Epilepsy is a common neurological disorder characterized by hyperexcitability in the brain. Its pathogenesis is classically associated with an imbalance of excitatory and inhibitory neurons. Calretinin (CR) is one of the three major types of calcium-binding proteins present in inhibitory GABAergic neurons. The functions of CR and its role in neural excitability are still unknown. Recent data suggest that CR neurons have diverse neurotransmitters, morphologies, distributions, and functions in different brain regions across various species. Notably, CR neurons in the hippocampus, amygdala, neocortex, and thalamus are extremely susceptible to excitotoxicity in the epileptic brain, but the causal relationship is unknown. In this review, we focus on the heterogeneous functions of CR neurons in different brain regions and their relationship with neural excitability and epilepsy. Importantly, we provide perspectives on future investigations of the role of CR neurons in epilepsy.
Amygdala/metabolism* ; Calbindin 2/metabolism* ; Epilepsy ; GABAergic Neurons ; Hippocampus/metabolism* ; Humans

The circling mice with tmie gene mutation are known as an animal deafness model, which showed hyperactive circling movement. Recently, the reinvestigation of circling mouse was performed to check the inner ear pathology as a main lesion of early hearing loss. In this trial, the inner ear organs were not so damaged to cause the hearing deficit of circling (cir/cir) mouse at 18 postnatal day (P18) though auditory brainstem response data indicated hearing loss of cir/cir mice at P18. Thus, another mechanism may be correlated with the early hearing loss of cir/cir mice at P18. Hearing loss in the early life can disrupt the ascending and descending information to inferior colliculus (IC) as integration site. There were many reports that hearing loss could result in the changes in Ca²⁺ concentration by either cochlear ablation or genetic defect. However, little was known to be reported about the correlation between the pathology of IC and Ca²⁺ changes in circling mice. Therefore, the present study investigated the distribution of calcium-binding proteins (CaBPs), calbindin-D28k, parvalbumin, and calretinin immunoreactivity (IR) in the IC to compare among wild-type (+/+), heterozygous (+/cir), and homozygous (cir/cir) mice by immunohistochemistry. The decreases of CaBPs IR in cir/cir were statistically significant in the neurons as well as neuropil of IC. Thus, this study proposed overall distributional alteration of CaBPs IR in the IC caused by early hearing defect and might be helpful to elucidate the pathology of central auditory disorder related with Ca²⁺ metabolism.
Animals ; Calbindin 1* ; Calbindin 2* ; Calcium-Binding Proteins ; Deafness ; Ear, Inner ; Evoked Potentials, Auditory, Brain Stem ; Hearing ; Hearing Loss ; Immunohistochemistry ; Inferior Colliculi* ; Metabolism ; Mice* ; Neurons ; Neuropil ; Parvalbumins ; Pathology

OBJECTIVETo analyze the clinicopathologic and immunohistochemical features of nodular histiocytic/mesothelial hyperplasia (NHMH) and to improve the knowledge of this disease.

METHODSSeven cases of NHMH were collected and the clinicopathologic and immunohistochemical data were analyzed with review of the literature.

RESULTSSeven male patients aged from 1.5 to 5.0 years (mean 2.8). The main clinical symptom was an inguinal mass.Grossly, main pathological changes were the mural nodule or free nodule in lumen, with diameter of 0.1-0.5 cm.Histologically, the tumor cell morphology was relatively single, cohesive polygonal or oval cells which were arranged in solid sheets or nests, usually with ovoid or deeply grooved nuclei and a moderate amount of pale pink cytoplasm in the nodular collection area. The nuclei had delicate chromatin and no obvious atypia, and mitosis was incidentally found. A few scattered lymphocytes were found in the stroma. The cyst wall was lined by a single layer of mesothelial cells.Immunohistochemically, the most cells in nodular lesion were strongly positive for the histiocytic marker CD68, vimentin and α1-antichymotrypsin, while lining mesothelial cells on the wall were positive for calretinin, MC, WT1, CK5/6, CKpan and EMA.

CONCLUSIONSNHMH is a rare and benign tumor-like lesion, and easy to be misdiagnozed, which should be distinguished from neuroendocrine tumors, Langerhans cell histiocytosis, seminoma, mesothelioma and so on. The correct diagnosis of this lesion depends on the clinical characteristics, morphology and immunohistochemistry.

Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Calbindin 2 ; metabolism ; Child, Preschool ; Diagnosis, Differential ; Epithelium ; metabolism ; pathology ; surgery ; Histiocytes ; metabolism ; pathology ; Histiocytosis, Langerhans-Cell ; metabolism ; pathology ; Humans ; Hyperplasia ; metabolism ; pathology ; surgery ; Infant ; Leukocyte Common Antigens ; metabolism ; Male ; Mesothelioma ; metabolism ; pathology ; Mucin-1 ; metabolism ; Neuroendocrine Tumors ; metabolism ; pathology ; Seminoma ; metabolism ; pathology ; Vimentin ; metabolism ; WT1 Proteins ; metabolism ; alpha 1-Antichymotrypsin ; metabolism

OBJECTIVETo study the pathogenesis, pathologic features and prognosis of fetal nuchal cystic hygroma.

