POSTEMBEDDING IMMUNOGOLD LABELING OF GAMMA-AMINOBUTYRIC-ACID IN LAMINA-II OF THE SPINAL TRIGEMINAL SUBNUCLEUS PARS-CAUDALIS .1. A QUALITATIVE STUDY

Citation
Jr. Almond et al., POSTEMBEDDING IMMUNOGOLD LABELING OF GAMMA-AMINOBUTYRIC-ACID IN LAMINA-II OF THE SPINAL TRIGEMINAL SUBNUCLEUS PARS-CAUDALIS .1. A QUALITATIVE STUDY, Synapse, 24(1), 1996, pp. 39-47
Citations number
55
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
08874476
Volume
24
Issue
1
Year of publication
1996
Pages
39 - 47
Database
ISI
SICI code
0887-4476(1996)24:1<39:PILOGI>2.0.ZU;2-V
Abstract
This study examines the normal synaptic organization of the feline spi nal trigeminal nucleus pars caudalis (PC). A primary goal of this stud y is to identify and characterize the synaptic complexes within PC bas ed on their specific neurotransmitter content. Post-embedding immunogo ld techniques are utilized with electron microscopy to determine the u ltrastructural localization of gamma-aminobutyric acid (GABA) immunore activity within lamina II of PC. The colloidal gold particles (10 nm) are randomly distributed over immunoreactive (IR) profiles without pre ference toward membranous or cytoplasmic regions. GABA immunoreactivit y occurs on small unmyelinated axons, on terminals which form synaptic contacts, and on some vesicle-containing dendrites. The GABA-IR termi nals form symmetric (type II) contacts onto unlabeled somata and dendr ites of-various sizes, and onto other unlabeled axon terminals. The GA BA-IR terminal in axo-axonic complexes is presynaptic to a round vesic le-containing terminal, which itself may form a type I asymmetric cont act onto an unlabeled dendrite or soma. A proportion of vesicle-contai ning dendrites show GABA-immunoreactivity and are postsynaptic to unla beled terminals with round vesicles. Other, but far fewer, vesicle-con taining dendrites are GABA negative and postsynaptic to GABA-IR termin als. 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. (C) 1996 Wiley-Liss, Inc.