@article{MTMT:34049040,
	title = {Closed-loop brain stimulation augments fear extinction in male rats},
	url = {https://m2.mtmt.hu/api/publication/34049040},
	author = {Sierra, Rodrigo Ordoñez and Lizeth Katherine, Pedraza Correa and Barcsai, Lívia and Pejin, Andrea and Li, Qun and Kozák, Gábor and Takeuchi, Yuichi and Nagy, Anett Júlia and Lőrincz, László Magor and Devinsky, Orrin and Buzsáki, György and Berényi, Antal},
	doi = {10.1038/s41467-023-39546-7},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {14},
	unique-id = {34049040},
	issn = {2041-1723},
	abstract = {Dysregulated fear reactions can result from maladaptive processing of trauma-related memories. In post-traumatic stress disorder (PTSD) and other psychiatric disorders, dysfunctional extinction learning prevents discretization of trauma-related memory engrams and generalizes fear responses. Although PTSD may be viewed as a memory-based disorder, no approved treatments target pathological fear memory processing. Hippocampal sharp wave-ripples (SWRs) and concurrent neocortical oscillations are scaffolds to consolidate contextual memory, but their role during fear processing remains poorly understood. Here, we show that closed-loop, SWR triggered neuromodulation of the medial forebrain bundle (MFB) can enhance fear extinction consolidation in male rats. The modified fear memories became resistant to induced recall (i.e., ‘renewal’ and ‘reinstatement’) and did not reemerge spontaneously. These effects were mediated by D2 receptor signaling-induced synaptic remodeling in the basolateral amygdala. Our results demonstrate that SWR-triggered closed-loop stimulation of the MFB reward system enhances extinction of fearful memories and reducing fear expression across different contexts and preventing excessive and persistent fear responses. These findings highlight the potential of neuromodulation to augment extinction learning and provide a new avenue to develop treatments for anxiety disorders.},
	year = {2023},
	eissn = {2041-1723},
	orcid-numbers = {Li, Qun/0000-0002-5501-8262; Kozák, Gábor/0000-0002-3473-9351; Takeuchi, Yuichi/0000-0001-7545-8401; Devinsky, Orrin/0000-0003-0044-4632; Buzsáki, György/0000-0002-3100-4800}
}

@article{MTMT:33806908,
	title = {Reinstating olfactory bulb-derived limbic gamma oscillations alleviates depression-like behavioral deficits in rodents},
	url = {https://m2.mtmt.hu/api/publication/33806908},
	author = {Li, Qun and Takeuchi, Yuichi and Wang, Jiale and Gellért, Levente and Barcsai, Lívia and Lizeth Katherine, Pedraza Correa and Nagy, Anett Júlia and Kozák, Gábor and Nakai, Shinya and Kato, Shigeki and Kobayashi, Kazuto and Ohsawa, Masahiro and Horváth, Gyöngyi and Kékesi, Gabriella and Lőrincz, László Magor and Devinsky, Orrin and Buzsáki, György and Berényi, Antal},
	doi = {10.1016/j.neuron.2023.04.013},
	journal-iso = {NEURON},
	journal = {NEURON},
	volume = {111},
	unique-id = {33806908},
	issn = {0896-6273},
	year = {2023},
	eissn = {1097-4199},
	pages = {2065-2075},
	orcid-numbers = {Gellért, Levente/0000-0003-2254-2970; Kozák, Gábor/0000-0002-3473-9351; Horváth, Gyöngyi/0000-0002-6025-4577; Kékesi, Gabriella/0000-0002-0185-2155}
}

