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Activation of multiple intracellular transduction signals by vasopressin in vasopressin-sensitive neurones of the rat supraoptic nucleus

Nancy Sabatier, Philippe Richard and Govindan Dayanithi

The intracellular mechanisms activated by the binding of vasopressin to its receptor(s) and which result in the increase of [Ca²⁺]_i were investigated in freshly dissociated supraoptic nucleus neurones. Various pharmacological agents were used to investigate the possible involvement of phospholipase C (PLC) and adenylate cyclase (AC) intracellular pathways in the transduction of the vasopressin action.

Both the PLC inhibitor U-73122 and the protein kinase C (PKC) inhibitor calphostin C, reduced the [Ca²⁺]_i rise elicited by vasopressin. The cAMP analogue, 8-Br-cAMP produced an increase in [Ca²⁺]_i and IBMX, a phosphodiesterase inhibitor, potentiated the response to vasopressin.

After pre-incubation with the AC inhibitor SQ-22536, 7 out of 18 vasopressin-sensitive neurones showed no inhibition of the vasopressin response, while the response to vasopressin was reduced by greater than 35 % in each of the other 11 neurones.

The activation of protein kinase A (PKA) with Sp-cAMPS caused an increase in [Ca²⁺]_i which was additive to the vasopressin-elicited [Ca²⁺]_i increase. After incubation with the PKA inhibitors Rp-cAMPS or H-89, the [Ca²⁺]_i responses triggered by Sp-cAMPS and vasopressin were, respectively, abolished and greatly reduced.

A combined administration of SQ-22536 (AC inhibitor) followed by U-73122 (PLC inhibitor), or U-73122 followed by H-89 (PKA inhibitor), virtually abolished the response to vasopressin.

In vasopressin-responsive neurones, the pituitary adenylate cyclase-activating polypeptide (PACAP) induced a [Ca²⁺]_i increase similar to the response to vasopressin and in both cases the increase was inhibited to the same extent by a combination of U-73122 and Rp-cAMPS.

In conclusion, we suggest that the autoregulation exerted specifically by vasopressin on vasopressin-sensitive neurones involves the activation of both PLC- and AC-linked pathways.

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