Proper layering is important for precisely timed activation of hippocampal mossy cells.
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Proper layering is important for precisely timed activation of hippocampal mossy cells. / Kowalski, Janina; Geuting, Markus; Paul, Sebastian; Dieni, Sandra; Laurens, Jean; Zhao, Shanting; Drakew, Alexander; Haas, Carola A; Frotscher, Michael; Vida, Imre.
In: CEREB CORTEX, Vol. 20, No. 9, 9, 2010, p. 2043-2054.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Proper layering is important for precisely timed activation of hippocampal mossy cells.
AU - Kowalski, Janina
AU - Geuting, Markus
AU - Paul, Sebastian
AU - Dieni, Sandra
AU - Laurens, Jean
AU - Zhao, Shanting
AU - Drakew, Alexander
AU - Haas, Carola A
AU - Frotscher, Michael
AU - Vida, Imre
PY - 2010
Y1 - 2010
N2 - The mammalian cortex exhibits a laminated structure that may underlie optimal synaptic connectivity and support temporally precise activation of neurons. In 'reeler' mice, the lack of the extracellular matrix protein Reelin leads to abnormal positioning of cortical neurons and disrupted layering. To address how these structural changes impact neuronal function, we combined electrophysiological and neuroanatomical techniques to investigate the synaptic activation of hippocampal mossy cells (MCs), the cell type that integrates the output of dentate gyrus granule cells (GCs). While somatodendritic domains of wild-type (WT) MCs were confined to the hilus, the somata and dendrites of reeler MCs were often found in the molecular layer, where the perforant path (PP) terminates. Most reeler MCs received aberrant monosynaptic excitatory input from the PP, whereas the disynaptic input to MCs via GCs was decreased and inhibition was increased. In contrast to the uniform disynaptic discharge of WT MCs, many reeler cells discharged with short, monosynaptic latencies, while others fired with long latencies over a broad temporal window in response to PP activation. Thus, disturbed lamination results in aberrant synaptic connectivity and altered timing of action potential generation. These results highlight the importance of a layered cortical structure for information processing.
AB - The mammalian cortex exhibits a laminated structure that may underlie optimal synaptic connectivity and support temporally precise activation of neurons. In 'reeler' mice, the lack of the extracellular matrix protein Reelin leads to abnormal positioning of cortical neurons and disrupted layering. To address how these structural changes impact neuronal function, we combined electrophysiological and neuroanatomical techniques to investigate the synaptic activation of hippocampal mossy cells (MCs), the cell type that integrates the output of dentate gyrus granule cells (GCs). While somatodendritic domains of wild-type (WT) MCs were confined to the hilus, the somata and dendrites of reeler MCs were often found in the molecular layer, where the perforant path (PP) terminates. Most reeler MCs received aberrant monosynaptic excitatory input from the PP, whereas the disynaptic input to MCs via GCs was decreased and inhibition was increased. In contrast to the uniform disynaptic discharge of WT MCs, many reeler cells discharged with short, monosynaptic latencies, while others fired with long latencies over a broad temporal window in response to PP activation. Thus, disturbed lamination results in aberrant synaptic connectivity and altered timing of action potential generation. These results highlight the importance of a layered cortical structure for information processing.
KW - Animals
KW - Mice
KW - Cell Adhesion Molecules, Neuronal deficiency
KW - Extracellular Matrix Proteins deficiency
KW - Nerve Tissue Proteins deficiency
KW - Serine Endopeptidases deficiency
KW - Neurons cytology
KW - Action Potentials genetics
KW - Mice, Neurologic Mutants
KW - Neurogenesis genetics
KW - Body Patterning genetics
KW - Mice, Inbred Strains
KW - Mossy Fibers, Hippocampal abnormalities
KW - Synaptic Transmission genetics
KW - Animals
KW - Mice
KW - Cell Adhesion Molecules, Neuronal deficiency
KW - Extracellular Matrix Proteins deficiency
KW - Nerve Tissue Proteins deficiency
KW - Serine Endopeptidases deficiency
KW - Neurons cytology
KW - Action Potentials genetics
KW - Mice, Neurologic Mutants
KW - Neurogenesis genetics
KW - Body Patterning genetics
KW - Mice, Inbred Strains
KW - Mossy Fibers, Hippocampal abnormalities
KW - Synaptic Transmission genetics
M3 - SCORING: Zeitschriftenaufsatz
VL - 20
SP - 2043
EP - 2054
JO - CEREB CORTEX
JF - CEREB CORTEX
SN - 1047-3211
IS - 9
M1 - 9
ER -