@article{MTMT:34759393,
	title = {Intrinsic running capacity associates with hippocampal electrophysiology and long-term potentiation in rats},
	url = {https://m2.mtmt.hu/api/publication/34759393},
	author = {Mäkinen, E.E. and Lensu, S. and Wikgren, J. and Pekkala, S. and Koch, L.G. and Britton, S.L. and Nokia, M.S.},
	doi = {10.1016/j.neulet.2024.137665},
	journal-iso = {NEUROSCI LETT},
	journal = {NEUROSCIENCE LETTERS},
	volume = {823},
	unique-id = {34759393},
	issn = {0304-3940},
	year = {2024},
	eissn = {1872-7972}
}

@article{MTMT:34280745,
	title = {Impairments in hippocampal oscillations accompany the loss of LTP induced by GIRK activity blockade},
	url = {https://m2.mtmt.hu/api/publication/34280745},
	author = {Contreras, Ana and Djebari, Souhail and Temprano-Carazo, Sara and Munera, Alejandro and Gruart, Agnes and Delgado-Garcia, Jose M. and Jimenez-Diaz, Lydia and Navarro-Lopez, Juan D.},
	doi = {10.1016/j.neuropharm.2023.109668},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {238},
	unique-id = {34280745},
	issn = {0028-3908},
	abstract = {Learning and memory occurrence requires of hippocampal long-term synaptic plasticity and precise neural activity orchestrated by brain network oscillations, both processes reciprocally influencing each other. As G-protein-gated inwardly rectifying potassium (GIRK) channels rule synaptic plasticity that supports hippocampaldependent memory, here we assessed their unknown role in hippocampal oscillatory activity in relation to synaptic plasticity induction.In alert male mice, pharmacological GIRK modulation did not alter neural oscillations before long-term potentiation (LTP) induction. However, after an LTP generating protocol, both gain- and loss-of basal GIRK activity transformed LTP into long-term depression, but only specific suppression of constitutive GIRK activity caused a disruption of network synchronization (6, & alpha;, & gamma; bands), even leading to long-lasting ripples and fast ripples pathological oscillations. Together, our data showed that constitutive GIRK activity plays a key role in the tuning mechanism of hippocampal oscillatory activity during long-term synaptic plasticity processes that underlies hippocampaldependent cognitive functions.},
	keywords = {SYNAPTIC PLASTICITY; In vivo; Dorsal hippocampus; GIRK channel; tertiapin-Q; Neuronal oscillations},
	year = {2023},
	eissn = {1873-7064},
	orcid-numbers = {Contreras, Ana/0000-0002-2185-0851; Munera, Alejandro/0000-0002-5405-2848}
}

@article{MTMT:34114129,
	title = {Toward the Identification of Neurophysiological Biomarkers for Alzheimer's Disease in Down Syndrome: A Potential Role for Cross-Frequency Phase-Amplitude Coupling Analysis},
	url = {https://m2.mtmt.hu/api/publication/34114129},
	author = {Victorino, D.B. and Faber, J. and Pinheiro, D.J.L.L. and Scorza, F.A. and Almeida, A.C.G. and Costa, A.C.S. and Scorza, C.A.},
	doi = {10.14336/AD.2022.0906},
	journal-iso = {AGING DIS},
	journal = {AGING AND DISEASE},
	volume = {14},
	unique-id = {34114129},
	issn = {2152-5250},
	abstract = {Cross-frequency coupling (CFC) mechanisms play a central role in brain activity. Pathophysiological mechanisms leading to many brain disorders, such as Alzheimer's disease (AD), may produce unique patterns of brain activity detectable by electroencephalography (EEG). Identifying biomarkers for AD diagnosis is also an ambition among research teams working in Down syndrome (DS), given the increased susceptibility of people with DS to develop early-onset AD (DS-AD). Here, we review accumulating evidence that altered theta-gamma phase-amplitude coupling (PAC) may be one of the earliest EEG signatures of AD, and therefore may serve as an adjuvant tool for detecting cognitive decline in DS-AD. We suggest that this field of research could potentially provide clues to the biophysical mechanisms underlying cognitive dysfunction in DS-AD and generate opportunities for identifying EEG-based biomarkers with diagnostic and prognostic utility in DS-AD. Copyright: © 2022 Victorino DB. et al.},
	year = {2023},
	eissn = {2152-5250},
	pages = {428-449}
}

@article{MTMT:32591465,
	title = {The interacting rotifer-biopolymers are anti- and disaggregating agents for human-type beta-amyloid in vitro},
	url = {https://m2.mtmt.hu/api/publication/32591465},
	author = {Datki, Zsolt László and Balázs, Evelin and Gálik, Bence and Sinka, Rita and Zeitler, Lavínia and Bozsó, Zsolt and Kálmán, János and Hortobágyi, Tibor and Oláh, Zita},
	doi = {10.1016/j.ijbiomac.2021.12.184},
	journal-iso = {INT J BIOL MACROMOL},
	journal = {INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES},
	volume = {201},
	unique-id = {32591465},
	issn = {0141-8130},
	year = {2022},
	eissn = {1879-0003},
	pages = {262-269},
	orcid-numbers = {Datki, Zsolt László/0000-0002-2537-4741; Sinka, Rita/0000-0003-4040-4184; Bozsó, Zsolt/0000-0002-5713-3096; Kálmán, János/0000-0001-5319-5639; Hortobágyi, Tibor/0000-0001-5732-7942; Oláh, Zita/0000-0002-6372-532X}
}

