Simulation and Analysis of Microspines Interlocking Behavior on Rocky Surfaces: An In-Depth Study of the Isolated Spine

Microspine grippers address a large variety of possible applications, especially in field robotics and manipulation in extreme environments. Predicting and modeling the gripper behavior remains a major challenge to this day. One of the most complex aspects of these predictions is how to model the spine to rock interaction of the spine tip with the local asperity. This paper proposes a single spine model, in order to fill the gap of knowledge in this specific field. A new model for the anchoring resistance of a single spine is proposed and discussed. The model is then applied to a simulation campaign. With the aid of simulations and analytic functions, we correlated performance characteristics of a spine with a set of quantitative, macroscopic variables related to the spine, the substrate and its usage. Eventually, this paper presents some experimental comparison tests and discusses traversal phenomena observed during the tests.

Altered dendritic spine function and integration in a mouse model of fragile X syndrome

Cellular and circuit hyperexcitability are core features of fragile X syndrome and related autism spectrum disorder models. However, the cellular and synaptic bases of this hyperexcitability have proved elusive. We report in a mouse model of fragile X syndrome, glutamate uncaging onto individual dendritic spines yields stronger single-spine excitation than wild-type, with more silent spines. Furthermore, fewer spines are required to trigger an action potential with near-simultaneous uncaging at multiple spines. This is, in part, from increased dendritic gain due to increased intrinsic excitability, resulting from reduced hyperpolarization-activated currents, and increased NMDA receptor signaling. Using super-resolution microscopy we detect no change in dendritic spine morphology, indicating no structure-function relationship at this age. However, ultrastructural analysis shows a 3-fold increase in multiply-innervated spines, accounting for the increased single-spine glutamate currents. Thus, loss of FMRP causes abnormal synaptogenesis, leading to large numbers of poly-synaptic spines despite normal spine morphology, thus explaining the synaptic perturbations underlying circuit hyperexcitability.

Rhinogobius maculagenys, A new species of freshwater goby (Teleostei: Gobiidae) from Hunan, China

A new freshwater goby, Rhinogobius maculagenys sp. nov., was collected from Hunan Province in Southern China. This species can be distinguished from all congeners by a combination of the following features: first dorsal fin with 6 spines; second dorsal fin with a single spine and 7–9 segmented rays; anal fin with a single spine and 6–8 segmented rays; pectoral fin with 16 segmented rays; 32–34 longitudinal scales; 9–13 transverse scales; 11+16=27 vertebrae; pore ω1 missing; head and body yellowish brown; cheek and opercle yellowish brown with over 30 small orange spots, branchiostegal membrane yellow with over 10 small orange spots in males and white and spotless in females; first dorsal fin trapezoidal in males and nearly semicircular in females, with large bright blue blotch in front of second spine; spines 4 and 5 longest, rear tip extending to base of second branched ray of second dorsal fin in males when adpressed, but just reaching or not reaching anterior margin of second dorsal fin in females; caudal fin with 5–6 vertical rows of brown spots; flank with several longitudinal rows of blackish-brown spots; and belly pale white.

Altered dendritic spine function and integration in a mouse model of Fragile X Syndrome

Cellular and circuit hyperexcitability are core features of Fragile X Syndrome and related autism spectrum disorder models. However, a synaptic basis for this hyperexcitability has proved elusive. We show in a mouse model of Fragile X Syndrome, glutamate uncaging onto individual dendritic spines yields stronger single-spine excitation than wild-type, with more silent spines. Furthermore, near-simultaneous uncaging at multiple spines revealed fewer spines are required to trigger an action potential. This arose, in part, from increased dendritic gain due to increased intrinsic excitability, resulting from reduced hyperpolarization-activated currents. Super-resolution microscopy revealed no change in dendritic spine morphology, pointing to an absence of a structure-function relationship. However, ultrastructural analysis revealed a 3-fold increase in multiply-innervated spines, accounting for the increased single-spine excitatory currents following glutamate uncaging. Thus, loss of FMRP causes abnormal synaptogenesis, leading to large numbers of poly-synaptic spines despite normal spine morphology, thus explaining the synaptic perturbations underlying circuit hyperexcitability.