Nuclear and mitochondrial genome datasets for spiny lobsters genus Panulirus (Decapoda: Achelata: Palinuridae).

Spiny lobsters (Decapoda: Palinuridae) in the genus Panulirus are targets of lucrative fisheries globally and have relevant ecological functions in tropical and subtropical environments. Only a few, but increasing, number of genetic and genomic resources exist for them. Nuclear and mitochondrial genome assemblies can provide insights into their phylogenetic relationships and support fishery management strategies in species that are heavily exploited. Herein, using Illumina short reads whole genome sequencing, we assembled the nuclear and mitochondrial genomes of a total of 14 species. Genomic DNA was extracted from specimens deposited at Clemson University Crustacean Collection and sequenced in a HiSeq X Ten system. The number of paired-end (PE) reads generated for the different studied species varied between 219,917,346 in P. argus and 70,215,423 in P. cygnus. Nuclear and mitochondrial genomes were 'de novo' assembled. Nuclear genomes ranged between 1,624,400,357 bp in P. guttatus and 935,571,898 bp in P. cygnus with scaffold numbers varying between 466,583 in P. versicolor and 852,228 in P. longipes. Mitochondrial genomes varied between 15,613 bp and 15,768 bp in P. pascuensis and P. versicolor, respectively. The totality of the short reads, nuclear, and mitochondrial genome assemblies are available at NCBI's GenBank.

Insights into the nuclear and mitochondrial genome of the Lemon shark Negaprion brevirostris using low-coverage sequencing: Genome size, repetitive elements, mitochondrial genome, and phylogenetic placement.

The Lemon shark Negaprion brevirostris is an important species experiencing conservation issues that is in need of genomic resources. Herein, we conducted a genome survey sequencing in N. brevirostris and determined genome size, explored repetitive elements, assembled and annotated the 45S rRNA DNA operon, and assembled and described in detail the mitochondrial genome. Lastly, the phylogenetic position of N. brevirostris in the family Carcharhinidae was examined using translated protein coding genes. The estimated haploid genome size ranged between 2.29 and 2.58 Gbp using a k-mer analysis, which is slightly below the genome size estimated for other sharks belonging to the family Carcharhinidae. Using a k-mer analysis, approx. 64-71 % of the genome of N. brevirostris was composed of repetitive elements. A relatively large proportion of the 'repeatome' could not be annotated. Taking into account only annotated repetitive elements, Class I - Long Interspersed Nuclear Element (LINE) were the most abundant repetitive elements followed by Class I - Penelope and Satellite DNA. The nuclear ribosomal operon was fully assembled. The AT-rich complete mitochondrial genome was 16,703 bp long and encoded 13 protein coding genes, 2 ribosomal RNA genes, and 22 transfer RNA genes. Negaprion brevirostris is closely related to the genera Carcharhinus, Glyphis and Lamiopsis in the family Carcharinidae. This new genomic resources will aid with the development of conservation plans for this large coastal shark.

Systemic morphine treatment induces changes in firing patterns and responses of nociceptive afferent fibers in mouse glabrous skin.

Patients receiving opioids for pain may experience decreased effectiveness of the drug and even abnormal pain sensitivity-hyperalgesia and/or allodynia. We hypothesized that peripheral nociceptor hyperexcitability contributes to opioid-induced hyperalgesia and tested this using an in vitro mouse glabrous skin-nerve preparation. Mice were injected intraperitoneally with escalating doses of morphine (5, 8, 10, 15 mg/kg) or saline every 12 hours for 48 hours and killed approximately 12 hours after the last injection. Receptive fields of nociceptors were tested for mechanical, heat, and cold sensitivity. Activity was also measured during an initial 2-minute period and during 5-minute periods between stimuli. Aberrant activity was common in fibers from morphine-treated mice but rare in saline-treated mice. Resting background activity was elevated in C-fibers from morphine-treated mice. Both C- and Aδ-fibers had afterdischarge in response to mechanical, heat, and/or cold stimulation of the skin as well as spontaneous, unevoked activity. Compared to saline, morphine treatment increased the proportion of fibers displaying polymodal rather than mechanical-only responses. A significant increase in Aδ-mechanoreceptive fibers responding to cold accounted for most of this change. In agreement with this, morphine-treated mice showed increased sensitivity in the cold tail flick test. In morphine-treated mice, aberrant activity and hyperexcitability of nociceptors could contribute to increased pain sensitivity. Importantly, this activity is likely driving central sensitization, a phenomenon contributing to abnormal sensory processing and chronic pain. If similar changes occur in human patients, aberrant nociceptor activity is likely to be interpreted as pain and could contribute to opioid-induced hyperalgesia.

Pain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord.

Withdrawal from prescribed opioids results in increased pain sensitivity, which prolongs the treatment. This pain sensitivity is attributed to neuroplastic changes that converge at the spinal cord dorsal horn. We have recently reported that repeated morphine administration triggers an insertion of GluA2-lacking (Ca(2+)-permeable) α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPAR) in the hippocampus. This finding together with the reported involvement of AMPAR in the mechanisms underlying inflammatory pain led us to hypothesize a role for spinal AMPAR in opioid-induced pain behavior. Mice treated with escalating doses of morphine showed hypersensitivity to mechanical stimulation. Intrathecal administration of a Ca(2+)-permeable AMPAR selective blocker disrupted morphine-induced mechanical sensitivity. Analysis of the expression and phosphorylation levels of AMPAR subunits (GluA1/2/3/4) in homogenates and in postsynaptic density fractions from spinal cord dorsal horns showed an increase in GluA4 expression and phosphorylation in the postsynaptic density after morphine. Co-immunoprecipitation analyses suggested an increase in GluA4 homomers (Ca(2+)-permeable AMPAR) and immunohistochemical staining localized the increase in GluA4 levels in laminae III-V. The excitatory postsynaptic currents (EPSCs) recorded in laminae III-V showed enhanced sensitivity to Ca(2+)-permeable AMPAR blockers in morphine-treated mice. Furthermore, current-voltage relationships of AMPAR-mediated EPSCs showed that rectification index (an indicator of Ca(2+)-permeable AMPAR contribution) is increased in morphine-treated but not in saline-treated mice. These effects could be reversed by infusion of GluA4 antibody through patch pipette. This is the first direct evidence for a role of GluA4-containing AMPAR in morphine-induced pain and highlights spinal GluA4-containing AMPAR as targets to prevent the morphine-induced pain sensitivity.