@article{MTMT:32640861,
	title = {Accelerated Aging Characterizes the Early Stage of Alzheimer’s Disease},
	url = {https://m2.mtmt.hu/api/publication/32640861},
	author = {Leparulo, A. and Bisio, M. and Redolfi, N. and Pozzan, T. and Vassanelli, S. and Fasolato, C.},
	doi = {10.3390/cells11020238},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {11},
	unique-id = {32640861},
	abstract = {For Alzheimer’s disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies track the progression of the disease at different ages, and most ignore how the aging process affects control mice. In this work, we addressed this problem by comparing the aging process of PS2APP (AD) and wild-type (WT) mice at the level of spontaneous brain electrical activity under anesthesia. Using local field potential recordings, obtained with a linear probe that traverses the posterior parietal cortex and the entire hippocampus, we analyzed how multiple electrical parameters are modified by aging in AD and WT mice. With this approach, we highlighted AD specific features that appear in young AD mice prior to plaque deposition or that are delayed at 12 and 16 months of age. Furthermore, we identified aging characteristics present in WT mice but also occurring prematurely in young AD mice. In short, we found that reduction in the relative power of slow oscillations (SO) and Low/High power imbalance are linked to an AD phenotype at its onset. The loss of SO connectivity and cortico-hippocampal coupling between SO and higher frequencies as well as the increase in UP-state and burst durations are found in young AD and old WT mice. We show evidence that the aging process is accelerated by the mutant PS2 itself and discuss such changes in relation to amyloidosis and gliosis. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {Adult; Female; Male; PHENOTYPE; immunohistochemistry; hippocampus; ARTICLE; MOUSE; Genotype; risk factor; gene mutation; Nerve Degeneration; nonhuman; animal model; animal experiment; oscillation; brain cortex; task performance; Delta waves; Delta rhythm; Electroencephalography; Electroencephalogram; Aging; spike; anesthesia; electric activity; action potential; PRION PROTEIN; cerebrospinal fluid; reactive oxygen metabolite; Alzheimer's disease; microglia; nerve cell plasticity; Alzheimer disease; pyramidal nerve cell; interneuron; POSTERIOR PARIETAL CORTEX; ASTROCYTE; Electroporation; dopaminergic nerve cell; estrus cycle; nerve cell network; amyloid beta protein; Purkinje cell; Amyloid-β; tau protein; functional connectivity; functional connectivity; Local field potential; slow oscillations; wild type mouse; presenilin-2; spikes; PRESENILIN 2; PS2APP; phase-amplitude-coupling; UP-DOWN states},
	year = {2022},
	eissn = {2073-4409}
}

@article{MTMT:32287233,
	title = {Synaptic Plasticity and Oscillations in Alzheimer's Disease: A Complex Picture of a Multifaceted Disease},
	url = {https://m2.mtmt.hu/api/publication/32287233},
	author = {Andrade-Talavera, Yuniesky and Rodriguez-Moreno, Antonio},
	doi = {10.3389/fnmol.2021.696476},
	journal-iso = {FRONT MOL NEUROSCI},
	journal = {FRONTIERS IN MOLECULAR NEUROSCIENCE},
	volume = {14},
	unique-id = {32287233},
	issn = {1662-5099},
	abstract = {Brain plasticity is widely accepted as the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). By using diverse induction protocols like high-frequency stimulation (HFS) or spike-timing dependent plasticity (STDP), such crucial cognition-relevant plastic processes are shown to be impaired in Alzheimer's disease (AD). In AD, the severity of the cognitive impairment also correlates with the level of disruption of neuronal network dynamics. Currently under debate, the named amyloid hypothesis points to amyloid-beta peptide 1-42 (A beta 42) as the trigger of the functional deviations underlying cognitive impairment in AD. However, there are missing functional mechanistic data that comprehensively dissect the early subtle changes that lead to synaptic dysfunction and subsequent neuronal network collapse in AD. The convergence of the study of both, mechanisms underlying brain plasticity, and neuronal network dynamics, may represent the most efficient approach to address the early triggering and aberrant mechanisms underlying the progressive clinical cognitive impairment in AD. Here we comment on the emerging integrative roles of brain plasticity and network oscillations in AD research and on the future perspectives of research in this field.},
	keywords = {PLASTICITY; OSCILLATIONS; Alzheimer's disease; transcranial magnetic stimulation; spike timing-dependent plasticity; Alzheimer's disease models},
	year = {2021},
	eissn = {1662-5099},
	orcid-numbers = {Andrade-Talavera, Yuniesky/0000-0002-5295-0169}
}

