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Post‐embedding immunogold labeling of gamma‐aminobutyric acid in lamina II of the spinal trigeminal subnucleus pars caudalis: I. A qualitative study
Author(s) -
Almond J.R.,
Westrum L.E.,
Henry M.A.
Publication year - 1996
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199609)24:1<39::aid-syn5>3.0.co;2-h
Subject(s) - immunogold labelling , anatomy , neuroscience , lamina , spinal trigeminal nucleus , chemistry , biology , nociception , ultrastructure , biochemistry , receptor
This study examines the normal synaptic organization of the feline spinal trigeminal nucleus pars caudalis (PC). A primary goal of this study is to identify and characterize the synaptic complexes within PC based on their specific neurotransmitter content. Post‐embedding immunogold techniques are utilized with electron microscopy to determine the ultrastructural localization of gamma‐aminobutyric acid (GABA) immunoreactivity within lamina II of PC. The colloidal gold particles (10 nm) are randomly distributed over immunoreactive (IR) profiles without preference toward membranous or cytoplasmic regions. GABA immunoreactivity occurs on small unmyelinated axons, on terminals which form synaptic contacts, and on some vesicle‐containing dendrites. The GABA‐IR terminals form symmetric (type II) contacts onto unlabeled somata and dendrites of various sizes, and onto other unlabeled axon terminals. The GABA‐IR terminal in axo‐axonic complexes is presynaptic to a round vesicle‐containing terminal, which itself may form a type I asymmetric contact onto an unlabeled dendrite or soma. A proportion of vesicle‐containing dendrites show GABA‐immunoreactivity and are postsynaptic to unlabeled terminals with round vesicles. Other, but far fewer, vesicle‐containing dendrites are GABA negative and postsynaptic to GABA‐IR terminals. In summary, the findings are consistent with the localization of GABA in intrinsic neurons, and may be associated with presynaptic and postsynaptic inhibition within nociceptive related pathways. © 1996 Wiley‐Liss, Inc.