Catecholaminergic, GABAergic, and hippocamposeptal innervation of GABAergic "somatospiny" neurons in the rat lateral septal area.
This study deals with the neurochemical characterization of the rat lateral septal area (LSA) somatospiny neurons and their innervation by hippocamposeptal, catecholaminergic, and GABAergic fibers. Electron microscopic single and double immunostaining methods were used to label catecholaminergic fibers and GABAergic cells and boutons. Axon terminals originating in the hippocampus were labeled by acute anterograde axon degeneration induced by fimbria-fornix transection 36 hours before sacrifice. Three types of experiments were performed. The convergent catecholaminergic and hippocamposeptal innervation of LSA somatospiny neurons was studied by combining immunostaining for tyrosine hydroxylase (TH) with fimbria-fornix transection. GABAergic neurons and their hippocamposeptal afferents were identified and characterized in colchicine pretreated animals immunostained for glutamic acid decarboxylase (GAD) combined with fimbria-fornix transection. The third experiment aimed at simultaneously visualizing the relationships between catecholaminergic boutons, hippocamposeptal excitatory amino acid containing axon terminals and GABAergic profiles by double immunostaining for TH (the PAP technique) and GAD (the immunogold method) combined with fimbria-fornix transection. The results are summarized as follows: 1) The same LSA somatospiny neurons receive synaptic inputs from the hippocampus and TH immunoreactive fibers which form pericellular baskets around these cells. 2) LSA somatospiny neurons are GABAergic and are postsynaptic targets of GABAergic boutons with unknown origin and hippocamposeptal axon terminals. 3) The double immunostaining experiment, finally, provided direct evidence that the same GABAergic somatospiny neurons are postsynaptic targets of both catecholaminergic and hippocamposeptal afferents. The synaptic interconnections described in this study provide anatomical basis for a better understanding of the action of catecholamines, excitatory amino acids, and GABA on the activity of LSA neurons.
Jakab
R L
RL
Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, Connecticut 06510.
Leranth
C
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D000818:Animals; D001369:Axons / Q000737:chemistry; D002395:Catecholamines / Q000032:analysis*; D005968:Glutamate Decarboxylase / Q000032:analysis; D006624:Hippocampus / Q000737:chemistry*; D007124:Immunoenzyme Techniques; D009410:Nerve Degeneration / Q000502:physiology; D009474:Neurons / Q000737:chemistry*; D051381:Rats; D011919:Rats, Inbred Strains; D012688:Septum Pellucidum / Q000737:chemistry* / Q000166:cytology; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis; D005680:gamma-Aminobutyric Acid / Q000032:analysis*
D002395:Catecholamines; D005680:gamma-Aminobutyric Acid; D014446:Tyrosine 3-Monooxygenase; D005968:Glutamate Decarboxylase