Actions of @entity1812 on electrical and synaptic behavior of neurones in the myenteric plexus of XXXX small intestine.

@entity5230 @entity1421 @entity840 @entity19616 @entity2918 @entity842 @entity750 @entity1812 @entity934
1. Electrophysiologic methods were used to study actions of @entity1812 (BK) in neurones of the myenteric plexus of @entity840 small intestine in vitro. Exposure to BK depolarized the membrane potential and elevated excitability in AH- and S-type neurones. Neuronal input resistance associated with the depolarizing responses was either decreased or unchanged in S-type and increased in AH-type neurones. 2. The selective B(2) BK receptor antagonist @entity19616 , but not the selective B(1) receptor antagonist des-arg(10)- @entity19616 , suppressed the BK-evoked responses. RT-PCR confirmed the expression of B(2) receptor mRNA, but not B(1) receptor mRNA. 3. Binding of fluorescently- labeled @entity19616 (HOE741) was localized to ganglion cells in whole-mount preparations. BK B(2) receptors were coexpressed with immunoreactivity for calbindin or @entity842 synthase. 4. Exposure to BK suppressed the amplitude of both fast and slow excitatory postsynaptic potentials. Depolarizing responses evoked by application of @entity750 or substance P and nicotinic responses to @entity934 were not reduced by BK. This suggested that BK action on neurotransmission was presynaptic suppression of neurotransmitter release. Presence of @entity19616 in the bathing solution suppressed or abolished the presynaptic inhibitory action of BK. 5. The cyclooxygenase inhibitor, @entity5230 , suppressed both the direct excitatory action of BK and its presynaptic inhibitory action. Application of @entity1421 , D(2), F(2alpha) or I(2) mimicked the BK-evoked responses. 6. The results suggest that BK acts at B(2) BK receptors on myenteric neurones to stimulate the formation of @entity2918 . Once formed and released, the prostaglandins act to elevate the excitability of ganglion cells in the myenteric plexus and to suppress the synaptic release of neurotransmitters.
