RT Journal Article
SR Electronic
T1 Lack of cross-desensitization of somatostatin-14 and somatostatin-28 receptors coupled to potassium channels in rat neocortical neurons.
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 357
OP 361
VO 38
IS 3
A1 H L Wang
A1 M Dichter
A1 T Reisine
YR 1990
UL http://molpharm.aspetjournals.org/content/38/3/357.abstract
AB The effects of somatostatin-14 (SOM-14) and somatostatin-28 (SOM-28) on the delayed rectifier K+ current (IK) in rat neocortical neurons in culture were measured by using whole-cell patch clamp techniques. SOM-14 stimulated IK in a reversible manner. Continuous application of SOM-14 to the neocortical neurons led to a gradual desensitization of the SOM-14 response. Many cells became completely densensitized to SOM-14. SOM-28 also modulated IK in neocortical cells. However, SOM-28 reduced IK. This response was also reversible. Continuous application of SOM-28 to neocortical neurons led to a desensitization of the SOM-28 inhibition of IK. Many of the neurons that responded to SOM-28 became completely refractory to the peptide following prolonged SOM-28 pretreatment. While most neocortical neurons responded either to SOM-14 or to SOM-28, a population of neurons responded to both peptides. Chronic application of SOM-14 to these neurons completely desensitized the SOM-14 stimulation of IK but did not affect SOM-28 inhibition of this potassium current. Similarly, complete desensitization of SOM-28 responses in these cells was not associated with a modification of SOM-14 stimulation of IK. The lack of cross-desensitization between SOM-14 and SOM-28 induced responses suggests that these peptides act through different receptors to regulate IK.