The choroid plexus is an important physiological barrier and produces CSF and neurotrophic, angiogenic, and inflammatory factors involved in brain development. Choroid plexus abnormalities have been implicated in both schizophrenia and bipolar disorder. A previous choroid plexus transcriptomic analysis of schizophrenia identified an upregulation of immune and inflammatory genes that correlated with peripheral inflammatory markers. The purpose of this study was to examine choroid plexus volume in probands across the psychosis spectrum and in their first-degree and axis II cluster A relatives, as well as choroid plexus familiality and choroid plexus covariance with clinical, cognitive, brain, and peripheral marker measures. Methods: Choroid plexus volume was quantified (using Free-Surfer) in psychosis probands, their first-degree and axis II cluster A relatives, and healthy control subjects, organized by DSM-IV-TR diagnosis. Analyte, structural connectivity, and genotype data were collected from a subset of study subjects.

The aim of this study was to determine the effect of varying concentrations of acetylcholine on the vasoconstriction of the perfused mesenteric arteries of the rat caused by stimulation of their sympathetic postganglionic nerves. Perfusion was carried out with a peristaltic pump, and the constriction caused by stimulation was measured by the rise of pressure in the cannula tied in the artery. Two effects were found. At rates of stimulation between 2 and 8/sec, acetylcholine added to the perfusion fluid in very low concentrations (50 pg/ml) caused an increase in the vasoconstriction. An increase was also caused by adding a concentration of 2 ng/ml for 15 seconds. If, however, this or a greater concentration was added for a longer time, it had the opposite effect and the vasoconstriction was greatly reduced or blocked. This reduction or block was not due in the main to a reduction or block of the vasoconstrictor action of norepinephrine. Block of response to stimulation was also produced by guanethidine. The block produced by acetylcholine resembled the block produced by guanethidine in two respects. The block was removed by raising the calcium concentration, and it was also removed by adding rf-amphetamine to the perfusion fluid. The block produced by a given concentration of acetylcholine was abolished by a much higher concentration of atropine or hyoscine.ADDITIONAL KEY WORDS autonomic control of mesenteric arteries cholinergic blockade of norepinephrine release d-amphetamine potentiation of perfusion pressure responses atropine calcium cocaine reversal of blockade • The block of sympathetic neurotransmission by acetylcholine was first observed by Briicke (1) in the pilomotor muscles of the cat's tail. Coon and Rothman (2) confirmed

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