Electrophysiological events during neuroeffector transmission in the spleen of XXXX and @entity35 .

@entity10969 @entity706 @entity3159 @entity840 @entity9006 @entity2922 @entity35 @entity669 @entity5747
Intracellular recordings were made from smooth muscle cells of arterioles and the capsule of the spleen of @entity840 and @entity35 , and the responses to periarterial or subcapsular nerve stimulation were recorded. The innervation of the spleen was studied using fluorescence and immunohistochemical techniques. @entity2922 -containing axons were associated with smooth muscle of the splenic capsule, trabeculae, arterioles and amongst cells of the periarteriolar @entity706 . Axons immunoreactive for @entity10969 (NPY) and @entity669 hydroxylase were distributed in an identical manner to @entity2922 -containing axons, whereas axons immunoreactive for substance P or calcitonin gene-related peptide were present at a very low density in spleens from both species. In segments of arterioles, single transmural stimuli evoked excitatory junction potentials (EJPs) of 1-10 mV amplitude. EJPs facilitated during short trains of stimuli (1-10 Hz) and summated at 10 Hz, often initiating a muscle action potential. EJPs persisted in the presence of @entity3159 (1 microM) and @entity9006 (1 microM), but were abolished by the P2x-purinoceptor antagonist @entity5747 (1 mM). Spontaneous depolarizations were observed in smooth muscle cells of arterioles and capsule. Some events in arterioles were observed in the presence of @entity5747 and so may originate postjunctionally independently of transmitter release. As single transmural stimuli failed to evoke a depolarization in capsular smooth muscle, spontaneous depolarizations in this tissue probably also arise postjunctionally. Short trains of high frequency stimuli (10-35 Hz) evoked biphasic depolarizations of capsular smooth muscle cells. The initial component peaked 2.5 s following the onset of stimulation; the second component peaked 15 s following the onset and decayed exponentially with a time constant of 15 s. By fitting a product of exponentials to the second component, it was possible to define the initial component, which decayed with a time constant of around 1.5 s. Neurally evoked depolarizations of capsular smooth muscle were abolished by 1 microM TTX. Blockade of alpha 1-adrenoceptors with @entity3159 reduced the initial component of the depolarization, whereas alpha 2-adrenoceptor blockade with @entity9006 virtually abolished the second component. In some cells a small, faster depolarization persisted after alpha-adrenoceptor blockade. The slow alpha 2-adrenoceptor-mediated depolarization was identical to that recorded in the @entity35 tail artery and in the @entity840 mesenteric vein. The data indicate that sympathetic neuroeffector transmission from noradrenergic axons containing NPY to splenic arterial and capsular smooth muscle occur by different mechanisms.