@article{MTMT:32286384,
	title = {Efficacy of preclinical pharmacological interventions against alterations of neuronal network oscillations in Alzheimer's disease: A systematic review},
	url = {https://m2.mtmt.hu/api/publication/32286384},
	author = {Isla, Arturo G. and Balleza-Tapia, Hugo and Fisahn, Andre},
	doi = {10.1016/j.expneurol.2021.113743},
	journal-iso = {EXP NEUROL},
	journal = {EXPERIMENTAL NEUROLOGY},
	volume = {343},
	unique-id = {32286384},
	issn = {0014-4886},
	abstract = {Despite the development of multiple pharmacological approaches over the years aimed at treating Alzheimer's Disease (AD) only very few have been approved for clinical use in patients. To date there still exists no diseasemodifying treatment that could prevent or rescue the cognitive impairment, particularly of memory aquisition, that is characteristic of AD. One of the possibilities for this state of affairs might be that the majority of drug discovery efforts focuses on outcome measures of decreased neuropathological biomarkers characteristic of AD, without taking into acount neuronal processes essential to the generation and maintenance of memory processes. Particularly, the capacity of the brain to generate theta (theta) and gamma (gamma) oscillatory activity has been strongly correlated to memory performance. Using a systematic review approach, we synthesize the existing evidence in the literature on pharmacological interventions that enhance neuronal theta (theta) and/or gamma (gamma) oscillations in non-pathological animal models and in AD animal models. Additionally, we synthesize the main outcomes and neurochemical systems targeted. We propose that functional biomarkers such as cognition-relevant neuronal network oscillations should be used as outcome measures during the process of research and development of novel drugs against cognitive impairment in AD.},
	keywords = {THETA OSCILLATIONS; Alzheimer's disease; systematic review; MEMORY IMPAIRMENT; GAMMA OSCILLATIONS},
	year = {2021},
	eissn = {1090-2430},
	orcid-numbers = {Isla, Arturo G./0000-0002-8176-3522}
}

@article{MTMT:32337186,
	title = {Absence of Pannexin 1 Stabilizes Hippocampal Excitability After Intracerebral Treatment With A beta (1-42) and Prevents LTP Deficits in Middle-Aged Mice},
	url = {https://m2.mtmt.hu/api/publication/32337186},
	author = {Sudkamp, Nicolina and Shchyglo, Olena and Manahan-Vaughan, Denise},
	doi = {10.3389/fnagi.2021.591735},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {13},
	unique-id = {32337186},
	issn = {1663-4365},
	abstract = {Beta-amyloid protein [A beta(1-42)] plays an important role in the disease progress and pathophysiology of Alzheimer's disease (AD). Membrane properties and neuronal excitability are altered in the hippocampus of transgenic AD mouse models that overexpress amyloid precursor protein. Although gap junction hemichannels have been implicated in the early pathogenesis of AD, to what extent Pannexin channels contribute to A beta(1-42)-mediated brain changes is not yet known. In this study we, therefore, investigated the involvement of Pannexin1 (Panx1) channels in A beta-mediated changes of neuronal membrane properties and long-term potentiation (LTP) in an animal model of AD. We conducted whole-cell patch-clamp recordings in CA1 pyramidal neurons 1 week after intracerebroventricular treatments of adult wildtype (wt) and Panx1 knockout (Panx1-ko) mice with either oligomeric A beta(1-42), or control peptide. Panx1-ko hippocampi treated with control peptide exhibited increased neuronal excitability compared to wt. In addition, action potential (AP) firing frequency was higher in control Panx1-ko slices compared to wt. A beta-treatment reduced AP firing frequency in both cohorts. But in A beta-treated wt mice, spike frequency adaptation was significantly enhanced, when compared to control wt and to A beta-treated Panx1-ko mice. Assessment of hippocampal LTP revealed deficits in A beta-treated wt compared to control wt. By contrast, Panx1-ko exhibited LTP that was equivalent to LTP in control ko hippocampi. Taken together, our data show that in the absence of Pannexin1, hippocampi are more resistant to the debilitating effects of oligomeric A beta. Both A beta-mediated impairments in spike frequency adaptation and in LTP that occur in wt animals, are ameliorated in Panx1-ko mice. These results suggest that Panx1 contributes to early changes in hippocampal neuronal and synaptic function that are triggered by oligomeric A beta.},
	keywords = {hippocampus; CA1; LTP; amyloidosis; beta-Amyloid; Alzheimer; rodent; pannexin 1 (Panx1)},
	year = {2021},
	eissn = {1663-4365}
}

@article{MTMT:33264551,
	title = {What electrophysiology tells us about Alzheimer's disease: a window into the synchronization and connectivity of brain neurons},
	url = {https://m2.mtmt.hu/api/publication/33264551},
	author = {Babiloni, C. and Blinowska, K. and Bonanni, L. and Cichocki, A. and De, Haan W. and Del, Percio C. and Dubois, B. and Escudero, J. and Fernández, A. and Frisoni, G. and Guntekin, B. and Hajos, M. and Hampel, H. and Ifeachor, E. and Kilborn, K. and Kumar, S. and Johnsen, K. and Johannsson, M. and Jeong, J. and LeBeau, F. and Lizio, R. and Lopes, da Silva F. and Maestú, F. and McGeown, W.J. and McKeith, I. and Moretti, D.V. and Nobili, F. and Olichney, J. and Onofrj, M. and Palop, J.J. and Rowan, M. and Stocchi, F. and Struzik, Z.M. and Tanila, H. and Teipel, S. and Taylor, J.P. and Weiergräber, M. and Yener, G. and Young-Pearse, T. and Drinkenburg, W.H. and Randall, F.},
	doi = {10.1016/j.neurobiolaging.2019.09.008},
	journal-iso = {NEUROBIOL AGING},
	journal = {NEUROBIOLOGY OF AGING: AGE-RELATED PHENOMENA NEURODEGENERATION AND NEUROPATHOLOGY},
	volume = {85},
	unique-id = {33264551},
	issn = {0197-4580},
	year = {2020},
	eissn = {1558-1497},
	pages = {58-73}
}