METHODSForty autopsied cases of fetal nuchal cystic hygroma were collected during January 2003 to December 2012. The clinical history, pathologic changes and immunohistochemical (EnVision method) findings were reviewed, and the pathogenesis and pathologic characteristics were analyzed.

RESULTSOf the 40 cases, 16 (40.0%) showed single malformation and 24 (60.0%) were associated with multiple malformations in other organs and/or systems.Nineteen cases were septated and 21 were not. The associated malformations occurred in the respiratory system, skeletal system and urinary system.In the cases of combined malformations of umbilical cord, 3 were single umbilical artery malformations and 1 was torsion and stricture of umbilical cord.Four cases had chromosomal analysis, and all were trisomy-21.

CONCLUSIONSFetal nuchal cystic hygroma is a rare disease. The etiology is unknown, but it is not neoplastic.Lymphangioma is divided into 3 types:capillary lymphangioma, cavernous lymphangioma and cystic hygroma according to their expansile growth pattern. The overall prognosis is determined by any co-existing chromosomal anomalies, associated malformations and the time of diagnosis of the cystic hygroma.

Antibodies, Monoclonal, Murine-Derived ; metabolism ; Autopsy ; Calbindin 2 ; metabolism ; Female ; Fetus ; pathology ; Humans ; Hydrops Fetalis ; metabolism ; pathology ; Lymphangioma, Cystic ; metabolism ; pathology ; Male ; Pregnancy ; Pregnancy Outcome

Calbindin 2 ; metabolism ; Colon ; metabolism ; Hirschsprung Disease ; metabolism ; Humans

Acetylcholinesterase ; analysis ; Antibodies, Monoclonal, Murine-Derived ; metabolism ; Australia ; Biopsy ; Calbindin 2 ; analysis ; Child ; Diagnosis, Differential ; Endoscopy, Gastrointestinal ; Eosinophilic Esophagitis ; pathology ; Hirschsprung Disease ; metabolism ; pathology ; Humans ; Intestinal Diseases ; pathology ; Lymphangiectasis, Intestinal ; immunology ; pathology ; Multiple Endocrine Neoplasia Type 2b ; pathology ; Nervous System Diseases ; pathology ; Quality Control

The α2A adrenoceptors (α2A-ARs) are the most common adrenergic receptor subtype found in the prefrontal cortex (PFC). It is generally accepted that stimulation of postsynaptic α2A-ARs on pyramidal neurons are key to PFC functions, such as working memory. However, the expression of α2A-ARs in interneurons is largely unknown. In the present study using double-labeling immunofluorencence technique, we investigated the expression of α2A-ARs in major types of rat PFC interneurons expressing calcium-binding proteins parvalbumin (PV), calretinin (CR), and calbindin (CB). Our data demonstrated that α2A-ARs are highly expressed in calcium-binding protein immunoreactive interneurons of rat PFC, suggesting that stimulation of α2A-ARs may alter neural networks comprising pyramidal neurons and interneurons, thereby exerting a beneficial effect on PFC cognitive functions. The present study provides the morphological basis for a potential mechanism by which stimulation of α2A-ARs induces cognitive improvement.
Animals ; Calbindin 2 ; metabolism ; Calbindins ; metabolism ; Interneurons ; metabolism ; Parvalbumins ; metabolism ; Prefrontal Cortex ; cytology ; Rats ; Receptors, Adrenergic, alpha-2 ; metabolism

Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Calbindin 2 ; metabolism ; Cholecystitis ; pathology ; Cisplatin ; administration & dosage ; Cystitis ; pathology ; Diagnosis, Differential ; Female ; Glutamates ; administration & dosage ; Guanine ; administration & dosage ; analogs & derivatives ; Humans ; Inflammation ; pathology ; Keratins ; metabolism ; Lung Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; Male ; Mesothelioma ; drug therapy ; metabolism ; pathology ; surgery ; Middle Aged ; Pemetrexed ; Peritoneal Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; Survival Rate ; Vimentin ; metabolism

Calbindin 2 ; metabolism ; Heart Neoplasms ; metabolism ; pathology ; surgery ; Humans ; Male ; Middle Aged ; MyoD Protein ; metabolism ; Myogenin ; metabolism ; Rhabdomyosarcoma, Embryonal ; metabolism ; pathology ; surgery

Adenocarcinoma ; pathology ; Adenomatoid Tumor ; metabolism ; pathology ; surgery ; Adenomyoma ; pathology ; Adult ; Antibodies, Monoclonal, Murine-Derived ; metabolism ; Biomarkers, Tumor ; metabolism ; Calbindin 2 ; metabolism ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Keratins ; metabolism ; Leiomyoma ; pathology ; Lymphatic Vessel Tumors ; metabolism ; pathology ; Middle Aged ; Uterine Neoplasms ; metabolism ; pathology ; surgery ; Young Adult