A morphometric MRI study of the hippocampus in first-episode, neuroleptic-naïve schizophrenia.

Magnetic resonance imaging (MRI) studies have frequently, although not unambiguously, reported hippocampal volume deficit in schizophrenia. Data on the hippocampal volumes in first-episode schizophrenia, however, are sparse. In addition, a recent topographic MRI study proposed a regionally specific volume loss in the hippocampus of chronic schizophrenics, but to date no reports have replicated this finding. In this study two-dimensional MRI-based topographic brain mapping was used to study the possibility of regional changes in the hippocampus of 22 controls and 18 patients with first-episode, neuroleptic-naïve schizophrenia. Compared to controls, there were no significant differences between hippocampal volumes, regional volumes, or length of the hippocampus in the patients with schizophrenia. These data are at odds with the previous reports on hippocampal volume loss in first-episode schizophrenia, and with the hypothesis of regionally specific hippocampal volume deficit in schizophrenia.

Striatal dopamine transporter binding in neuroleptic-naive patients with schizophrenia studied with positron emission tomography.

OBJECTIVE: Recent in vivo imaging studies indicate a dysregulated presynaptic function of the striatal dopaminergic system in patients with schizophrenia. To further explore the basis of this phenomenon, the authors studied brain dopamine transporter binding in vivo in patients with first-episode, never-medicated schizophrenia. METHOD: Nine patients with schizophrenia and nine healthy matched comparison subjects were recruited. Striatal dopamine transporter binding was measured with positron emission tomography and a specific dopamine transporter ligand, [(18)F]CFT, a radiolabeled form of 2beta-carbomethoxy-3beta-(4-fluorophenyl)tropane. RESULTS: Average caudate and putamen dopamine transporter binding potentials were almost identical in the patients and comparison subjects, but the patients lacked the right-left asymmetry of the caudate dopamine transporter binding seen in the comparison group. CONCLUSIONS: Average striatal dopamine transporter density is unaltered in neuroleptic-naive patients with schizophrenia. However, patients lack asymmetry in caudate dopamine transporter binding, which conforms with disrupted brain lateralization in this disorder.

Effect of atropine on bile flow and biliary excretion of 3H-ouabain in the isolated perfused rat liver.

Effects of choleresis produced by atropine (4-10(-4)M) on the biliary elimination of 3H-ouabain and on the biliary clearance rate of 14C-erythritol were studied in the isolated perfused rat liver. The increased bile flow produced by atropine was associated with decreased level of 3H-ouabain in the bile. The cumulative biliary elimination of ouabain was not affected. Atropine choleresis caused an increase in the erythritol clearance rate and a reduction in the bile to plasma ratios of erythritol as compared to the controls. The results suggest that the choleresis induced by atropine is not entirely of canalicular origin but possibly reabsorption mechanisms in the bile ducts or ductules are also involved.

The effect of acetylcholine on biliary excretion of ouabain in the physostigmine pretreated isolated perfused rat liver.

The effect of acetylcholine (ACh) on bile flow and biliary excretion of 3H-ouabain was studied in the physostigmine pretreated isolated perfused rat liver. ACh added into the perfusion medium to give a concentration of 1 X 10(-4)M after the addition of physostigmine (2 X 1 X 10(-5)M) transiently decreased bile flow and biliary concentration of tritium, originated from 3H-ouabain. A deficit of 34 mul of bile during the decreased bile flow could be calculated, compared to the control group. This deficit in bile flow possibly reflects an inhibitory secretory effect of ACh on canalicular bile secretion, or enhanced reabsorption of water in the biliary tree. The decline in the concentration of 3H-oubain in the bile after the addition of ACh indicates that ACh inhibits biliary transport of ouabain by an unknown mechanism, in addition to its effect on bile flow. Physostigmine alone possibly was without an effect on biliary elimination of ouabain. The results show that ACh retards the biliary elimination of ouabain through its influence on bile flow and biliary concentraton of ouabain.

Effects of acetylcholine and atropine on the bile flow and biliary excretion of digoxin in the isolated perfused rat liver.

The effects of acetylcholine (ACh). physostigmine, and atropine on bile flow and biliary elimination of digoxin were investigated using isolated rat liver perfusion. 1. ACh in the presence of physostigmine caused a temporary reduction in the bile secretion, while physostigmine alone had no effect on the bile flow. 2. The biliary concentration of radioactivity derived from 3H-digoxin was slightly decreased after an addition of physostigmine alone. This effect of physostigmine was not potentiated by ACh. 3. The addition of ACh decreased transiently the biliary elimination of digoxin, as a result of the reduced bile flow. 4. Atropine in the concentration range of 10(-6)-10(-5) M in the perfusion medium did not affect bile flow or biliary excretion of digoxin; repeated addition of atropine (2 X 2 X 10(-4) M) caused a choleresis lasting over the perfusion period. 5. This choleresis induced by atropine was associated with decreased concentration of tritium in the bile but slightly increased biliary elimination of total radioactivity. 6. The results allow us to draw the conclusion that ACh in the presence of physostigmine has an inhibitory action on bile flow and biliary elimination of digoxin in the isolated perfused rat liver.