@article{MTMT:31639846,
	title = {Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in a micro-in vivo system},
	url = {https://m2.mtmt.hu/api/publication/31639846},
	author = {Balázs, Evelin and Oláh, Zita and Gálik, Bence and Bozsó, Zsolt and Kálmán, János and Datki, Zsolt László},
	doi = {10.1016/j.ibror.2020.10.002},
	journal-iso = {IBRO REP},
	journal = {IBRO REPORTS},
	volume = {9},
	unique-id = {31639846},
	year = {2020},
	eissn = {2451-8301},
	pages = {319-323},
	orcid-numbers = {Oláh, Zita/0000-0002-6372-532X; Bozsó, Zsolt/0000-0002-5713-3096; Kálmán, János/0000-0001-5319-5639; Datki, Zsolt László/0000-0002-2537-4741}
}

@article{MTMT:31314638,
	title = {Dissociation of somatostatin and parvalbumin interneurons circuit dysfunctions underlying hippocampal theta and gamma oscillations impaired by amyloid β oligomers in vivo},
	url = {https://m2.mtmt.hu/api/publication/31314638},
	author = {Chung, H. and Park, K. and Jang, H.J. and Kohl, M.M. and Kwag, J.},
	doi = {10.1007/s00429-020-02044-3},
	journal-iso = {BRAIN STRUCT FUNC},
	journal = {BRAIN STRUCTURE & FUNCTION},
	volume = {225},
	unique-id = {31314638},
	issn = {1863-2653},
	abstract = {Accumulation of amyloid β oligomers (AβO) in Alzheimer’s disease (AD) impairs hippocampal theta and gamma oscillations. These oscillations are important in memory functions and depend on distinct subtypes of hippocampal interneurons such as somatostatin-positive (SST) and parvalbumin-positive (PV) interneurons. Here, we investigated whether AβO causes dysfunctions in SST and PV interneurons by optogenetically manipulating them during theta and gamma oscillations in vivo in AβO-injected SST-Cre or PV-Cre mice. Hippocampal in vivo multi-electrode recordings revealed that optogenetic activation of channelrhodopsin-2 (ChR2)-expressing SST and PV interneurons in AβO-injected mice selectively restored AβO-induced reduction of the peak power of theta and gamma oscillations, respectively, and resynchronized CA1 pyramidal cell (PC) spikes. Moreover, SST and PV interneuron spike phases were resynchronized relative to theta and gamma oscillations, respectively. Whole-cell voltage-clamp recordings in CA1 PC in ex vivo hippocampal slices from AβO-injected mice revealed that optogenetic activation of SST and PV interneurons enhanced spontaneous inhibitory postsynaptic currents (IPSCs) selectively at theta and gamma frequencies, respectively. Furthermore, analyses of the stimulus–response curve, paired-pulse ratio, and short-term plasticity of SST and PV interneuron-evoked IPSCs ex vivo showed that AβO increased the initial GABA release probability to depress SST/PV interneuron’s inhibitory input to CA1 PC selectively at theta and gamma frequencies, respectively. Our results reveal frequency-specific and interneuron subtype-specific presynaptic dysfunctions of SST and PV interneurons’ input to CA1 PC as the synaptic mechanisms underlying AβO-induced impairments of hippocampal network oscillations and identify them as potential therapeutic targets for restoring hippocampal network oscillations in early AD. © 2020, The Author(s).},
	keywords = {SOMATOSTATIN; hippocampus; hippocampus; ARTICLE; MOUSE; priority journal; controlled study; nonhuman; animal tissue; animal model; animal experiment; oscillation; stimulus response; unclassified drug; protein expression; in vivo study; Alzheimer's disease; ex vivo study; Alzheimer disease; interneuron; Oligomer; parvalbumin; 4 aminobutyric acid release; amyloid beta protein; hippocampal slice; NETWORK OSCILLATIONS; Blue light; optogenetics; whole cell patch clamp; channelrhodopsin; voltage clamp technique; channelrhodopsin 2; somatostatin interneuron; parvalbumin interneuron; Amyloid beta oligomers},
	year = {2020},
	eissn = {1863-2661},
	pages = {935-954}
}

