Hippocampal corticotropin releasing hormone: pre- and postsynaptic location and release by stress.

Neuropeptides modulate neuronal function in hippocampus, but the organization of hippocampal sites of peptide release and actions is not fully understood. The stress-associated neuropeptide corticotropin releasing hormone (CRH) is expressed in inhibitory interneurons of rodent hippocampus, yet physiological and pharmacological data indicate that it excites pyramidal cells. Here we aimed to delineate the structural elements underlying the actions of CRH, and determine whether stress influenced hippocampal principal cells also via actions of this endogenous peptide. In hippocampal pyramidal cell layers, CRH was located exclusively in a subset of GABAergic somata, axons and boutons, whereas the principal receptor mediating the peptide's actions, CRH receptor 1 (CRF1), resided mainly on dendritic spines of pyramidal cells. Acute 'psychological' stress led to activation of principal neurons that expressed CRH receptors, as measured by rapid phosphorylation of the transcription factor cyclic AMP responsive element binding protein. This neuronal activation was abolished by selectively blocking the CRF1 receptor, suggesting that stress-evoked endogenous CRH release was involved in the activation of hippocampal principal cells.

Mechanism of lumen enlargement with direct stenting versus predilatation stenting: influence of remodelling and plaque characteristics assessed by volumetric intracoronary ultrasound.

OBJECTIVE: To compare the effects of arterial remodelling and plaque characteristics on the mechanisms of direct stenting and predilatation stenting. Direct stenting has become routine in some laboratories and differs technically from predilatation stenting. METHODS: Pre- and post-interventional volumetric intravascular ultrasound (IVUS) was undertaken in 30 patients with direct stenting and in 30 with predilatation stenting of non-calcified native coronary lesions, using the same stent design and stent length. Lumen, vessel (external elastic membrane (EEM)), and plaque (plaque + media) volumes were calculated. Remodelling was determined by comparing the EEM area at the centre of the lesion with the EEM areas at proximal and distal reference sites. Plaque eccentricity was defined as the thinnest plaque diameter to the thickest plaque diameter ratio. Plaque composition was characterised as soft, mixed, or dense. RESULTS: All volumetric IVUS changes were similar in the two groups. Pre-intervention remodelling remained uninfluenced after direct stenting, but was neutralised after predilatation stenting. Eccentric lesions responded to intervention by a greater luminal gain owing to greater vessel expansion in direct stenting. Plaque composition influenced luminal gain in direct stenting, the gain being greatest in the softest plaques; in predilatation stenting, luminal gain was equivalent but vessel expansion was greater for "dense" plaque and plaque reduction greater for "soft" plaque. CONCLUSIONS: In non-calcified lesions, the mechanisms of lumen enlargement after direct or predilatation stenting are significantly influenced by atherosclerotic remodelling, plaque eccentricity, and plaque composition.

Estrogen up-regulates estrogen receptor alpha and synaptophysin in slice cultures of rat hippocampus.

Previous studies have shown that estrogen application increases the density of synaptic input and the number of spines on CA1 pyramidal neurons. Here, we have investigated whether Schaffer collaterals to CA1 pyramidal cells are involved in this estrogen-induced synaptogenesis on CA1 pyramidal neurons. To this end, we studied estrogen-induced expression of both estrogen receptor (ER) subtypes (ERalpha and ERbeta) together with the presynaptic marker synaptophysin in the rat hippocampus. In tissue sections as well as in slice cultures mRNA expression of ERalpha, ERbeta and synaptophysin was higher in CA3 than in CA1, and mRNA expression and immunoreactivity for both ER subtypes were found in both principal cells and interneurons. By using quantitative image analysis we found stronger nuclear immunoreactivity for ERalpha in CA3 than in CA1. In slice cultures, supplementation of the medium with 10(-8) M estradiol led to an increase of nuclear immunoreactivity for ERalpha, but not for ERbeta, which was accompanied by a dramatic up-regulation of synaptophysin immunoreactivity in stratum radiatum of CA1. Together these findings indicate that estrogen effects on hippocampal neurons are more pronounced in CA3 than in CA1 and that ER activation in CA3 neurons leads to an up-regulation of a presynaptic marker protein in the axons of these cells, the Schaffer collaterals. We conclude that estradiol-induced spine formation on CA1 pyramidal cells may be mediated presynaptically, very likely by activation of ERalpha in CA3 pyramidal cells, followed by an increase in Schaffer collateral synapses.

