Immune complex deposits have been found in the choroid plexus in patients with systemic lupus erythematosus, and it can be assumed that an immune complex injury to the choroid plexus might be related to the neuropsychiatric disorder seen in patients with SLE. Acute serum sickness was experimentally induced in rabbits by intravenous injection of crystalized BSA. Prednisolone in conventionl dosage was administered to study the immunologic injury of the choroid plexus as well as the mechanisms involved in the prednisolone effect. Light, electron microscopic and immunofluorescent studies were made. The host immunoglobulins(IgG, IgA, IgM) and beta 1 C globulin were demonstrated in the choroid plexus. Histopathological findings included mild to moderate interstitial and perivascular lymphocyte and plasma cell infiltrations and edema. Control animals showed no immune deposits and no histopathologic changes. Electron microscopic findings comparing the immunofluorescent and histopathologic changes were minimal, and showed sparse, vague electron dense deposits particularly in the interstitial spaces, knob-like focal thickening of vascular basement membrane, swelling of endothelial cells, and some accentuation of interstitial cells. The morphologic and functional similarities of the choroid plexus and glomerular basement membrane, the findings in morphologic, electron microscopic and immunofluorescent examinations of the experimental rabbits, along with the observed effects of prednisolone, together with similar reports in the recent literature suggest that immunologic injury of the choroid plexus could be considered as a new disease entity. This immunologic injury might play a significant role in neuropsychiatric disorders in the long standing immune complex deposit diseases. The very interesting finding is the nature and function of the interstitial cell between the endothelial (vascular) and epithelial side basement membranes, and speculation as to whether or not the role of this interstitial cell in choroid plexus injury may be in its possible analogy with glomerular mesangial cells.
Acute Disease ; Animal ; Choroid Plexus/drug effects ; Choroid Plexus/immunology* ; Choroid Plexus/pathology ; Lupus Erythematosus, Systemic/etiology ; Prednisolone/pharmacology* ; Rabbits ; Serum Sickness/chemically induced ; Serum Sickness/complications* ; Serum Sickness/immunology

OBJECTIVETo explore the effects of acrylamide on the permeability of blood cerebrospinal fluid barrier (BCB) and tight junction protein ZO-1 of choroid plexus in rats and to provide a theoretical basis for explaining the mechanism of nerve injury induced by acrylamide.

METHODSThirty two male Sprague-Dawley rats were randomly divided into ACR and control groups. ACR group was exposed to 20 mg/kg ACR daily for 5 days a week by intraperitoneal injection (i.p.) for 4 weeks. Control group was exposed to normal saline. The neurobehavioral tests (including sensatory and motor functions) were performed every week. At the end of exposure, Evan blue (EB) and Sodium fluorescein (NaFI) content in rat CSF were detected for determining the BCB permeability, Real-time PCR was used to measure the expression levels of ZO-1 mRNA in the epithelium cells of choroid plexus, and laser scanning confocal microscope (LSCM) was utilized to observe the distribution of ZO-1 protein.

RESULTSNeurobehavioral tests showed that the tail-flick latencies of ACR group were 27.77% and 53.71% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). The hind lamb splay distances of ACR group were 131.76% and 153.77% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). Evan blue (EB) and Sodium fluorescein (NaFI) content of ACR group were significantly higher than those of control group (P < 0.05). In the 4th week, the expression level of ZO-1 mRNA in ACR group was 0.21 +/- 0.07, which was significantly lower than that (0.31 +/- 0.11) in control group (P < 0.05). In the 4th week, the ZO-1 protein expression level of choroid plexus in ACR group was significantly lower than that in control group (P < 0.05).

CONCLUSIONAcrylamide could increased the BCB permeability of rats, which may be involved in the central nervous injury induced by ACR.

Acrylamide ; toxicity ; Animals ; Blood-Brain Barrier ; drug effects ; Choroid Plexus ; metabolism ; Male ; Permeability ; drug effects ; Rats ; Rats, Sprague-Dawley ; Zonula Occludens-1 Protein ; metabolism

OBJECTIVETo investigate the effects of lead exposure on the copper concentration in the brain and serum and the expression of copper transporters in the choroid plexus among rats.

METHODSSixty specific pathogen-free Sprague-Dawley rats were randomly divided into a control group and three lead-exposed groups, with 8 mice in each group. The lead-exposed groups were orally administrated with 500 (low-dose group)), 1 000 (middle-dose group), and 2 000 mg/L (high-dose group) lead acetate in drinking water for eight weeks. And the rats in control group were given 2 000 mg/L sodium acetate in drinking water. The content of lead and copper in the serum, hippocampus, cortex, choroid plexus, bones, and cerebrospinal fluid (CSF) was determined by inductively coupled plasma-mass spectrometry (ICP-MS). Confocal and real-time PCR methods were applied to measure the expression of copper transporters including copper transporter 1 (Ctr1), antioxidant protein 1 (ATX1), and Cu ATPase (ATP7A).

RESULTSCompared with the control group, the lead-exposed groups showed significantly higher lead concentrations in the serum, cortex, hippocampus, choroid plexus, CSF, and bones (P < 0.05) and significantly higher copper concentrations in the CSF, choroid plexus, serum, and hippocampus (P < 0.05). Confocal images showed that Ctr1 protein was expressed in the cytoplasm and cell membrane of choroid plexus in control group. However, Ctr1 migrated to CSF surface microvilli after lead exposure. Ctr1 fluorescence intensity gradually increased with increasing dose of lead, except that the middle-dose group had a higher Ctr1 fluorescence intensity than the high-dose group. In addition, the middle- and high-dose groups showed a lower ATX1 fluorescence intensity compared with the control group. Real-time PCR data indicated that the three lead-exposed groups showed significantly higher mRNA levels of Ctr1 and ATP7A compared with the control group (P < 0.05).

CONCLUSIONCopper homeostasis in the choroid plexus is affected by lead exposure to induce copper homeostasis disorders in brain tissue, which may be one of the mechanisms of lead neurotoxicity.

Adenosine Triphosphatases ; Animals ; Brain ; Cation Transport Proteins ; drug effects ; Choroid Plexus ; drug effects ; metabolism ; Copper ; metabolism ; Homeostasis ; Organometallic Compounds ; toxicity ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley