[Human brain trypsin(ogen) 4-like (HT-4) immunoreactivity was localized in glial cells of human cerebral cortex and spinal cord. After a short post mortem delay (two hours), cortical and spinal cord regions were dissected, frozen or immersed into a fixative solution. Sections of 10 and 50 µm thickness were cut and immunostained by antibodies raised against recombinant human trypsin 4. HT-4-like immunoreactive glial cells and fibers were stained in the white matter, low to moderate levels of immunostaining were also observed in the matrix of the cerebral cortex and the spinal cord. To characterize HT-4-like immunopositive glial cells, alternate sections were immunostained for astrocytes and oligodendrocytes. HT-4 is present predominantly in astrocytes, but some of the oligodendrocytes and microglial cells may also contain this enzyme.]

[Background and purpose - Understanding the trafficking of G-protein-coupled receptors is of particular importance. In the central nervous system, although some Gprotein- coupled receptors were reported to internalize in vivo, little is known about their trafficking downstream of the endocytic event. Methods - The distribution of the major somatostatin receptor subtype, the sst2, was monitored in the hippocampus using immunofluorescence from 10 minutes to seven days after in vivo injection of the receptor agonist octreotide. Results - From 10 min to 3 h after agonist injection, intensity of receptor immunoreactivity gradually decreased in the molecular layer of dentate gyrus and in the strata oriens and radiatum of CA1. Concomitantly, in the granular and pyramidal layers, small spherical immunofluorescent particles became apparent in perikarya, shortly after agonist stimulation (i.e. 30 min, 60 min). After longer survival times (i.e. 3 h, 6 h, 24 h), immunolabeling was confined to larger, intensely-stained intracytoplasmic vesicles. From 48 h to 7 d after agonist injection, distribution and intensity of sst2 receptor immunoreactivity became similar to that of control animals. The sst2 receptor labeling extensively colocalized with TGN38 and syntaxin 6 after OCT injection. Colocalization with trans-Golgi markers was observed as soon as 1 h after OCT injection and still present 24 h after. By contrast, colocalization with the endoplasmic reticulum marker PDI and the cis-Golgi marker GM130 was never observed. Conclusions - Our results suggest that upon agonist stimulation, dendritic receptors are retrogradely transported to a trans-Golgi network domain enriched in the t-SNARE syntaxin-6 and TGN38 proteins before recycling.]

[3D reconstruction from electronmicroscopic (EM) serial sections substantially differs from modeling body parts by linking convoluted planes delivered by CT and NMR. Namely, variations both in relative X-Y position and rotation of the target elements between the adjacent images and also additional problems caused by deformed, deteriorated or missing sections can only be overruled by an aligning paradigm, which exploits all the pixel-level information, and results in an optimal fitting with selected precision. This paper presents a complex computer program called Optimal Alignment®, which performs the precise elaboration of X-Y shift and relative rotation of two consecutive images. The required searching process will be customized by setting four independent parameters which relate the span and density of the pixel-scanning basic process. Optimalization of fitting accuracy versus running time can be achieved by a rather short training period. The potential precision of Optimal Alignment based on complex algorythms is far superior to manual aligning of EM photographs with the eye-wrist-mouse facility. The resulted database of alignment orientation parameters can serve as an advanced source for the 3D reconstructing programs. Optimal Alignment® software tool (supported by Hungarian Space Office grant TP 138) will be demonstrated on a basal forebrain NPY+ axonal reconstruction, performed in L. Záborszky’s laboratory (supported by NIH grant NSO23945).]

[While three decades ago, the co-existence of classical neurotransmitters and peptide neuromodulators in a single neuronal cell was considered to be rather exceptional, the phenomenon that neurons have a complex transmitter phenotype now appears to be the general rule. Parvicellular and magnocellular neurosecretory systems consist of neuronal cells which are specialized in secreting peptide neurohormones into the blood-stream to regulate hypophyseal functions. This mini-review, dedicated to the memory of Mariann Fodor, summarizes the current knowledge about the classical neurotransmitter content of different hypothalamic neurosecretory systems, with a special focus on the occurrence and putative functions of glutamate in parvicellular and magnocellular neurosecretory cells.]

[The unparalleled global rates of obesity and type 2 diabetes, together with the associated cardiovascular morbidity and mortality, are referred to as the "diabesity pandemic". Changes in lifestyle occurring worldwide, including the increased consumption of high-caloric foods and reduced exercise, are regarded as the main causal factors. Central obesity and insulin resistance have emerged as important linking components. Understanding the aetiology of the cluster of pathologies that leads to the increased risk is instrumental in the development of preventive and therapeutic strategies. Historically, skeletal muscle, adipose tissue and liver were regarded as key insulin target organs involved in insulinmediated regulation of peripheral carbohydrate, lipid and protein metabolism. The consequences of impaired insulin action in these organs were deemed to explain the functional and structural abnormalities associated with insulin resistance. The discovery of insulin receptors in the central nervous system, the detection of insulin in the cerebrospinal fluid after peripheral insulin administration and the well-documented effects of intracerebroventricularly injected insulin on energy homeostasis, have identified the brain as an important target for insulin action. In addition to its critical role as a peripheral signal integrating the complex network of hypothalamic neuropeptides and neurotransmitters that influence parameters of energy balance, central nervous insulin signalling is also implicated in the regulation of peripheral glucose metabolism. This review summarizes the evidence of insulin action in the brain as part of the multifaceted circuit involved in the central regulation of energy and glucose homeostasis, and discuss the role of impaired central nervous insulin signalling as a pathogenic factor in the obesity and type 2 diabetes epidemic.]