@article{MTMT:33789524,
	title = {Differential Serotonergic Modulation of Synaptic Inputs to the Olfactory Cortex},
	url = {https://m2.mtmt.hu/api/publication/33789524},
	author = {Piszár, Ildikó and Lőrincz, László Magor},
	doi = {10.3390/ijms24031950},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33789524},
	issn = {1661-6596},
	abstract = {Serotonin (5-hydroxytriptamine, 5-HT) is an important monoaminergic neuromodulator involved in a variety of physiological and pathological functions. It has been implicated in the regulation of sensory functions at various stages of multiple modalities, but its mechanisms and functions in the olfactory system have remained elusive. Combining electrophysiology, optogenetics and pharmacology, here we show that afferent (feed-forward) pathway-evoked synaptic responses are boosted, whereas feedback responses are suppressed by presynaptic 5-HT1B receptors in the anterior piriform cortex (aPC) in vitro. Blocking 5-HT1B receptors also reduces the suppressive effects of serotonergic photostimulation of baseline firing in vivo. We suggest that by regulating the relative weights of synaptic inputs to aPC, 5-HT finely tunes sensory inputs in the olfactory cortex.},
	keywords = {synaptic transmission; neuromodulation; interneuron; Olfactory cortex},
	year = {2023},
	eissn = {1422-0067}
}

@article{MTMT:33789523,
	title = {Higher-order thalamic nuclei facilitate the generalization and maintenance of spike-and-wave discharges of absence seizures},
	url = {https://m2.mtmt.hu/api/publication/33789523},
	author = {Atherton, Zoe and Nagy, Olivér and Barcsai, Lívia and Sere, Péter and Zsigri, Nikolett and Földi, Tamás and Gellért, Levente and Berényi, Antal and Crunelli, Vincenzo and Lőrincz, László Magor},
	doi = {10.1016/j.nbd.2023.106025},
	journal-iso = {NEUROBIOL DIS},
	journal = {NEUROBIOLOGY OF DISEASE},
	volume = {178},
	unique-id = {33789523},
	issn = {0969-9961},
	abstract = {Spike-and-wave discharges (SWDs), generated by the cortico-thalamo-cortical (CTC) network, are pathological, large amplitude oscillations and the hallmark of absence seizures (ASs). SWDs begin in a cortical initiation network in both humans and animal models, including the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), where it is located in the primary somatosensory cortex (S1). The behavioral manifestation of an AS occurs when SWDs spread from the cortical initiation site to the whole brain, however, the mechanisms behind this rapid propagation remain unclear. Here we investigated these processes beyond the principal CTC network, in higher-order (HO) thalamic nuclei (lateral posterior (LP) and posterior (PO) nuclei) since their diffuse connectivity and known facilitation of intracortical communications make these nuclei key candidates to support SWD generation and maintenance. In freely moving GAERS, multi-site LFP in LP, PO and multiple cortical regions revealed a novel feature of SWDs: during SWDs there are short periods (named SWD-breaks) when cortical regions far from S1, such the primary visual cortex (V1), become transiently unsynchronized from the ongoing EEG rhythm. Inactivation of HO nuclei with local muscimol injections or optogenetic perturbation of HO nuclei activity increased the occurrence of SWD-breaks and the former intervention also increased the SWD propagation-time from S1. The neural underpinnings of these findings were explored further by silicon probe recordings from single units of PO which uncovered two previously unknown groups of excitatory neurons based on their burst firing dynamics at SWD onset. Moreover, a switch from tonic to burst firing at SWD onset was shown to be an important feature since it was much less prominent for non-generalized events, i.e. SWDs that remained local to S1. Additionally, one group of neurons showed a reverse of this switch during SWD-breaks, demonstrating the importance of this firing pattern throughout the SWD. In summary, these results support the view that multiple HO thalamic nuclei are utilized at SWD onset and contribute to cortical synchrony throughout the paroxysmal discharge.},
	keywords = {EPILEPSY; somatosensory cortex; Thalamus; Ensemble recordings; Higher-order thalamic nuclei},
	year = {2023},
	eissn = {1095-953X},
	orcid-numbers = {Gellért, Levente/0000-0003-2254-2970}
}

