Three-dimensional organization of dendrites and local axon collaterals of shell and core medium-sized spiny projection neurons of the rat nucleus accumbens

Medium-sized spiny projection neurons (MSN) in the head of the primate caudate nucleus are thought to have preferred dendritic orientations that tend to parallel the orientations of the striosomes. Moreover, recurrent axon collaterals of MSN in the rat dorsal striatum have been categorized into two types, i.e., restricted and widespread. The nucleus accumbens (Acb) has a highly complex compartmental organization, and the spatial organization of dendritic and axonal arbors of MSN has not yet been systematically studied. In this study, using single-cell juxtacellular labeling with neurobiotin as well as anterograde neuroanatomical tracing with biotinylated dextran amine, we investigated the three-dimensional (3D) organization of dendrites and axons of MSN of the rat Acb in relation to subregional (shell-core) and compartmental (patch-matrix) boundaries. Our results show that dendritic arbors of MSN in both the Acb shell and core subregions are preferentially oriented, i.e., they are flattened in at least one of the 3D-planes. The preferred orientations are influenced by shell-core and patch-matrix boundaries, suggesting parallel and independent processing of information. Dendritic orientations of MSN of the Acb core are more heterogeneous than those of the shell and the dorsal striatum, suggesting a more complex distribution of striatal inputs within the core. Although dendrites respect the shell-core and patch-matrix boundaries, recurrent axon collaterals may cross these boundaries. Finally, different degrees of overlap between dendritic and axonal arborizations of individual MSN were identified, suggesting various possibilities of lateral inhibitory interactions within and between, functionally distinct territories of the Acb

Towards a monolithic optical cavity for atom detection and manipulation

We study a Fabry-Perot cavity formed from a ridge waveguide on a AlGaAs substrate. We experimentally determined the propagation losses in the waveguide at 780 nm, the wavelength of Rb atoms. We have also made a numerical and analytical estimate of the losses induced by the presence of the gap which would allow the interaction of cold atoms with the cavity field. We found that the intrinsic finesse of the gapped cavity can be on the order of F ~ 30, which, when one takes into account the losses due to mirror transmission, corresponds to a cooperativity parameter for our system C ~ 1

Protein kinase D at the Golgi controls NLRP3 inflammasome activation

The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein kinase D (PKD), a key effector of DAG. Upon PKD inactivation, self-oligomerized NLRP3 is retained at MAMs adjacent to Golgi, blocking assembly of the active inflammasome. Importantly, phosphorylation of NLRP3 by PKD at the Golgi is sufficient to release NLRP3 from MAMs, resulting in assembly of the active inflammasome. Moreover, PKD inhibition prevents inflammasome autoactivation in peripheral blood mononuclear cells from patients carrying NLRP3 mutations. Hence, Golgi-mediated PKD signaling is required and sufficient for NLRP3 inflammasome activation.PMC558412

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

International audienceUpregulation of extracellular chondroitin sulfate proteoglycans (CSPG) is a primary cause for the failure of axons to regenerate after spinal cord injury (SCI), and the beneficial effect of their degradation by chondroitinase ABC (ChABC) is widely documented. Little is known, however, about the effect of ChABC treatment on astrogliosis and revascularization, two important factors influencing axon regrowth. This was investigated in the present study. Immediately after a spinal cord hemisection at thoracic level 8-9, we injected ChABC intrathecally at the sacral level, repeated three times until 10 days post-injury. Our results show an effective cleavage of CSPG glycosaminoglycan chains and stimulation of axonal remodeling within the injury site, accompanied by an extended period of astrocyte remodeling (up to 4 weeks). Interestingly, ChABC treatment favored an orientation of astrocytic processes directed toward the injury, in close association with axons at the lesion entry zone, suggesting a correlation between axon and astrocyte remodeling. Further, during the first weeks post-injury, ChABC treatment affected the morphology of laminin-positive blood vessel basement membranes and vessel-independent laminin deposits: hypertrophied blood vessels with detached or duplicated basement membrane were more numerous than in lesioned untreated animals. In contrast, at later time points, laminin expression increased and became more directly associated with newly formed blood vessels, the size of which tended to be closer to that found in intact tissue. Our data reinforce the idea that ChABC injection in combination with other synergistic treatments is a promising therapeutic strategy for SCI repair

Chartings of the terminal fields from each cortical functional region, illustrating the collective diffuse projections superimposed on the focal terminal fields at four chosen AP levels: (a and b) rostral striatum (AP 26); (c–e) n

<p><b>Copyright information:</b></p><p>Taken from "Relationship between the corticostriatal terminals from areas 9 and 46, and those from area 8A, dorsal and rostral premotor cortex and area 24c: an anatomical substrate for cognition to action"</p><p></p><p>The European Journal of Neuroscience 2007;26(7):2005-2024.</p><p>Published online Jan 2007</p><p>PMCID:PMC2121143.</p><p>© The Authors (2007). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</p> Ac (AP 22); (f) AC (AP 18.5); and (g) caudal striatum (AP 10). Yellow, areas 9 and 46; orange, area 24b; white, area 8A-FEF; green, SEF, PMdr and 24c. In (a) and (d), orange is transparent to better illustrate the convergence between focal projections from area 24b with those from areas 9 and 46; in (d)– (e), yellow is transparent to better illustrate the convergence between focal projections from areas 9 and 46 with those from areas 8A-FEF, SEF, PMdr and 24c (the convergence area appears in green); in (c), (f) and (g), white is transparent. Note that diffuse projections from each cortical region distribute to a larger striatal area, extending the territory covered by the focal projections. Scale bar, 5 mm

3-D rendering of the combined focal projections from all the frontal regions, illustrating the overlap between corticostriatal projections

<p><b>Copyright information:</b></p><p>Taken from "Relationship between the corticostriatal terminals from areas 9 and 46, and those from area 8A, dorsal and rostral premotor cortex and area 24c: an anatomical substrate for cognition to action"</p><p></p><p>The European Journal of Neuroscience 2007;26(7):2005-2024.</p><p>Published online Jan 2007</p><p>PMCID:PMC2121143.</p><p>© The Authors (2007). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</p> The white lines in (a) the lateral view of the striatum indicate the level of sections illustrated in (b) and (c) (b and c) Coronal slices through the 3-D model with the corresponding Nissl section at the AP levels corresponding to (b) the rostral striatum (AP 26) and to (c) the n. Ac (AP 22). Note that the striatal sections shown in (b) and (c) have different magnifications. Black arrows indicate key striatal regions receiving convergent projections from areas 9 and 46, 8A-FEF, SEF, PMdr and 24c. Yellow dotted line, areas 9 and rostral 46; dark yellow, caudal area 46; white, area 8A-FEF; green, SEF; blue-green dotted line, PMdr; grey, 24c. Scale bars, 2 mm