Genetic and morphological identification of pelagic juvenile rockfish collected from the Gulf of Alaska

Pelagic juvenile rockfish (Sebastes spp.) collected in surveys designed to assess juvenile salmonids and other species in the Gulf of Alaska in 1998 and 2000–2003 provide an opportunity to document the occurrence of the pelagic juveniles of several species of rockfish. Often, species identification of rockfish is difficult or impossible at this stage of development (~20 to 60 mm), and few species indigenous to Alaska waters have been described. Use of mitochondrial DNA markers for rockfish species allowed unequivocal identification of ten species (S. aleutianus, S. alutus, S. borealis, S. entomelas, S. flavidus, S. melanops, S. pinniger, S. proriger, S. reedi, and S. ruberrimus) in subsamples from the collections. Other specimens were genetically assignable to groups of two or three species. Sebastes borealis, S. crameri, and S. reedi were identified using morphological data. Combining genetic and morphological data allowed successful resolution of the other species as S. emphaeus, probably S. ciliatus (although S. polyspinis cannot be totally ruled out), and S. polyspinis. Many specimens were initially morphologically indistinguishable from S. alutus, and several morphological groups included fish genetically identified as S. alutus. This paper details the characteristics of these pelagic juveniles to facilitate morphological identification of these species in future collections. (PDF file contains 32 pages.)

Behavioral, neurochemical and morphological changes induced by the overexpression of munc18-1a in brain of mice: relevance to schizophrenia

Overexpression of the mammalian homolog of the unc-18 gene (munc18-1) has been described in the brain of subjects with schizophrenia. Munc18-1 protein is involved in membrane fusion processes, exocytosis and neurotransmitter release. A transgenic mouse strain that overexpresses the protein isoform munc18-1a in the brain was characterized. This animal displays several schizophrenia-related behaviors, supersensitivity to hallucinogenic drugs and deficits in prepulse inhibition that reverse after antipsychotic treatment. Relevant brain areas (that is, cortex and striatum) exhibit reduced expression of dopamine D-1 receptors and dopamine transporters together with enhanced amphetamine-induced in vivo dopamine release. Magnetic resonance imaging demonstrates decreased gray matter volume in the transgenic animal. In conclusion, the mouse overexpressing brain munc18-1a represents a new valid animal model that resembles functional and structural abnormalities in patients with schizophrenia.