Relationship between postsynaptic NK1 receptor distribution and nerve terminals innervating myenteric neurons in the guinea‐pig ileum
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posted on 2024-08-23, 01:26 authored by AL Portbury, I Grkovic, HM Young, John FurnessJohn FurnessAbstractThe amounts of neurokinin 1 (NK1) receptor immunolabelling on the membranes of myenteric cell bodies at appositions with tachykinin‐immunoreactive nerve terminals, other nerve terminals, and glial cells were compared at the ultrastructural level using pre‐embedding, double‐label immunocytochemistry. NK1 receptor immunoreactivity was revealed using silver‐intensified, 1 nm gold, and tachykinin‐immunoreactive nerve terminals were revealed using diaminobenzidine. The density of NK1 receptor immunolabelling (silver particles per length of cell membrane) on the membrane at appositions with tachykinin‐immunoreactive nerve terminals was not significantly different from that at appositions with other (nonimmunoreactive) nerve terminals or with glial cells. Synaptic specializations (“active zones”) were present at a small proportion of the appositions between NK1 receptor‐immunoreactive cell bodies and tachykinin‐immunoreactive or other nerve terminals. The density of NK1 receptor immunolabelling at synaptic specializations was lower than that at regions of appositions where no synaptic specializations were present. The presence of NK1 receptor on the cell surface in areas not directly apposed to tachykinin‐containing nerve terminals suggests that tachykinins that diffuse away from their site of release may still exert an action via NK1 receptors. Although NK1 receptors do not appear to be targetted to particular sites on the surfaces of myenteric nerve cell bodies and proximal dendrites, they are reduced in density at regions of the membrane‐forming synaptic specializations. Anat Rec 263:248–254, 2001. © 2001 Wiley‐Liss, Inc.
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Journal
The Anatomical RecordVolume
263Pagination
248-254Location
United StatesPublisher DOI
ISSN
0003-276XeISSN
1097-0185Language
enPublication classification
C1.1 Refereed article in a scholarly journalIssue
3Publisher
WileyPublication URL
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