@article{MTMT:33789490,
	title = {HCN channels and absence seizures},
	url = {https://m2.mtmt.hu/api/publication/33789490},
	author = {Crunelli, Vincenzo and David, Francois and Morais, Tatiana P and Lőrincz, László Magor},
	doi = {10.1016/j.nbd.2023.106107},
	journal-iso = {NEUROBIOL DIS},
	journal = {NEUROBIOLOGY OF DISEASE},
	volume = {181},
	unique-id = {33789490},
	issn = {0969-9961},
	abstract = {Hyperpolarization-activation cyclic nucleotide-gated (HCN) channels were for the first time implicated in absence seizures (ASs) when an abnormal Ih (the current generated by these channels) was reported in neocortical layer 5 neurons of a mouse model. Genetic studies of large cohorts of children with Childhood Absence Epilepsy (where ASs are the only clinical symptom) have identified only 3 variants in HCN1 (one of the genes that code for the 4 HCN channel isoforms, HCN1-4), with one (R590Q) mutation leading to loss-of-function. Due to the multi-faceted effects that HCN channels exert on cellular excitability and neuronal network dynamics as well as their modulation by environmental factors, it has been difficult to identify the detailed mechanism by which different HCN isoforms modulate ASs. In this review, we systematically and critically analyze evidence from established AS models and normal non-epileptic animals with area- and time-selective ablation of HCN1, HCN2 and HCN4. Notably, whereas knockout of rat HCN1 and mouse HCN2 leads to the expression of ASs, the pharmacological block of all HCN channel isoforms abolishes genetically determined ASs. These seemingly contradictory results could be reconciled by taking into account the well-known opposite effects of Ih on cellular excitability and network function. Whereas existing evidence from mouse and rat AS models indicates that pan-HCN blockers may provide a novel approach for the treatment of human ASs, the development of HCN isoform-selective drugs would greatly contribute to current research on the role for these channels in ASs generation and maintenance as well as offer new potential clinical applications.},
	keywords = {CORTEX; Thalamus; THALAMIC RETICULAR NUCLEUS; I(h); Spike-and-wave discharges; network resonance; Dendritic summation; HCN1–4},
	year = {2023},
	eissn = {1095-953X}
}

@article{MTMT:32820872,
	title = {Differential Serotonergic Modulation of Principal Neurons and Interneurons in the Anterior Piriform Cortex},
	url = {https://m2.mtmt.hu/api/publication/32820872},
	author = {Piszár, Ildikó and Lőrincz, László Magor},
	doi = {10.3389/fnana.2022.821695},
	journal-iso = {FRONT NEUROANAT},
	journal = {FRONTIERS IN NEUROANATOMY},
	volume = {16},
	unique-id = {32820872},
	issn = {1662-5129},
	year = {2022},
	eissn = {1662-5129}
}

@article{MTMT:32551790,
	title = {Temporally Targeted Interactions With Pathologic Oscillations as Therapeutical Targets in Epilepsy and Beyond},
	url = {https://m2.mtmt.hu/api/publication/32551790},
	author = {Földi, Tamás and Lőrincz, László Magor and Berényi, Antal},
	doi = {10.3389/fncir.2021.784085},
	journal-iso = {FRONT NEURAL CIRCUIT},
	journal = {FRONTIERS IN NEURAL CIRCUITS},
	volume = {15},
	unique-id = {32551790},
	issn = {1662-5110},
	year = {2021},
	eissn = {1662-5110}
}

@article{MTMT:32167983,
	title = {Activity of the Lateral Hypothalamus during Genetically Determined Absence Seizures},
	url = {https://m2.mtmt.hu/api/publication/32167983},
	author = {Sere, Péter and Nikolett, Zsigri and Raffai, Tímea and Furdan, Szabina and Győri, Fanni and Vincenzo, Crunelli and Lőrincz, László Magor},
	doi = {10.3390/ijms22179466},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {32167983},
	issn = {1661-6596},
	year = {2021},
	eissn = {1422-0067}
}

