Biogenic amines regulate a variety of behaviors. Their functions are predominantly mediated through G-protein-coupled 7-transmembrane domain receptors (GPCR), 16 of which are predicted to exist in the genome sequence of the nematode Caenorhabditis elegans. We describe here the expression pattern of several of these aminergic receptors, including two serotonin receptors (ser-1 and ser-4), one tyramine receptor (ser-2), and two dopamine receptors (dop-1 and dop-2). Moreover, we describe distinct but partially overlapping expression patterns of different splice forms of the ser-2 tyramine receptor locus. We find that each of the aminergic receptor genes is expressed in restricted regions of the nervous system and that many of them reveal significant overlap with the expression of regulatory factors of the LIM homeobox (Lhx) gene family. We demonstrate that the expression of several of the biogenic amine receptors is abrogated in specific cell types in Lhx gene mutants, thus establishing a role for these Lhx genes in regulating aspects of neurotransmission. We extend these findings with other cell fate markers and show that the lim-4 Lhx gene is required for several but not all aspects of RID motor neuron differentiation and that the lim-6 Lhx gene is required for specific aspects of RIS interneuron differentiation. We also use aminergic receptor gfp reporter fusions as tools to visualize the anatomy of specific neurons in Lhx mutant backgrounds and find that the development of the elaborate dendritic branching pattern of the PVD harsh touch sensory neuron requires the mec-3 Lhx gene. Lastly, we analyze a mutant allele of the ser-2 tyramine receptor, a target of the ttx-3 Lhx gene in the AIY interneuron class. ser-2 mutants display none of the defects previously shown to be associated with loss of AIY function.

Caenorhabditis elegans feeds by rhythmically contracting its pharynx to ingest bacteria. The rate of pharyngeal contraction is increased by serotonin and suppressed by octopamine. Using an electrophysiological assay, we show that serotonin and octopamine regulate two additional aspects of pharyngeal behavior. Serotonin decreases the duration of the pharyngeal action potential and enhances activity of the pharyngeal M3 motor neurons. Gramine, a competitive serotonin antagonist, and octopamine have effects opposite to those of serotonin: gramine and octopamine increase action potential duration and suppress M3 activity. The effects of serotonin, gramine and octopamine on action potential duration are dependent on the pharyngeal motor neurons MC and M3. When the MC and M3 motor neurons are functionally defective, serotonin and octopamine do not regulate the action potential. Our data suggest that serotonin alters pharyngeal physiology to allow for rapid contraction-relaxation cycles. Reciprocal regulation of pharyngeal behavior by serotonin and octopamine provides a mechanism for adapting to the presence and absence of food, respectively.

Background Peripheral nerve damage resulting in pain, loss of sensation, or motor function may necessitate a reconstruction with a bridging material. The RANGER® Registry was designed to evaluate outcomes following nerve repair with processed nerve allograft (Avance® Nerve Graft; Axogen; Alachua, FL). Here we report on the results from the largest peripheral nerve registry to‐date. Methods This multicenter IRB‐approved registry study collected data from patients repaired with processed nerve allograft (PNA). Sites followed their own standard of care for patient treatment and follow‐up. Data were assessed for meaningful recovery, defined as ≥S3/M3 to remain consistent with previously published results, and comparisons were made to reference literature. Results The study included 385 subjects and 624 nerve repairs. Overall, 82% meaningful recovery (MR) was achieved across sensory, mixed, and motor nerve repairs up to gaps of 70 mm. No related adverse events were reported. There were no significant differences in MR across the nerve type, age, time‐to‐repair, and smoking status subgroups in the upper extremity ( p > .05). Significant differences were noted by the mechanism of injury subgroups between complex injures (74%) as compared to lacerations (85%) or neuroma resections (94%) ( p = .03) and by gap length between the <15 mm and 50–70 mm gap subgroups, 91 and 69% MR, respectively ( p = .01). Results were comparable to historical literature for nerve autograft and exceed that of conduit. Conclusions These findings provide clinical evidence to support the continued use of PNA up to 70 mm in sensory, mixed and motor nerve repair throughout the body and across a broad patient population.

High levels of posttraumatic stress disorder symptoms are common in the recovery period after pediatric orthopaedic trauma, even among patients with relatively minor injury. Children admitted to the hospital after injury are at higher risk for such symptoms.

PMCI is characterized by kinematic dysfunction of the proximal carpal row and is often associated with a painful ulnar catch-up "clunk" as the wrist moves from radial to ulnar deviation. Clinical and laboratory findings suggest that palmar midcarpal instability is caused by a functional loss of midcarpal constraints, primarily the dorsal radiocarpal (dorsal radiocarpal) ligament and the ulnar arm of the palmar arcuate ligament, which permits hypermobility of the proximal carpal row.Management of PMCI should always begin with a trial of non-operative management. This includes the use of activity modification, non-steroidal anti-inflammatory medications, proprioceptive retraining, and splinting. In our experience, non-operative management has proven effective in the management of most symptomatic PMCI patients. However, surgical management is an option for those that do not respond to non-operative treatment.Surgical management of PMCI has been limited in the past with small numbers and limited follow-up available. Here we present multiple surgical techniques preferred by the authors for the management of PMCI that has not responded to nonoperative management. Surgical Techniques Extensor Carpi Ulnaris Ligament ReconstructionBetween 1981 and 1989, we performed 15 surgical procedures in 13 patients with symptomatic palmar midcarpal instability that had failed non-operative management.1 Nine of the 15 procedures performed were to address the PMCI with soft-tissue procedures, including rerouting of the ECU tendon to stabilize the triquetrohamate joint. The remaining 6 procedures consisted of limited midcarpal arthrodesis. All of the extensor carpi ulnaris (ECU) rerouting soft-tissue procedures failed at an average of 48 months of follow-up, leading the authors to believe that perhaps limited midcarpal arthrodesis might be a more definitive surgical procedure. Dorsal ReefingIn patients with mild to moderate PMCI (symptomatic clunking that can be prevented with dorsally directed pressure on the pisiform or trapezoid ridge), reefing of the dorsal radiocarpal ligament is our preferred method of surgical treatment. The dorsal radiocarpal ligament is one AbstractPalmar midcarpal instability (PMCI) is an uncommon and poorly understood disorder. Its etiology is believed to be due to traumatic or congenital laxity of the ligaments (volar and dorsal) that stabilize the proximal row. This laxity results in hypermobility of the proximal carpal row and unphysiologic coupling of the midcarpal joint. Clinically, the condition is manifested by a painful clunk with ulnar and radial wrist deviation. The purpose of this article is to chronicle our personal experience with this condition and to review our current treatment recommendations and outcomes.