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Neurobiology of Disease

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https://www.readbyqxmd.com/read/29141182/optogenetic-activation-of-5-ht-neurons-in-the-dorsal-raphe-suppresses-seizure-induced-respiratory-arrest-and-produces-anticonvulsant-effect-in-the-dba-1-mouse-sudep-model
#1
Honghai Zhang, Haiting Zhao, Chang Zeng, Christa Van Dort, Carl L Faingold, Norman E Taylor, Ken Solt, Hua-Jun Feng
Sudden unexpected death in epilepsy (SUDEP) is a devastating epilepsy complication. Seizure-induced respiratory arrest (S-IRA) occurs in many witnessed SUDEP patients and animal models as an initiating event leading to death. Thus, understanding the mechanisms underlying S-IRA will advance the development of preventive strategies against SUDEP. Serotonin (5-HT) is an important modulator for many vital functions, including respiration and arousal, and a deficiency of 5-HT signaling is strongly implicated in S-IRA in animal models, including the DBA/1 mouse...
November 13, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29113829/increased-motor-neuron-resilience-by-small-molecule-compound-that-regulate-igf-ii-expression
#2
Teresia M Osborn, Jonathan Beagan, Ole Isacson
The selective vulnerability of motor neurons in amyotrophic lateral sclerosis (ALS) is evident by sparing of a few subpopulations during this fast progressing and debilitating degenerative disease. By studying the gene expression profile of resilient vs. vulnerable motor neuron populations we can gain insight in what biomolecules and pathways may contribute to the resilience and vulnerability. Several genes have been found to be differentially expressed in the vulnerable motor neurons of the cervical spinal cord as compared to the spared motor neurons in CN3/4...
November 4, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29108985/serotonergic-neurons-mediate-the-anxiolytic-effect-of-l-dopa-neuronal-correlates-in-the-amygdala
#3
Emilie Faggiani, Frederic Naudet, Marcus L F Janssen, Yasin Temel, Abdelhamid Benazzouz
Anxiety in Parkinson's disease is a comorbid non-motor symptom that alters the quality of life of patients. Its neuronal substrates and those of l-Dopa treatment are still poorly known. Using different combinations of monoaminergic system lesions in the rat, we addressed the contribution of these systems in the efficacy of l-DOPA on anxiety and on the neuronal activity of basolateral amygdala (BLA), a brain structure involved in anxiety. Anxiety, locomotor activity and motor performance were assessed using the elevated plus maze, the open field and the skinner box, respectively...
November 3, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29100987/istradefylline-reduces-memory-deficits-in-aging-mice-with-amyloid-pathology
#4
Anna G Orr, Iris Lo, Heike Schumacher, Kaitlyn Ho, Michael Gill, Weikun Guo, Daniel H Kim, Anthony Knox, Takashi Saito, Takaomi C Saido, Jeffrey Simms, Carlee Toddes, Xin Wang, Gui-Qiu Yu, Lennart Mucke
Adenosine A2A receptors are putative therapeutic targets for neurological disorders. The adenosine A2A receptor antagonist istradefylline is approved in Japan for Parkinson's disease and is being tested in clinical trials for this condition elsewhere. A2A receptors on neurons and astrocytes may contribute to Alzheimer's disease (AD) by impairing memory. However, it is not known whether istradefylline enhances cognitive function in aging animals with AD-like amyloid plaque pathology. Here, we show that elevated levels of Aβ, C-terminal fragments of the amyloid precursor protein (APP), or amyloid plaques, but not overexpression of APP per se, increase astrocytic A2A receptor levels in the hippocampus and neocortex of aging mice...
October 31, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29097328/lovastatin-suppresses-hyperexcitability-and-seizure-in-angelman-syndrome-model
#5
Leeyup Chung, Alexandra L Bey, Aaron J Towers, Xinyu Cao, Il Hwan Kim, Yong-Hui Jiang
Epilepsy is prevalent and often medically intractable in Angelman syndrome (AS). AS mouse model (Ube3a(m-/p+)) shows reduced excitatory neurotransmission but lower seizure threshold. The neural mechanism linking the synaptic dysfunction to the seizure remains elusive. We show that the local circuits of Ube3a(m-/p+)in vitro are hyperexcitable and display a unique epileptiform activity, a phenomenon that is reminiscent of the finding in fragile X syndrome (FXS) mouse model. Similar to the FXS model, lovastatin suppressed the epileptiform activity and audiogenic seizures in Ube3a(m-/p+)...
October 31, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29107639/cjun-n-terminal-kinase-jnk-mediates-cortico-striatal-signaling-in-a-model-of-parkinson-s-disease
#6
Giada Spigolon, Anna Cavaccini, Massimo Trusel, Raffaella Tonini, Gilberto Fisone
The cJun N-terminal kinase (JNK) signaling pathway has been extensively studied with regard to its involvement in neurodegenerative processes, but little is known about its functions in neurotransmission. In a mouse model of Parkinson's disease (PD), we show that the pharmacological activation of dopamine D1 receptors (D1R) produces a large increase in JNK phosphorylation. This effect is secondary to dopamine depletion, and is restricted to the striatal projection neurons that innervate directly the output structures of the basal ganglia (dSPN)...
October 28, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29079454/the-adenosine-a2a-receptor-agonist-t1-11-ameliorates-neurovisceral-symptoms-and-extends-the-lifespan-of-a-mouse-model-of-niemann-pick-type-c-disease
#7
Antonella Ferrante, Antonella Pezzola, Andrea Matteucci, Antonella Di Biase, Lucilla Attorri, Monica Armida, Alberto Martire, Yijuang Chern, Patrizia Popoli
Niemann-Pick C is a fatal neurovisceral disorder caused, in 95% of cases, by mutation of NPC1 gene. Therapeutic options are extremely limited and new "druggable" targets are highly warranted. We previously demonstrated that the stimulation of the adenosine A2A receptor (A2AR) normalized the pathological phenotype of cellular models of NPC1. Since the validation of A2ARs as a therapeutic target for NPC1 can be obtained only conducting studies in in vivo models of the disease, in the present paper, the effects of two agonists of A2ARs were evaluated in the mouse model Balb/c Npc1(nih), hereafter indicated as NPC1-/-...
October 25, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29074125/status-epilepticus-triggers-long-lasting-activation-of-complement-c1q-c3-signaling-in-the-hippocampus-that-correlates-with-seizure-frequency-in-experimental-epilepsy
#8
Nicole D Schartz, Season K Wyatt-Johnson, Lauren R Price, Samantha A Colin, Amy L Brewster
Status epilepticus (SE) triggers a myriad of neurological alterations that include unprovoked seizures, temporal lobe epilepsy (TLE), and cognitive deficits. Although SE-induced loss of hippocampal dendritic structures and synaptic remodeling are often associated with this pathophysiology, the underlying mechanisms remain elusive. Recent evidence points to the classical complement pathway as a potential mechanism. Signaling through the complement protein C1q to C3, which is cleaved into smaller biologically active fragments including C3b and iC3b, contributes to the elimination of synaptic structures in the normal developing brain and in models of neurodegenerative disorders...
October 23, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29045814/role-of-kcc2-dependent-potassium-efflux-in-4-aminopyridine-induced-epileptiform-synchronization
#9
Oscar C González, Zahra Shiri, Giri P Krishnan, Timothy L Myers, Sylvain Williams, Massimo Avoli, Maxim Bazhenov
A balance between excitation and inhibition is necessary to maintain stable brain network dynamics. Traditionally, seizure activity is believed to arise from the breakdown of this delicate balance in favor of excitation with loss of inhibition. Surprisingly, recent experimental evidence suggests that this conventional view may be limited, and that inhibition plays a prominent role in the development of epileptiform synchronization. Here, we explored the role of the KCC2 co-transporter in the onset of inhibitory network-induced seizures...
October 16, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29037828/chemogenetic-modulation-of-cholinergic-interneurons-reveals-their-regulating-role-on-the-direct-and-indirect-output-pathways-from-the-striatum
#10
Patrick Aldrin-Kirk, Andreas Heuer, Daniella Rylander Ottosson, Marcus Davidsson, Bengt Mattsson, Tomas Björklund
The intricate balance between dopaminergic and cholinergic neurotransmission in the striatum has been thoroughly difficult to characterize. It was initially described as a seesaw with a competing function of dopamine versus acetylcholine. Recent technical advances however, have brought this view into question suggesting that the two systems work rather in concert with the cholinergic interneurons (ChIs) driving dopamine release. In this study, we have utilized two transgenic Cre-driver rat lines, a choline acetyl transferase ChAT-Cre transgenic rat and a novel double-transgenic tyrosine hydroxylase TH-Cre/ChAT-Cre rat to further elucidate the role of striatal ChIs in normal motor function and in Parkinson's disease...
October 14, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29031639/oscillatory-neural-representations-in-the-sensory-thalamus-predict-neuropathic-pain-relief-by-deep-brain-stimulation
#11
Yongzhi Huang, Alexander L Green, Jonathan Hyam, James Fitzgerald, Tipu Z Aziz, Shouyan Wang
OBJECTIVE: Understanding the function of sensory thalamic neural activity is essential for developing and improving interventions for neuropathic pain. However, there is a lack of investigation of the relationship between sensory thalamic oscillations and pain relief in patients with neuropathic pain. This study aims to identify the oscillatory neural characteristics correlated with pain relief induced by deep brain stimulation (DBS), and develop a quantitative model to predict pain relief by integrating characteristic measures of the neural oscillations...
October 13, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29024713/a-lack-of-glun2a-containing-nmda-receptors-confers-a-vulnerability-to-redox-dysregulation-consequences-on-parvalbumin-interneurons-and-their-perineuronal-nets
#12
Romain Cardis, Jan-Harry Cabungcal, Daniella Dwir, Kim Q Do, Pascal Steullet
The GluN2A subunit of NMDA receptors (NMDARs) plays a critical role during postnatal brain development as its expression increases while Glun2B expression decreases. Mutations and polymorphisms in GRIN2A gene, coding for GluN2A, are linked to developmental brain disorders such as mental retardation, epilepsy, schizophrenia. Published data suggest that GluN2A is involved in maturation and phenotypic maintenance of parvalbumin interneurons (PVIs), and these interneurons suffer from a deficient glutamatergic neurotransmission via GluN2A-containing NMDARs in schizophrenia...
October 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29024712/brief-activation-of-gabaergic-interneurons-initiates-the-transition-to-ictal-events-through-post-inhibitory-rebound-excitation
#13
Michael Chang, Joshua A Dian, Suzie Dufour, Lihua Wang, Homeira Moradi Chameh, Meera Ramani, Liang Zhang, Peter L Carlen, Thilo Womelsdorf, Taufik A Valiante
Activation of γ-aminobutyric acid (GABAA) receptors have been associated with the onset of epileptiform events. To investigate if a causal relationship exists between GABAA receptor activation and ictal event onset, we activated inhibitory GABAergic networks in the superficial layer (2/3) of the somatosensory cortex during hyperexcitable conditions using optogenetic techniques in mice expressing channelrhodopsin-2 in all GABAergic interneurons. We found that a brief 30ms light pulse reliably triggered either an interictal-like event (IIE) or ictal-like ("ictal") event in the in vitro cortical 4-Aminopyridine (4-AP) slice model...
October 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29017795/long-term-effects-of-sleep-deprivation-on-neuronal-activity-in-four-hypothalamic-areas
#14
Karim Fifel, Johanna H Meijer, Tom Deboer
Lack of adequate sleep has become increasingly common in our 24/7 society. Unfortunately diminished sleep has significant health consequences including metabolic and cardiovascular disease and mental disorders including depression. The pathways by which reduced sleep adversely affects physiology and behavior are unknown. We found that 6h of sleep deprivation in adult male rats induces changes in neuronal activity in the lateral hypothalamus, the paraventricular nucleus, the arcuate nucleus and the mammillary bodies...
October 7, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28993242/a-distinct-microrna-expression-profile-is-associated-with-%C3%AE-11-c-methyl-l-tryptophan-amt-pet-uptake-in-epileptogenic-cortical-tubers-resected-from-patients-with-tuberous-sclerosis-complex
#15
Shruti Bagla, Daniela Cukovic, Eishi Asano, Sandeep Sood, Aimee Luat, Harry T Chugani, Diane C Chugani, Alan A Dombkowski
Tuberous sclerosis complex (TSC) is characterized by hamartomatous lesions in various organs and arises due to mutations in the TSC1 or TSC2 genes. TSC mutations lead to a range of neurological manifestations including epilepsy, cognitive impairment, autism spectrum disorders (ASD), and brain lesions that include cortical tubers. There is evidence that seizures arise at or near cortical tubers, but it is unknown why some tubers are epileptogenic while others are not. We have previously reported increased tryptophan metabolism measured with α[(11)C]-methyl-l-tryptophan (AMT) positron emission tomography (PET) in epileptogenic tubers in approximately two-thirds of patients with tuberous sclerosis and intractable epilepsy...
