Neuronal gap junctions in the mouse main olfactory bulb: morphological analyses on transgenic mice.
In the present study we analyzed the structural features of extraglomerular gap junction-forming processes in mouse olfactory bulb electron microscopically. This work complements a previous study in which we analyzed the structural features of neuronal gap junction-forming processes within the glomerulus itself. Furthermore we examined connexin 36 expressing cells in the mouse olfactory bulb by analyzing transgenic mice in which the connexin 36 coding sequence was replaced with histological reporters. In extraglomerular regions, the mitral/tufted cell somata, dendrites and axon hillocks made gap junctions and mixed synapses with interneuronal processes. These gap junctions and synapses were associated with various types of interneuronal processes, including a particular type of sheet-like or calyx-like process contacting the somata or large dendrites of mitral/tufted cells. In the olfactory bulbs of the transgenic mice, connexin 36 was expressed in mitral cells, tufted cells, presumed granule cells and periglomerular cells. Multiple immunofluorescent labelings further revealed that presumed interneurons expressing connexin 36 in the periglomerular region rarely expressed calbindin, calretinin or tyrosine hydroxylase and are likely to comprise a chemically uncharacterized class of neurons. Similarly, interneurons expressing connexin 36 in the granule cell layer were rarely positive for calretinin, which was expressed in numerous presumed granule cells in the mouse main olfactory bulb. In summary, these findings revealed that mitral/tufted cells make gap junctions with diverse types of neurons; in the glomeruli gap junction-forming interneuronal processes originated from some types of periglomerular cells but others from a hitherto uncharacterized neuron type(s), and in the extraglomerular region gap-junction forming processes originate mainly from a subset of cells within the granule cell layer.
Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. kosaka@a3rd.med.kyushu-u.ac.jp
T
T
Kosaka
M R
MR
Deans
D L
DL
Paul
K
K
Kosaka
D000818:Animals; D064026:Calbindins; D002766:Cholecystokinin / Q000378:metabolism; D017630:Connexins / Q000235:genetics / Q000378:metabolism; D017629:Gap Junctions / Q000000981:diagnostic imaging* / Q000378:metabolism; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D046529:Microscopy, Electron, Transmission / Q000379:methods; D016253:Microscopy, Immunoelectron / Q000379:methods; D009474:Neurons / Q000166:cytology* / Q000648:ultrastructure; D009830:Olfactory Bulb / Q000166:cytology* / Q000648:ultrastructure; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014463:Ultrasonography; D001616:beta-Galactosidase / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism; D000097004:Gap Junction delta-2 Protein
D064026:Calbindins; D002766:Cholecystokinin; D017630:Connexins; D064030:S100 Calcium Binding Protein G; D014446:Tyrosine 3-Monooxygenase; D001616:beta-Galactosidase; D005680:gamma-Aminobutyric Acid; D000097004:Gap Junction delta-2 Protein