L. Acsady et al., IMMUNOSTAINING FOR SUBSTANCE-P RECEPTOR LABELS GABAERGIC CELLS WITH DISTINCT TERMINATION PATTERNS IN THE HIPPOCAMPUS, Journal of comparative neurology, 378(3), 1997, pp. 320-336
A specific antiserum against substance P receptor (SPR) labels nonprin
cipal neurons in the cerebral cortex of the rat (T. Kaneko et al. [199
4], Neuroscience 60:199-211; Y. Nakaya et al. [1994], J. Comp. Neurol.
347:249-274). In the present study, we aimed to identify the types of
SPR-immunoreactive neurons in the hippocampus according to their cont
ent of neurochemical markers, which label interneuron populations with
distinct termination patterns. Markers for perisomatic inhibitory cel
ls, parvalbumin and cholecystokinin (CCK), colocalized with SPR in pyr
amidallike basket cells in the dentate gyrus and in large multipolar o
r bitufted cells within all hippocampal subfields respectively. A dens
e meshwork of SPR-immunoreactive spiny dendrites in the hilus and stra
tum lucidum of the CA3 region belonged largely to inhibitory cells ter
minating in the distal dendritic region of granule cells as indicated
by the somatostatin and neuropeptide Y (NPY) content. In addition, SPR
and NPY were colocalized in numerous multipolar interneurons with den
drites branching close to the soma. Twenty-five percent of the SPR-imm
unoreactive cells overlapped with calretinin-positive neurons in all h
ippocampal subfields, showing that interneurons specialized to contact
other gamma-aminobutyric acid-ergic cells may also contain SPR. On th
e basis of the known termination pattern of the colocalized markers, w
e conclude that SPR-positive interneurons are functionally heterogeneo
us and participate in different inhibitory processes: (1) perisomatic
inhibition of principal cells (CCK-containing cells, and parvalbumin-p
ositive cells in the dentate gyrus), (2) feedback dendritic inhibition
in the entorhinal termination zone (somatostatin and NPY-containing c
ells), and (3) innervation of other interneurons (calretinin-containin
g cells). (C) 1997 Wiley-Liss, Inc.