@article{MTMT:31939733,
	title = {Acute Effects of Two Different Species of Amyloid-β on Oscillatory Activity and Synaptic Plasticity in the Commissural CA3-CA1 Circuit of the Hippocampus},
	url = {https://m2.mtmt.hu/api/publication/31939733},
	author = {Gauthier-Umanã, C. and Munõz-Cabrera, J. and Valderrama, M. and Múnera, A. and Nava-Mesa, M.O.},
	doi = {10.1155/2020/8869526},
	journal-iso = {NEURAL PLAST},
	journal = {NEURAL PLASTICITY},
	volume = {2020},
	unique-id = {31939733},
	issn = {2090-5904},
	abstract = {Recent evidence indicates that soluble amyloid-β (Aβ) species induce imbalances in excitatory and inhibitory transmission, resulting in neural network functional impairment and cognitive deficits during early stages of Alzheimer's disease (AD). To evaluate the in vivo effects of two soluble Aβ species (Aβ25-35 and Aβ1-40) on commissural CA3-to-CA1 (cCA3-to-CA1) synaptic transmission and plasticity, and CA1 oscillatory activity, we used acute intrahippocampal microinjections in adult anaesthetized male Wistar rats. Soluble Aβ microinjection increased cCA3-to-CA1 synaptic variability without significant changes in synaptic efficiency. High-frequency CA3 stimulation was rendered inefficient by soluble Aβ intrahippocampal injection to induce long-term potentiation and to enhance synaptic variability in CA1, contrasting with what was observed in vehicle-injected subjects. Although soluble Aβ microinjection significantly increased the relative power of γ-band and ripple oscillations and significantly shifted the average vector of θ-to-γ phase-amplitude coupling (PAC) in CA1, it prevented θ-to-γ PAC shift induced by high-frequency CA3 stimulation, opposite to what was observed in vehicle-injected animals. These results provide further evidence that soluble Aβ species induce synaptic dysfunction causing abnormal synaptic variability, impaired long-term plasticity, and deviant oscillatory activity, leading to network activity derailment in the hippocampus. © 2020 Cécile Gauthier-Umanã et al.},
	keywords = {Adult; Male; MEMORY; ARTICLE; controlled study; nonhuman; animal experiment; HIPPOCAMPAL CA3 REGION; synaptic transmission; urethan; nerve cell plasticity; long term potentiation; hippocampal CA1 region; microinjection; acute drug administration; amyloid beta protein[1-40]; amyloid beta protein[25-35]; xylazine; rat; oscillatory potential},
	year = {2020},
	eissn = {1687-5443}
}

@article{MTMT:34565241,
	title = {Impaired Potentiation of Theta Oscillations During a Visual Cortical Plasticity Paradigm in Individuals With Schizophrenia},
	url = {https://m2.mtmt.hu/api/publication/34565241},
	author = {Hamilton, H.K. and Roach, B.J. and Cavus, I. and Teyler, T.J. and Clapp, W.C. and Ford, J.M. and Tarakci, E. and Krystal, J.H. and Mathalon, D.H.},
	doi = {10.3389/fpsyt.2020.590567},
	journal-iso = {FRONT PSYCHIATRY},
	journal = {FRONTIERS IN PSYCHIATRY},
	volume = {11},
	unique-id = {34565241},
	issn = {1664-0640},
	year = {2020},
	eissn = {1664-0640}
}

@article{MTMT:31290261,
	title = {Hippocampal long-term synaptic depression and memory deficits induced in early amyloidopathy are prevented by enhancing G-protein-gated inwardly rectifying potassium channel activity},
	url = {https://m2.mtmt.hu/api/publication/31290261},
	author = {Sánchez-Rodríguez, I. and Djebari, S. and Temprano-Carazo, S. and Vega-Avelaira, D. and Jiménez-Herrera, R. and Iborra-Lázaro, G. and Yajeya, J. and Jiménez-Díaz, L. and Navarro-López, J.D.},
	doi = {10.1111/jnc.14946},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {153},
	unique-id = {31290261},
	issn = {0022-3042},
	abstract = {Hippocampal synaptic plasticity disruption by amyloid-β (Aβ) peptides + thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures in neuronal excitability maintenance seems to be an underlying mechanism. G-protein-gated inwardly rectifying potassium (GirK) channels control neural excitability by hyperpolarization in response to many G-protein-coupled receptors activation. Here, in early in vitro and in vivo amyloidosis mouse models, we study whether GirK channels take part of the hippocampal synaptic plasticity impairments generated by Aβ1–42. In vitro electrophysiological recordings from slices showed that Aβ1–42 alters synaptic plasticity by switching high-frequency stimulation (HFS) induced long-term potentiation (LTP) to long-term depression (LTD), which led to in vivo hippocampal-dependent memory deficits. Remarkably, selective pharmacological activation of GirK channels with ML297 rescued both HFS-induced LTP and habituation memory from Aβ1–42 action. Moreover, when GirK channels were specifically blocked by Tertiapin-Q, their activation with ML297 failed to rescue LTP from the HFS-dependent LTD induced by Aβ1–42. On the other hand, the molecular analysis of the recorded slices by western blot showed that the expression of GIRK1/2 subunits, which form the prototypical GirK channel in the hippocampus, was not significantly regulated by Aβ1–42. However, immunohistochemical examination of our in vivo amyloidosis model showed Aβ1–42 to down-regulate hippocampal GIRK1 subunit expression. Together, our results describe an Aβ-mediated deleterious synaptic mechanism that modifies the induction threshold for hippocampal LTP/LTD and underlies memory alterations observed in amyloidosis models. In this scenario, GirK activation assures memory formation by preventing the transformation of HFS-induced LTP into LTD. (Figure presented.). © 2019 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry},
	keywords = {hippocampus; SYNAPTIC PLASTICITY; habituation; brain slices; GIRK channels; amyloid-β1–42 peptide; LABORAS},
	year = {2020},
	eissn = {1471-4159},
	pages = {362-376}
}

@article{MTMT:31239913,
	title = {Brain arrhythmias induced by amyloid beta and inflammation: Involvement in alzheimer’s disease and other inflammation-related pathologies},
	url = {https://m2.mtmt.hu/api/publication/31239913},
	author = {Peña-Ortega, F.},
	doi = {10.2174/1567205017666191213162233},
	journal-iso = {CURR ALZHEIMER RES},
	journal = {CURRENT ALZHEIMER RESEARCH},
	volume = {16},
	unique-id = {31239913},
	issn = {1567-2050},
	abstract = {A variety of neurological diseases, including Alzheimer’s disease (AD), involve amyloid beta (Aβ) accumulation and/or neuroinflammation, which can alter synaptic and neural circuit functions. Consequently, these pathological conditions induce changes in neural network rhythmic activity (brain arrhythmias), which affects many brain functions. Neural network rhythms are involved in information processing, storage and retrieval, which are essential for memory consolidation, executive functioning and sensory processing. Therefore, brain arrhythmias could have catastrophic effects on circuit function, underlying the symptoms of various neurological diseases. Moreover, brain arrhythmias can serve as biomarkers for a variety of brain diseases. The aim of this review is to provide evidence linking Aβ and inflammation to neural network dysfunction, focusing on alterations in brain rhythms and their impact on cognition and sensory processing. I reviewed the most common brain arrhythmias characterized in AD, in AD transgenic models and those induced by Aβ. In addition, I reviewed the modulations of brain rhythms in neuroinflammatory diseases and those induced by immunogens, interleukins and microglia. This review reveals that Aβ and inflammation produce a complex set of effects on neural network function, which are related to the induction of brain arrhythmias and hyperexcitability, both closely related to behavioral alterations. Understanding these brain arrhythmias can help to develop therapeutic strategies to halt or prevent these neural network alterations and treat not only the arrhythmias but also the symptoms of AD and other inflammation-related pathologies. © 2019 Bentham Science Publishers.},
	keywords = {Inflammation; ANTIGEN; GAMMA; LIPOPOLYSACCHARIDE; cytokine; review; human; priority journal; nonhuman; animal model; Theta; OSCILLATIONS; Health; Tumor Necrosis Factor; ENCEPHALITIS; microglia; amyloid; brain disease; interleukin 1beta; neuromodulation; Alzheimer disease; amyloid beta protein; epileptiform; brain arrhythmia},
	year = {2019},
	eissn = {1875-5828},
	pages = {1108-1131}
}

@article{MTMT:30775278,
	title = {Role of girk channels in long-term potentiation of synaptic inhibition in an in vivo mouse model of early amyloid-β pathology},
	url = {https://m2.mtmt.hu/api/publication/30775278},
	author = {Sánchez-Rodríguez, I. and Gruart, A. and Delgado-García, J.M. and Jiménez-Díaz, L. and Navarro-López, J.D.},
	doi = {10.3390/ijms20051168},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {30775278},
	issn = {1661-6596},
	abstract = {Imbalances of excitatory/inhibitory synaptic transmission occur early in the pathogenesis of Alzheimer’s disease (AD), leading to hippocampal hyperexcitability and causing synaptic, network, and cognitive dysfunctions. G-protein-gated potassium (GirK) channels play a key role in the control of neuronal excitability, contributing to inhibitory signaling. Here, we evaluate the relationship between GirK channel activity and inhibitory hippocampal functionality in vivo. In a non-transgenic mouse model of AD, field postsynaptic potentials (fPSPs) from the CA3–CA1 synapse in the dorsal hippocampus were recorded in freely moving mice. Intracerebroventricular (ICV) injections of amyloid-β (Aβ) or GirK channel modulators impaired ionotropic (GABAA-mediated fPSPs) and metabotropic (GirK-mediated fPSPs) inhibitory signaling and disrupted the potentiation of synaptic inhibition. However, the activation of GirK channels prevented Aβ-induced changes in GABAA components. Our data shows, for the first time, the presence of long-term potentiation (LTP) for both the GABAA and GirK-mediated inhibitory postsynaptic responses in vivo. In addition, our results support the importance of an accurate level of GirK-dependent signaling for dorsal hippocampal performance in early amyloid pathology models by controlling the excess of excitation that disrupts synaptic plasticity processes. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {Animals; Adult; Male; Male; metabolism; MICE; AGONISTS; hippocampus; ARTICLE; PATHOPHYSIOLOGY; PATHOPHYSIOLOGY; MOUSE; signal transduction; signal transduction; animal; Injections; physiology; comparative study; controlled study; nonhuman; animal model; animal experiment; drug effect; 4 aminobutyric acid A receptor; SYNAPSES; SYNAPTIC PLASTICITY; LONG-TERM POTENTIATION; HIPPOCAMPAL CA3 REGION; synaptic transmission; evoked response; injection; latent period; synapse; Disease Models, Animal; disease model; in vivo study; In vivo; nerve cell plasticity; Alzheimer disease; Alzheimer disease; Alzheimer disease; G protein coupled inwardly rectifying potassium channel; G protein coupled inwardly rectifying potassium channel; postsynaptic potential; amyloid beta protein; amyloid beta protein; metabotropic receptor; Glutamatergic synapse; G Protein-Coupled Inwardly-Rectifying Potassium Channels; Amyloid beta-Peptides; intracerebroventricular drug administration; long term potentiation; long term potentiation; hippocampal CA1 region; synaptic inhibition; antagonists and inhibitors; neuronal excitability; GIRK channels; Aβ1–42; FIPSP; Freely moving mice; Inhibitory LTP},
	year = {2019},
	eissn = {1422-0067}
}

@article{MTMT:3323000,
	title = {Exceptional in vivo catabolism of neurodegeneration-related aggregates},
	url = {https://m2.mtmt.hu/api/publication/3323000},
	author = {Datki, Zsolt László and Oláh, Zita and Hortobágyi, Tibor and Borbélyné Mácsai, Lilla and Zsuga, Katalin and Fülöp, Lívia and Bozsó, Zsolt and Gálik, Bence and Ács, Éva and Földi, Angéla and Szarvas, A and Kálmán, János},
	doi = {10.1186/s40478-018-0507-3},
	journal-iso = {ACTA NEUROPATH COMM},
	journal = {ACTA NEUROPATHOLOGICA COMMUNICATIONS},
	volume = {6},
	unique-id = {3323000},
	issn = {2051-5960},
	year = {2018},
	eissn = {2051-5960},
	orcid-numbers = {Datki, Zsolt László/0000-0002-2537-4741; Oláh, Zita/0000-0002-6372-532X; Hortobágyi, Tibor/0000-0001-5732-7942; Borbélyné Mácsai, Lilla/0000-0002-9503-6449; Fülöp, Lívia/0000-0002-8010-0129; Bozsó, Zsolt/0000-0002-5713-3096; Ács, Éva/0000-0003-1774-157X; Kálmán, János/0000-0001-5319-5639}
}

@article{MTMT:30585473,
	title = {Trophic modulation of gamma oscillations: The key role of processing protease for Neuregulin-1 and BDNF precursors},
	url = {https://m2.mtmt.hu/api/publication/30585473},
	author = {Tamura, Hideki and Shiosaka, Sadao and Morikawa, Shota},
	doi = {10.1016/j.neuint.2017.12.002},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {119},
	unique-id = {30585473},
	issn = {0197-0186},
	abstract = {Gamma oscillations within the cerebral cortex and hippocampus are associated with cognitive processes, including attention, sensory perception, and memory formation; a deficit in gamma regulation is a common symptom of neurologic and psychiatric disorders. Accumulating evidence has suggested that gamma oscillations result from the synchronized activity of cell assemblies coordinated mainly by parvalbumin-positive inhibitory interneurons. The modulator molecules for pan/albumin-positive interneurons are major research targets and have the potential to control the specific oscillatory rhythm and behavior originating from neural coordination. Neuregulin-1 and brain-derived neurotrophic factor have been focused on as synaptic trophic factors that are associated with gamma oscillations. Synaptic activity converts precursor trophic factors into their biologically active forms by proteolytic cleavage, which could, in turn, modulate cell excitability and synaptic plasticity through each receptor's signaling. From these findings, the processing of trophic factors by proteases in a synaptic microenvironment might involve gamma oscillations during cognition. Here, we review the trophic modulation of gamma oscillations through extracellular proteolysis and its implications in neuronal diseases. (C) 2017 Elsevier Ltd. All rights reserved.},
	keywords = {MEMORY; Alzheimer's disease; BDNF; GAMMA OSCILLATION; Neuropsin (KLK8); Neureuglin-1},
	year = {2018},
	eissn = {1872-9754},
	pages = {2-10}
}

@article{MTMT:27029821,
	title = {Metabotropic glutamate receptor, mGlu5, regulates hippocampal synaptic plasticity and is required for tetanisation-triggered changes in theta and gamma oscillations},
	url = {https://m2.mtmt.hu/api/publication/27029821},
	author = {Bikbaev, Arthur and Manahan-Vaughan, Denise},
	doi = {10.1016/j.neuropharm.2016.06.004},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {115},
	unique-id = {27029821},
	issn = {0028-3908},
	year = {2017},
	eissn = {1873-7064},
	pages = {20-29}
}

