Gene Therapy
https://www.readbyqxmd.com/read/27404844/chemogenetic-silencing-of-the-midline-and-intralaminar-thalamus-blocks-amygdala-kindled-seizures
#10
Evan Wicker, Patrick A Forcelli
Temporal lobe epilepsy is the most common form of medically-intractable epilepsy. While seizures in TLE originate in structures such as hippocampus, amygdala, and temporal cortex, they propagate through a crucial relay: the midline/intralaminar thalamus. Prior studies have shown that pharmacological inhibition of midline thalamus attenuates limbic seizures. Here, we examined a recently developed technology, Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), as a means of chemogenetic silencing to attenuate limbic seizures...
September 2016: Experimental Neurology
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