The course of the occipital artery--an anatomical investigation for biopsy in suspected vasculitis.

BACKGROUND: The occipital artery can show an inflammation in cranial arteritis. For biopsy it is essential to know the course of the occipital artery. METHODS: In 6 randomly selected specimens of the head, the occipital artery and vein were sought and examined. In addition, the topographical proximity of the greater occipital nerve was considered. COURSE: The occipital artery followed a tortuous course, including an occasional hairpin bend in four out of 6 specimens. Lateral distance of the occipital artery from the external occipital protuberance of the occiput: The occipital artery runs at a mean distance of 3.92 cm on the right side and 4.4 cm on the left side from the midline. Variations of the course: A comparison between the right and left side showed a marked side-difference in the course of the vessel. The extent of tortuosity varied distinctly. In most of the arteries, the angle between superior nuchal line and occipital artery was 90 degrees. External diameter: The average external diameter of the occipital artery (in the area where it crosses with the superior nuchal line) was 2.3 mm on the right side and 2.7 mm on the left side. CONCLUSION: Because the greater occipital nerve enters the subcutis below the external protuberance of the occiput and shortly afterwards crosses the occipital artery, we recommend to carry out the biopsy of the occipital artery between 1 to 3 cm above (cranially) and 4 to 5 cm lateral to the external protuberance.

The alvear pathway of the rat hippocampus.

Neurons of the entorhinal cortex project to the hippocampus proper and dentate gyrus. This projection is called the "perforant pathway" because it perforates the subiculum; current usage applies this term to all entorhino-hippocampal fibers. However, entorhinal fibers also reach Ammon's horn via the alveus ("alvear pathway"), an alternative route first described by Cajal. The anterograde tracer Phaseolus vulgaris leucoagglutinin (PHAL) was used in order to analyze the contribution of this pathway to the temporo-ammonic projection. In the temporal portion of the rat hippocampus, most of the entorhinal fibers reach Ammon's horn after perforating the subiculum (classical perforant pathway). At more septal levels, the number of entorhinal fibers that take the alvear pathway increases; in the septal portion of the hippocampal formation, most of the entorhinal fibers to hippocampal subfield CA1 reach this subfield via the alveus. These fibers make sharp right-angle turns in the alveus, perforate the pyramidal cell layer, and finally terminate in the stratum lacunosum-moleculare. The crossed temporo-ammonic fibers reach their termination area in the stratum lacunosum-moleculare of CA1 almost exclusively via the alveus. These data indicate that the alveus is a major route by which entorhinal fibers reach their targets in CA1.

Organization of identified fiber tracts in the rat fimbria-fornix: an anterograde tracing and electron microscopic study.

The fimbria is a major route for afferent and efferent fibers of the hippocampal formation. However, little is known about the intrinsic organization of the fimbria-fornix complex. In this study, the anterograde tracer Phaseolus vulgaris-leucoagglutinin (PHAL) was used to analyze the ultrastructure and topography of identified fiber tracts within the fimbria-fornix. Septo-hippocampal fibers are loosely distributed throughout the fimbria-fornix. Commissural fibers cross the midline in the ventral hippocampal commissure and form a tight fiber bundle in the fimbria. Crossed entorhino-hippocampal fibers cross the midline in the ventral hippocampal commissure rostral to the commissural fiber bundle, and crossed entorhino-entorhinal fibers pass through the dorsal hippocampal commissure. This suggests a topographical organization of fiber tracts within the fimbria-fornix that reflects the laminar organization of the hippocampal target structure: fibers of the diffusely terminating septohippocampal projection are loosely distributed throughout the fimbria-fornix, while those projections that are known to terminate in specific laminae of the hippocampal formation (commissural projection, crossed entorhino-hippocampal projection) form fiber bundles within the fimbria and the ventral hippocampal commissure.