Cellular correlate of assembly formation in oscillating hippocampal networks in vitro.
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Cellular correlate of assembly formation in oscillating hippocampal networks in vitro. / Bähner, Florian; Weiss, Elisa K; Birke, Gunnar; Maier, Nikolaus; Schmitz, Dietmar; Rudolph, Uwe; Frotscher, Michael; Traub, Roger D; Both, Martin; Draguhn, Andreas.
In: P NATL ACAD SCI USA, Vol. 108, No. 35, 35, 2011, p. 607-616.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Cellular correlate of assembly formation in oscillating hippocampal networks in vitro.
AU - Bähner, Florian
AU - Weiss, Elisa K
AU - Birke, Gunnar
AU - Maier, Nikolaus
AU - Schmitz, Dietmar
AU - Rudolph, Uwe
AU - Frotscher, Michael
AU - Traub, Roger D
AU - Both, Martin
AU - Draguhn, Andreas
PY - 2011
Y1 - 2011
N2 - Neurons form transiently stable assemblies that may underlie cognitive functions, including memory formation. In most brain regions, coherent activity is organized by network oscillations that involve sparse firing within a well-defined minority of cells. Despite extensive work on the underlying cellular mechanisms, a fundamental question remains unsolved: how are participating neurons distinguished from the majority of nonparticipators? We used physiological and modeling techniques to analyze neuronal activity in mouse hippocampal slices during spontaneously occurring high-frequency network oscillations. Network-entrained action potentials were exclusively observed in a defined subset of pyramidal cells, yielding a strict distinction between participating and nonparticipating neurons. These spikes had unique properties, because they were generated in the axon without prior depolarization of the soma. GABA(A) receptors had a dual role in pyramidal cell recruitment. First, the sparse occurrence of entrained spikes was accomplished by intense perisomatic inhibition. Second, antidromic spike generation was facilitated by tonic effects of GABA in remote axonal compartments. Ectopic spike generation together with strong somatodendritic inhibition may provide a cellular mechanism for the definition of oscillating assemblies.
AB - Neurons form transiently stable assemblies that may underlie cognitive functions, including memory formation. In most brain regions, coherent activity is organized by network oscillations that involve sparse firing within a well-defined minority of cells. Despite extensive work on the underlying cellular mechanisms, a fundamental question remains unsolved: how are participating neurons distinguished from the majority of nonparticipators? We used physiological and modeling techniques to analyze neuronal activity in mouse hippocampal slices during spontaneously occurring high-frequency network oscillations. Network-entrained action potentials were exclusively observed in a defined subset of pyramidal cells, yielding a strict distinction between participating and nonparticipating neurons. These spikes had unique properties, because they were generated in the axon without prior depolarization of the soma. GABA(A) receptors had a dual role in pyramidal cell recruitment. First, the sparse occurrence of entrained spikes was accomplished by intense perisomatic inhibition. Second, antidromic spike generation was facilitated by tonic effects of GABA in remote axonal compartments. Ectopic spike generation together with strong somatodendritic inhibition may provide a cellular mechanism for the definition of oscillating assemblies.
KW - Animals
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Cell Movement
KW - Models, Neurological
KW - Action Potentials
KW - Computer Simulation
KW - Probability
KW - Hippocampus/cytology/physiology
KW - Receptors, GABA-A/physiology
KW - Animals
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Cell Movement
KW - Models, Neurological
KW - Action Potentials
KW - Computer Simulation
KW - Probability
KW - Hippocampus/cytology/physiology
KW - Receptors, GABA-A/physiology
M3 - SCORING: Journal article
VL - 108
SP - 607
EP - 616
JO - P NATL ACAD SCI USA
JF - P NATL ACAD SCI USA
SN - 0027-8424
IS - 35
M1 - 35
ER -