October 7, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28986324/the-ubiquitin-conjugating-enzyme-ube2w-regulates-solubility-of-the-huntington-s-disease-protein-huntingtin
#16
Bo Wang, Li Zeng, Sean A Merillat, Svetlana Fischer, Joseph Ochaba, Leslie M Thompson, Sami J Barmada, Kenneth M Scaglione, Henry L Paulson
Huntington's disease (HD) is caused by a CAG repeat expansion that encodes a polyglutamine (polyQ) expansion in the HD disease protein, huntingtin (HTT). PolyQ expansion promotes misfolding and aggregation of mutant HTT (mHTT) within neurons. The cellular pathways, including ubiquitin-dependent processes, by which mHTT is regulated remain incompletely understood. Ube2W is the only ubiquitin conjugating enzyme (E2) known to ubiquitinate substrates at their amino (N)-termini, likely favoring substrates with disordered N-termini...
October 3, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28982592/human-amyloid-%C3%AE-peptide-and-tau-co-expression-impairs-behavior-and-causes-specific-gene-expression-changes-in-caenorhabditis-elegans
#17
Chenyin Wang, Valeria Saar, Ka Lai Leung, Liang Chen, Garry Wong
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the presence of extracellular amyloid plaques consisting of Amyloid-β peptide (Aβ) aggregates and neurofibrillary tangles formed by aggregation of hyperphosphorylated microtubule-associated protein tau. We generated a novel invertebrate model of AD by crossing Aβ1-42 (strain CL2355) with either pro-aggregating tau (strain BR5270) or anti-aggregating tau (strain BR5271) pan-neuronal expressing transgenic Caenorhabditis elegans...
October 2, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28982591/genetic-inactivation-of-mglu5-receptor-improves-motor-coordination-in-the-grm1-crv4-mouse-model-of-scar13-ataxia
#18
Simone Bossi, Ilaria Musante, Tommaso Bonfiglio, Tiziana Bonifacino, Laura Emionite, Maria Cerminara, Chiara Cervetto, Manuela Marcoli, Giambattista Bonanno, Roberto Ravazzolo, Anna Pittaluga, Aldamaria Puliti
Deleterious mutations in the glutamate receptor metabotropic 1 gene (GRM1) cause a recessive form of cerebellar ataxia, SCAR13. GRM1 and GRM5 code for the metabotropic glutamate type 1 (mGlu1) and type 5 (mGlu5) receptors, respectively. Their different expression profiles suggest they could have distinct functional roles. In a previous study, homozygous mice lacking mGlu1 receptors (Grm1(crv4/crv4)) and exhibiting ataxia presented cerebellar overexpression of mGlu5 receptors, that was proposed to contribute to the mouse phenotype...
October 2, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28962900/effects-of-tamoxifen-on-neuronal-morphology-connectivity-and-biochemistry-of-hypothalamic-ventromedial-neurons-impact-on-the-modulators-of-sexual-behavior
#19
Susana I Sá, Natércia Teixeira, Bruno M Fonseca
Tamoxifen (TAM) is a selective estrogen receptor modulator, widely used in the treatment and prevention of estrogen-dependent breast cancer. Although with great clinical results, women on TAM therapy still report several side effects, such as sexual dysfunction, which impairs quality of life. The anatomo-functional substrates of the human sexual behavior are still unknown; however, these same substrates are very well characterized in the rodent female sexual behavior, which has advantage of being a very simple reflexive response, dependent on the activation of estrogen receptors (ERs) in the ventrolateral division of the hypothalamic ventromedial nucleus (VMNvl)...
September 28, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28923597/targeting-demyelination-via-%C3%AE-secretases-promoting-sapp%C3%AE-release-to-enhance-remyelination-in-central-nervous-system
#20
Gemma Llufriu-Dabén, Alex Carrete, Elena Chierto, Jo Mailleux, Emeline Camand, Anne Simon, Tim Vanmierlo, Christiane Rose, Bernadette Allinquant, Jerome J A Hendriks, Charbel Massaad, Delphine Meffre, Mehrnaz Jafarian-Tehrani
Remyelination is an endogenous regenerative process of myelin repair in the central nervous system (CNS) with limited efficacy in demyelinating disorders. As strategies enhancing endogenous remyelination become a therapeutic challenge, we have focused our study on α-secretase-induced sAPPα release, a soluble endogenous protein with neuroprotective and neurotrophic properties. However, the role of sAPPα in remyelination is not known. Therefore, we investigated the remyelination potential of α-secretase-induced sAPPα release following CNS demyelination in mice...
September 18, 2017: Neurobiology of Disease
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