Proper layering is important for precisely timed activation of hippocampal mossy cells.
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.
Kowalski
Janina
J
Department of Neuroanatomy, Institute of Anatomy and Cell Biology, University of Freiburg, D-79104 Freiburg, Germany.
Geuting
Markus
M
Paul
Sebastian
S
Dieni
Sandra
S
Laurens
Jean
J
Zhao
Shanting
S
Drakew
Alexander
A
Haas
Carola A
CA
Frotscher
Michael
M
Vida
Imre
I
D000200:Action Potentials / Q000235:genetics; D000818:Animals; D019521:Body Patterning / Q000235:genetics; D015816:Cell Adhesion Molecules, Neuronal / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D016326:Extracellular Matrix Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D008818:Mice, Neurologic Mutants; D019599:Mossy Fibers, Hippocampal / Q000002:abnormalities / Q000378:metabolism* / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D055495:Neurogenesis / Q000235:genetics; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D000091042:Reelin Protein; D012697:Serine Endopeptidases / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D009435:Synaptic Transmission / Q000235:genetics
D015816:Cell Adhesion Molecules, Neuronal; D016326:Extracellular Matrix Proteins; D009419:Nerve Tissue Proteins; D000091042:Reelin Protein; C000717128:Reln protein, mouse; D012697:Serine Endopeptidases