TY  - JOUR
AU  - Fernández-Ruiz, A.
AU  - Oliva, A.
AU  - Soula, M.
AU  - Rocha-Almeida, F.
AU  - Nagy, Attila Gergő
AU  - Martin-Vazquez, G.
AU  - Buzsáki, G.
TI  - Gamma rhythm communication between entorhinal cortex and dentate gyrus neuronal assemblies
JF  - SCIENCE
J2  - SCIENCE
VL  - 372
PY  - 2021
IS  - 6537
PG  - 15
SN  - 0036-8075
DO  - 10.1126/science.abf3119
UR  - https://m2.mtmt.hu/api/publication/31980426
ID  - 31980426
N1  - Funding Agency and Grant Number: NARSAD Young Investigator Grant; Rosztoczy Foundation; NIH [MH107396, NS113283, U19NS104590]; NSF [1707316];  [K99MH120343];  [K99MH122582]; National Institute of Mental Health [K99MH122582] Funding Source: NIH RePORTER; National Institute of Neurological Disorders and Stroke [U19NS104590] Funding Source: NIH RePORTER
            Funding text: This work was supported by a K99 grant (K99MH120343), a NARSAD Young Investigator Grant (A.F.-R.), a K99 grant (K99MH122582) (A.O.), the Rosztoczy Foundation (G.N.), NIH grants (MH107396 and NS113283, U19NS104590), and NSF grant 1707316 (NeuroNex MINT; G.B.)
AB  - Gamma oscillations are thought to coordinate the spike timing of functionally specialized neuronal ensembles across brain regions. To test this hypothesis, we optogenetically perturbed gamma spike timing in the rat medial (MEC) and lateral (LEC) entorhinal cortices and found impairments in spatial and object learning tasks, respectively. MEC and LEC were synchronized with the hippocampal dentate gyrus through high- and low-gamma-frequency rhythms, respectively, and engaged either granule cells or mossy cells and CA3 pyramidal cells in a task-dependent manner. Gamma perturbation disrupted the learning-induced assembly organization of target neurons. Our findings imply that pathway-specific gamma oscillations route task-relevant information between distinct neuronal subpopulations in the entorhinal-hippocampal circuit. We hypothesize that interregional gamma-time-scale spike coordination is a mechanism of neuronal communication. Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - BRAGIN, A
AU  - Jandó, Gábor
AU  - Nádasdy, Zoltán
AU  - VANLANDEGHEM, M
AU  - Buzsáki, György
TI  - Dentate EEG spikes and associated interneuronal population bursts in the hippocampal hilar region of the rat
JF  - JOURNAL OF NEUROPHYSIOLOGY
J2  - J NEUROPHYSIOL
VL  - 73
PY  - 1995
IS  - 4
SP  - 1691
EP  - 1705
PG  - 15
SN  - 0022-3077
DO  - 10.1152/jn.1995.73.4.1691
UR  - https://m2.mtmt.hu/api/publication/1428425
ID  - 1428425
AB  - 1. This paper describes two novel population patterns in the dentate gyrus of the awake rat, termed type 1 and type 2 dentate spikes (DS1, DS2). Their cellular generation and spatial distribution were examined by simultaneous recording of field potentials and unit activity using multiple-site silicon probes and wire electrode arrays. 2. Dentate spikes were large amplitude (2-4 mV), short duration (<30 ms) field potentials that occurred sparsely during behavioral immobility and slow-wave sleep. Current-source density analysis revealed large sinks in the outer (DS1) and middle (DS2) thirds of the dentate molecular layer, respectively. DS1 and DS2 had similar longitudinal, lateral, and interhemispheric synchrony. 3. Dentate spikes invariably were coupled to synchronous population bursts of putative hilar interneurons. CA3 pyramidal cells, on the other hand were suppressed during dentate spikes. 4. After bilateral removal of the entorhinal cortex, dentate spikes disappeared, whereas sharp wave-associated bursts, reflecting synchronous discharge of the CA3-CA1 network, increased several fold. 5. These physiological characteristics of the dentate spikes sug gest that they are triggered by a population burst of layer II stellate cells of the lateral (DS1) and medial (DS2) entorhinal cortex. 6. We suggest that dentate spike-associated synchronized bursts of hilar-region interneurons provide a suppressive effect on the excitability of the CA3-CA1 network in the intact brain.
LA  - English
DB  - MTMT
ER  -