Apoptosis and proliferation in the trigeminal placode

The neurogenic trigeminal placode develops from the crescent-shaped panplacodal primordium which delineates the neural plate anteriorly. We show that, in Tupaia belangeri, the trigeminal placode is represented by a field of focal ectodermal thickenings which over time changes positions from as far rostral as the level of the forebrain to as far caudal as opposite rhombomere 3. Delamination proceeds rostrocaudally from the ectoderm adjacent to the rostral midbrain, and contributes neurons to the trigeminal ganglion as well as to the ciliary ganglion/oculomotor complex. Proliferative events are centered on the field prior to the peak of delamination. They are preceded, paralleled and, finally, outnumbered by apoptotic events which proceed rostrocaudally from non-delaminating to delaminating parts of the field. Apoptosis persists upon regression of the placode, thereby exhibiting a massive “wedge” of apoptotic cells which includes the postulated position of the “ventrolateral postoptic placode” (Lee et al. in Dev Biol 263:176–190, 2003), merges with groups of lens-associated apoptotic cells, and disappears upon lens detachment. In conjunction with earlier work (Washausen et al. in Dev Biol 278:86–102, 2005) our findings suggest that apoptosis contributes repeatedly to the disintegration of the panplacodal primordium, to the elimination of subsets of premigratory placodal neuroblasts, and to the regression of placodes

Vegetation and climate changes around the Lama Lake, Taymyr Peninsula during the Late Pleistocene and Holocene reconstructed from pollen records

A continuous lacustrine sequence from the western part of Lama Lake (69°32'N, 90°12'E),completed by a peat sequence from the lake catchment provides the first detailed environmentalreconstruction for the Late Glacial and Holocene on the Taymyr Peninsula. Scarce steppe-likecommunities with Artemisia, Poaceae, and Cyperaceae dominated during the Late Glacial. Tundra-like communities with Betula nana, Dryas, and Salix grew on more mesic sites. There are distinctclimatic signals, which may be correlated with the Bølling and Allerød warmings and Middle andYounger Dryas coolings. The Late Glacial/Preboreal transition, at about 10,000 14C yr BP, wascharacterized by changes from predominantly open herb communities to shrub tundra ones. Larchforest might have been established as early as 9700-9600 14C yr BP, whilst shrub alder came tothe area ca 9500-9400 14C yr BP, and spruce did not reach area before ca 9200 14C yr BP. Spruce-larch forests with shrub alder and tree birch dominated the vegetation around the Lama Lake fromca 9000 14C yr BP. Dwarf birch communities were also broadly distributed. Role of spruce in theforest gradually decreased after 4500 14C yr BP. Vegetation cover in the Lama Lake area becamesimilar to modern larch-spruce forest ca 2500 14C yr BP. A pollen-based biome reconstructionsupports a quantitative interpretation of the pollen spectra. Climate reconstructions obtained withinformation-statistical and plan-functional-type methods show very similar trends in reconstructedJuly temperature since ca 12,300 14C yr BP, while precipitation anomalies are less coherent,especially during the Late Glacial-Holocene transition

The vanilloid receptor TRPV1 is activated and sensitized by local anesthetics in rodent sensory neurons

Local anesthetics (LAs) block the generation and propagation of action potentials by interacting with specific sites of voltage-gated Na+ channels. LAs can also excite sensory neurons and be neurotoxic through mechanisms that are as yet undefined. Nonspecific cation channels of the transient receptor potential (TRP) channel family that are predominantly expressed by nociceptive sensory neurons render these neurons sensitive to a variety of insults. Here we demonstrated that the LA lidocaine activated TRP channel family receptors TRPV1 and, to a lesser extent, TRPA1 in rodent dorsal root ganglion sensory neurons as well as in HEK293t cells expressing TRPV1 or TRPA1. Lidocaine also induced a TRPV1-dependent release of calcitonin gene–related peptide (CGRP) from isolated skin and peripheral nerve. Lidocaine sensitivity of TRPV1 required segments of the putative vanilloid-binding domain within and adjacent to transmembrane domain 3, was diminished under phosphatidylinositol 4,5-bisphosphate depletion, and was abrogated by a point mutation at residue R701 in the proximal C-terminal TRP domain. These data identify TRPV1 and TRPA1 as putative key elements of LA-induced nociceptor excitation. This effect is sufficient to release CGRP, a key component of neurogenic inflammation, and warrants investigation into the role of TRPV1 and TRPA1 in LA-induced neurotoxicity