@article{MTMT:32037613,
	title = {Systemic administration of ivabradine, a hyperpolarization-activated cyclic nucleotide-gated channel inhibitor, blocks spontaneous absence seizures},
	url = {https://m2.mtmt.hu/api/publication/32037613},
	author = {Iacone, Yasmine and Morais, Tatiana P. and David, Francois and Delicata, Francis and Sandle, Joanna and Raffai, Tímea and Parri, Harri Rheinallt and Weisser, Johan Juhl and Bundgaard, Christoffer and Klewe, Ib Vestergaard and Tamás, Gábor and Thomsen, Morten Skott and Crunelli, Vincenzo and Lőrincz, László Magor},
	doi = {10.1111/epi.16926},
	journal-iso = {EPILEPSIA},
	journal = {EPILEPSIA},
	volume = {62},
	unique-id = {32037613},
	issn = {0013-9580},
	abstract = {Objective Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are known to be involved in the generation of absence seizures (ASs), and there is evidence that cortical and thalamic HCN channel dysfunctions may have a proabsence role. Many HCN channel blockers are available, but their role in ASs has been investigated only by localized brain injection or in in vitro model systems due to their limited brain availability. Here, we investigated the effect on ASs of orally administered ivabradine (an HCN channel blocker approved for the treatment of heart failure in humans) following injection of the P-glycoprotein inhibitor elacridar, which is known to increase penetration into the brain of drug substrates for this efflux transporter. The action of ivabradine was also tested following in vivo microinjection into the cortical initiation network (CIN) of the somatosensory cortex and in the thalamic ventrobasal nucleus (VB) as well as on cortical and thalamocortical neurons in brain slices. Methods We used electroencephalographic recordings in freely moving Genetic Absence Epilepsy Rats From Strasbourg (GAERSs) to assess the action of oral administration of ivabradine, with and without elacridar, on ASs. Ivabradine was also microinjected into the CIN and VB of GAERSs in vivo and applied to Wistar CIN and GAERS VB slices while recording patch-clamped cortical Layer 5/6 and thalamocortical neurons, respectively. Results Oral administration of ivabradine markedly and dose-dependently reduced ASs. Ivabradine injection into CIN abolished ASs and elicited small-amplitude 4-7-Hz waves (without spikes), whereas in the VB it was less potent. Moreover, ivabradine applied to GAERS VB and Wistar CIN slices selectively decreased HCN channel-dependent properties of cortical Layer 5/6 pyramidal and thalamocortical neurons, respectively. Significance These results provide the first demonstration of the antiabsence action of a systemically administered HCN channel blocker, indicating the potential of this class of drugs as a novel therapeutic avenue for ASs.},
	keywords = {MODEL; CORTEX; EPILEPSY; valproic acid; childhood; Pacemaker; anticonvulsant; THALAMOCORTICAL NEURONS; CHILDHOOD ABSENCE EPILEPSY; NETWORK MECHANISMS; rat; I-h current; OPERATIONAL CLASSIFICATION},
	year = {2021},
	eissn = {1528-1167},
	pages = {1729-1743},
	orcid-numbers = {Delicata, Francis/0000-0002-5339-5275; Tamás, Gábor/0000-0002-7905-6001}
}

@article{MTMT:31987689,
	title = {Reciprocal lateral hypothalamic and raphé GABAergic projections promote wakefulness},
	url = {https://m2.mtmt.hu/api/publication/31987689},
	author = {Gazea, Mary and Furdan, Szabina and Sere, Péter and Oesch, Lukas and Molnár, Benedek and Giovanni, Giuseppe Di and Fenno, Lief E. and Ramakrishnan, Charu and Mattis, Joanna and Deisseroth, Karl and Dymecki, Susan M. and Adamantidis, Antoine R. and Lőrincz, László Magor},
	doi = {10.1523/JNEUROSCI.2850-20.2021},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {41},
	unique-id = {31987689},
	issn = {0270-6474},
	year = {2021},
	eissn = {1529-2401},
	pages = {4840-4849},
	orcid-numbers = {Giovanni, Giuseppe Di/0000-0003-2006-563X; Ramakrishnan, Charu/0000-0002-3474-6332; Dymecki, Susan M./0000-0003-0910-9881; Adamantidis, Antoine R./0000-0003-2531-5175}
}