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Active Uptake of Substance P Carboxy‐Terminal Heptapeptide (5–11) into Rat Brain and Rabbit Spinal Cord Slices
Author(s) -
Nakata Yoshihiro,
Kusaka Yoshiko,
Yajima Haruaki,
Segawa Tomio
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb06323.x
Subject(s) - ouabain , substance p , spinal cord , chemistry , dinitrophenol , neurotransmitter , medicine , biochemistry , biology , sodium , neuropeptide , receptor , organic chemistry , neuroscience
We previously reported that nerve terminals and glial cells lack an active uptake system capable of terminating transmitter action of substance P (SP). In the present study, we demonstrated the existence of an active uptake system for SP carboxy‐terminal heptapeptide, (5–11)SP. When the slices from either rat brain or rabbit spinal cord were incubated with [ 3 H](5–11)SP, the uptake of (5–11)SP into slices was observed. The uptake system has the properties of an active transport mechanism: it is dependent on temperature and sensitive to hypoosmotic treatment and is inhibited by ouabain and dinitrophenol (DNP). In the brain, (5–11)SP was accumulated by means of a high‐affinity and a low‐affinity uptake system. The K m and the V max values for the high‐affinity system were 4.20 × 10 −8 m and 7.59 fmol/10 mg wet weight/min, respectively, whereas these values for the low‐affinity system were 1.00 × 10 −6 m and 100 fmol/10 mg wet weight/min, respectively. In the spinal cord, there was only one uptake system, with a K m value of 2.16 × 10 −7 m and V max value of 26.2 fmol/10 mg wet weight/min. These results suggest that when SP is released from nerve terminals, it is hydrolysed into (5–11)SP before or after acting as a neurotransmitter, which is in turn accumulated into nerve terminals. Therefore, the uptake system may represent a possible mechanism for the inactivation of SP.