ULTRASTRUCTURAL-LOCALIZATION OF NEUROTRANSMITTER IMMUNOREACTIVITY IN MOSSY CELL AXONS AND THEIR SYNAPTIC TARGETS IN THE RAT DENTATE GYRUS

Citation
Hj. Wenzel et al., ULTRASTRUCTURAL-LOCALIZATION OF NEUROTRANSMITTER IMMUNOREACTIVITY IN MOSSY CELL AXONS AND THEIR SYNAPTIC TARGETS IN THE RAT DENTATE GYRUS, Hippocampus, 7(5), 1997, pp. 559-570
Citations number
72
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
10509631
Volume
7
Issue
5
Year of publication
1997
Pages
559 - 570
Database
ISI
SICI code
1050-9631(1997)7:5<559:UONIIM>2.0.ZU;2-#
Abstract
Electrophysiologically identified and intracellularly biocytin-labeled messy cells in the dentate hilus of the rat were studied using electr on microscopy and postembedding immunogold techniques. Ultrathin secti ons containing a labeled messy cell or its axon collaterals were react ed with antisera against the excitatory neurotransmitter glutamate and against the inhibitory neurotransmitter gamma-aminobutyric acid (GABA ). From single-and double-immunolabeled preparations, we found that 1) messy cell axon terminals made asymmetric contacts onto postsynaptic targets in the hilus and stratum moleculare of the dentate gyrus and s howed immunoreactivity primarily for glutamate, but never for GABA; 2) in the hilus, glutamate-positive messy cell axon terminals targeted G ABA-positive dendritic shafts of hilar interneurons and GABA-negative dendritic spines; and 3) in the inner molecular layer, the messy cell axon formed asymmetric synapses with dendritic spines associated with GABA-negative (presumably granule cell) dendrites. The results of this study support the view that excitatory (glutamatergic) messy cell ter minals contact GABAergic interneurons and non-GABAergic neurons in the hilar region and GABA-negative granule cells in the stratum molecular e. This pattern of connectivity is consistent with the hypothesis that messy cells provide excitatory feedback to granule cells in a dentate gyrus associational network and also activate local hilar inhibitory elements. (C) 1997 Wiley-Liss, Inc.