@{MTMT:31840159,
	title = {mGlu5: A Metabotropic Glutamate Receptor at the Hub of Hippocampal Information Processing, Persistent Synaptic Plasticity, and Long-Term Memory},
	url = {https://m2.mtmt.hu/api/publication/31840159},
	author = {Hagena, Hardy and Manahan-Vaughan, Denise},
	booktitle = {mGLU Receptors.},
	doi = {10.1007/978-3-319-56170-7_5},
	unique-id = {31840159},
	abstract = {In the hippocampus, the metabotropic glutamate (mGlu) receptor, mGlu5, plays a very prominent role in synaptic information storage and memory. This receptor enables persistent (>24 h) forms of synaptic plasticity, in the form of long-term potentiation (LTP) and long-term depression (LTD), and is also required for plasticity forms that are directly modulated by spatial learning. mGlu5 supports hippocampal neuronal oscillations that occur during synaptic plasticity events, supports the stabilization of place fields, and regulates the direction of change in synaptic weights in specific synaptic subcompartments of the hippocampus. Furthermore, dysfunctions in this receptor are associated with potent disturbances of hippocampus-dependent cognition. We propose that the mGlu5 receptor lies at the hub of hippocampal information processing and is pivotal to the accurate, long-term, and reliable acquisition and encoding of new spatial experiences and cognitive representations.},
	keywords = {FREELY MOVING RATS; MEMORY; hippocampus; learning; POSTSYNAPTIC DENSITY PROTEINS; SYNAPTIC PLASTICITY; METHYL-D-ASPARTATE; In vivo; rodent; FRAGILE-X-SYNDROME; POSITIVE ALLOSTERIC MODULATOR; NR2B-CONTAINING NMDA RECEPTORS; Biochemistry & Molecular Biology; IMMEDIATE-EARLY GENE; mGlu5; MOSSY FIBER SYNAPSES; Slow-onset potentiation},
	year = {2017},
	pages = {79-101},
	orcid-numbers = {Hagena, Hardy/0000-0002-6421-4732}
}

@article{MTMT:26565341,
	title = {Changes in Neuronal Oscillations Accompany the Loss of Hippocampal LTP that Occurs in an Animal Model of Psychosis},
	url = {https://m2.mtmt.hu/api/publication/26565341},
	author = {Kalweit, Alexander N and Amanpour-Gharaei, Bezhad and Colitti-Klausnitzer, Jens and Manahan-Vaughan, Denise},
	doi = {10.3389/fnbeh.2017.00036},
	journal-iso = {FRONT BEHAV NEUROSCI},
	journal = {FRONTIERS IN BEHAVIORAL NEUROSCIENCE},
	volume = {11},
	unique-id = {26565341},
	year = {2017},
	eissn = {1662-5153}
}

@article{MTMT:3193785,
	title = {Multivalent foldamer-based affinity assay for selective recognition of Aβ oligomers},
	url = {https://m2.mtmt.hu/api/publication/3193785},
	author = {Olajos, Gábor and Bartus, Éva and Schuster, Ildikó and Lautner, Gergely and Gyurcsányi, Ervin Róbert and Szögi, Titanilla and Fülöp, Lívia and Martinek, Tamás},
	doi = {10.1016/j.aca.2017.01.013},
	journal-iso = {ANAL CHIM ACTA},
	journal = {ANALYTICA CHIMICA ACTA},
	volume = {960},
	unique-id = {3193785},
	issn = {0003-2670},
	abstract = {Abstract Mimicking the molecular recognition functionality of antibodies is a great challenge. Foldamers are attractive candidates because of their relatively small size and designable interaction surface. This paper describes a sandwich type enzyme-linked immunoassay with a tetravalent β-peptide foldamer helix array as capture element and enzyme labeled tracer antibodies. The assay was found to be selective to β-amyloid oligomeric species with surface features transiently present in ongoing aggregation. In optimized conditions, with special emphasis on the foldamer immobilization, a detection limit of 5 pM was achieved with a linear range of 10–500 pM. These results suggest that protein mimetic foldamers can be useful tools in biosensors and affinity assays.},
	keywords = {FOLDAMERS; MOLECULAR RECOGNITION; Antibody mimetics; Bioaffinity assay; β-Amyloid oligomers},
	year = {2017},
	eissn = {1873-4324},
	pages = {131-137},
	orcid-numbers = {Olajos, Gábor/0000-0002-2479-4891; Bartus, Éva/0000-0001-9976-6978; Schuster, Ildikó/0000-0001-9997-5729; Gyurcsányi, Ervin Róbert/0000-0002-9929-7865; Szögi, Titanilla/0000-0002-9854-7340; Fülöp, Lívia/0000-0002-8010-0129; Martinek, Tamás/0000-0003-3168-8066}
}

@article{MTMT:27147147,
	title = {Activation of G-protein-gated inwardly rectifying potassium (Kir3/GirK) channels rescues hippocampal functions in a mouse model of early amyloid-β pathology},
	url = {https://m2.mtmt.hu/api/publication/27147147},
	author = {Sanchez-Rodriguez, Irene and Temprano-Carazo, Sara and Najera, Alberto and Djebari, Souhail and Yajeya, Javier and Gruart, Agnes and Delgado-Garcia, Jose M and Jimenez-Diaz, Lydia and Navarro-Lopez, Juan D},
	doi = {10.1038/s41598-017-15306-8},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {7},
	unique-id = {27147147},
	issn = {2045-2322},
	year = {2017},
	eissn = {2045-2322}
}

@article{MTMT:26224480,
	title = {Toxin-Induced Experimental Models of Learning and Memory Impairment},
	url = {https://m2.mtmt.hu/api/publication/26224480},
	author = {More, Sandeep Vasant and Kumar, Hemant and Cho, Duk-Yeon and Yun, Yo-Sep and Choi, Dong-Kug},
	doi = {10.3390/ijms17091447},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {17},
	unique-id = {26224480},
	issn = {1661-6596},
	year = {2016},
	eissn = {1422-0067}
}