Two swimming modes in Trachymedusae; bell kinematics and the role of giant axons

Although members of the Rhopalonematidae family (Cnidaria, Hydrozoa, Trachymedusae) are known to exhibit unusually powerful jet swimming in addition to their more normal slow swimming behaviour, for the most part reports are rare and anecdotal. Many species are found globally at depths of 600 - 2000 m and so observation and collection depends on using remotely operated submersible vehicles. With a combination of in-situ video footage and laboratory measurements, we have quantified kinematic aspects of this dual swimming motion and its electrophysiology. The species included are from two Rhopalonematidae clades; they are Colobonema sericeum, Pantachogon haeckeli, Crossota millsae and two species of Benthocodon. Comparison is made with Aglantha digitale, a species from a third Rhopalonematidae clade brought to the surface by natural water movement. We find that although all Rhopalonematidae appear to have two swimming modes there are marked differences in their neural anatomy, kinematics and physiology. Giant motor axons, known to conduct impulses during fast swimming in A. digitale, are absent from C. sericeum and P. haeckeli. Slow swimming is also different; in C. sericeum and its relatives it is driven by contractions restricted to the base of the bell. These behavioural differences are related to the position of the different clades on a ribosomal DNA-based phylogenetic tree. This finding allows us to pinpoint the phylogenetic branch point leading to the appearance of giant motor axons and escape swimming. They place the remarkable dual swimming behaviour of members of the Rhopalonematidae family into an evolutionary context.

Decreased excitability of motor axons contributes substantially to contraction fatigability during neuromuscular electrical stimulation

The present study was designed to: 1) determine the time course of changes in motor axon excitability during and after neuromuscular electrical stimulation (NMES), and 2) characterise the relationship between contraction fatigability, NMES frequency, and changes at the axon, neuromuscular junction, and muscle. Eight neurologically-intact participants attended three sessions. NMES was delivered over the common peroneal nerve at 20, 40, or 60 Hz for 8 min (0.3 s “on”, 0.7 s “off”). Threshold tracking was used to measure changes in axonal excitability. Supramaximal stimuli were used to assess neuromuscular transmission and force-generating capacity of the tibialis anterior muscle. Torque decreased 49 and 62% during 8 min of 40 and 60 Hz NMES, respectively. Maximal twitch torque decreased only during 60 Hz NMES. Motor axon excitability decreased by 14, 27, and 35% during 20, 40, and 60 Hz NMES, respectively. Excitability recovered to baseline immediately (20 Hz), 2 min (40 Hz), and 4 min (60 Hz) following NMES. Overall, decreases in axonal excitability best predicted how torque declined over 8 min of NMES. During NMES, motor axons become less excitable and motor units “drop out” of the contraction, contributing substantially to contraction fatigability and its dependence on NMES frequency. NOVELTY BULLETS • The excitability of motor axons decreased during neuromuscular electrical stimulation (NMES) in a frequency-dependent manner. • As excitability decreased, axons failed to reach threshold and motor units dropped out of the contraction. • Overall, decreased excitability best predicted how torque declined and thus is a key contributor to fatigability during NMES.

Aberrant early growth of individual trigeminal sensory and motor axons in a series of mouse genetic models of 22q11.2 deletion syndrome

We identified divergent modes of initial axon growth that prefigure disrupted differentiation of the trigeminal nerve (CN V), a cranial nerve essential for suckling, feeding and swallowing (S/F/S), a key innate behavior compromised in multiple genetic developmental disorders including DiGeorge/22q11.2 Deletion Syndrome (22q11.2 DS). We combined rapid in vivo labeling of single CN V axons in LgDel+/− mouse embryos, a genomically accurate 22q11.2DS model, and 3D imaging to identify and quantify phenotypes that could not be resolved using existing methods. We assessed these phenotypes in three 22q11.2-related genotypes to determine whether individual CN V motor and sensory axons wander, branch and sprout aberrantly in register with altered anterior–posterior hindbrain patterning and gross morphological disruption of CN V seen in LgDel+/−. In the additional 22q11.2-related genotypes: Tbx1+/−, Ranbp1−/−, Ranbp1+/− and LgDel+/−:Raldh2+/−; axon phenotypes are seen when hindbrain patterning and CN V gross morphology is altered, but not when it is normal or restored toward WT. This disordered growth of CN V sensory and motor axons, whose appropriate targeting is critical for optimal S/F/S, may be an early, critical determinant of imprecise innervation leading to inefficient oropharyngeal function associated with 22q11.2 deletion from birth onward.