Hypothalamic and hormonal control of photoperiodically induced vernal functions in the white-crowned sparrow,Zonotrichia leucophrys gambelii

Summary The effects of implantation of testosterone propionate (TP) in various sites in the hypothalamus on the photoperiodically induced vernal premigratory functions in the White-crowned Sparrows were investigated in order to assess the role of the hypothalamo-hypophysial-testicular axis in the induction of these responses.Implantation of glass capillary tubes containing TP in the basal infundibular nucleus (IN), in the median eminence, or in the pars distalis inhibited the photoperiodically induced increase in plasma levels of luteinizing hormone (LH), as measured by radioimmunoassay, and testicular growth. The effective implants significantly lowered the levels of LH in birds held on nonstimulatory short days. These TP implants apparently inhibited release from the pars distalis of both LH and follicle-stimulating hormone (FSH). It is concluded that the site of sensitivity in the negative feedback by testosterone is either the basal IN or the pars distalis, or both. The implants of TP that inhibited the increase in plasma LH and testicular growth completely did not prevent the birds from fattening.These investigations were supported, in part, by research grants from the National Institutes of Health (HD-6527) and National Science Foundation (BMS 79-13933) to Professor Donald S. Farner. This paper is based on a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy from the University of WashingtonThe author is grateful to Professor Donald S. Farner for his guidance throughout the course of these investigations. The assistance of Mr. Philip W. Mattocks, Jr. in performing radioimmunoassays is sincerely appreciated     

索曼中毒运动终板乙酰胆碱酯酶活性和接头传递功能的关系

用大鼠的在体膈肌局部索曼(Soman)中毒法,观察了乙酰胆碱酯酶(ACHE)在运动终板的再生和肌接头传递功能的恢复过程,以及肟类药物(HI-6)对两过程的促进作用。提出终板 AChE 活性与高频间接刺激(100次/秒)引起膈肌强直收缩幅度有一定的关系。中毒早期(30分钟以内)HI-6对索曼抑制的膈肌终板 AChE 有一定的重活化作用,并能相应地恢复肌接头的传递功能。     

Neuroethological approaches to the study of motor development in chicks: Achievements and challenges

Chicks and chick embryos provide a useful model system for the study of related to the development of motor behaviors. EMG and kinematic analyses of leg movements have been used to provide new data on the organization of embryonic motility. These data suggest that the circuitry needed to produce a basic, coordinated motor pattern is available early in development. This circuitry then appears to be retained throughout life. Evidence from analysis of EMG patterns and leg deafferentation studies suggest that the output of this basic circuit can be modulated by sensory input to produce the motor patterns of later behaviors, such as hatching and walking. If the same circuitry is present throughout life, then mechanisms for initiation and termination of particular behaviors must be available to ensure that specific behaviors are turned on and off at appropriate times. For example, hatching can be turned on by a specific sensory signal: proprioceptive signals from the bent neck. In addition to reviewing current research on the development of chick motor behaviors, methodological considerations and suggestions for future research are presented. © 1992 John Wiley & Sons, Inc.     

Thermo-inducible expression of cloned early genes of bacteriophage Mu.

An EcoRI fragment, containing approx. 5100 base pairs (bp) of the immunity-end of bacteriophage Mu, was inserted into the multicopy plasmid pMB9 by in vitro recombination. The expression of early Mu genes, located on the cloned fragment, is thermo-inducible because of the presence of the ts mutation in gene c. The isolation of a transformant harbouring the recombinant plasmid, pGP1, was possible only when expression of Mu genes was prevented. pGP1 can be maintained at 28 degrees C at high copy number, but at 42 degrees C the pGP1 containing cells are killed due to the expression of the kil gene of Mu. The following Mu genes are present on pGP1: the ner gene, the integration and replication genes A and B, the cim gene, and the kil gene. pGP1 containing cells do not show Gam and Sot activity at 42 degrees C, therefore the leftmost EcoRI site on the Mu DNA is located between genes kil and gam or sot, or within the gam or sot gene.     

Mantis Shrimp Navigate Home Using Celestial and Idiothetic Path Integration

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Synaptic Connectivity between the Cortex and Claustrum Is Organized into Functional Modules

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Age‐related deterioration of motor function in male and female 5xFAD mice from 3 to 16 months of age

Alzheimer's disease (AD) is a neurodegenerative disorder that leads to age‐related cognitive and sensori‐motor dysfunction. There is an increased understanding that motor dysfunction contributes to overall AD severity, and a need to ameliorate these impairments. The 5xFAD mouse develops the neuropathology, cognitive and motor impairments observed in AD, and thus may be a valuable animal model to study motor deficits in AD. Therefore, we assessed age‐related changes in motor ability of male and female 5xFAD mice from 3 to 16 months of age, using a battery of behavioral tests. At 9‐10 months, 5xFAD mice showed reduced body weight, reduced rearing in the open‐field and impaired performance on the rotarod compared to wild‐type controls. At 12‐13 months, 5xFAD mice showed reduced locomotor activity on the open‐field, and impaired balance on the balance beam. At 15‐16 months, impairments were also seen in grip strength. Although sex differences were observed at specific ages, the development of motor dysfunction was similar in male and female mice. Given the 5xFAD mouse is commonly on a C57BL/6 × SJL hybrid background, a subset of mice may be homozygous recessive for the Dysf ^im mutant allele, which leads to muscular weakness in SJL mice and may exacerbate motor dysfunction. We found small effects of Dysf ^im on motor function, suggesting that Dysf ^im contributes little to motor dysfunction in 5xFAD mice. We conclude that the 5xFAD mouse may be a useful model to study mechanisms that produce motor dysfunction in AD, and to assess the efficacy of therapeutics on ameliorating motor impairment.     

Femtosecond Laser‐Etched MXene Microsupercapacitors with Double‐Side Configuration via Arbitrary On‐ and Through‐Substrate Connections

The capacitance of microsupercapacitors (MSCs) can double if both sides of substrates are used to construct MSCs. Nevertheless, achieving electric connections of MSCs through substrates is a challenge due to the difficulty in precisely positioning each MSC couple that has two of the same MSCs units on two sides. In this work, taking advantage of the synchronous etching on both sides of transparent polyethylene terephthalate substrates by femtosecond laser pulses, a double‐sided configuration is attained with high precision in the alignment of back‐to‐back MSC couples and versatile double‐side MSCs are realized via arbitrary on‐ and through‐substrate connections of MXene MSC units. The MXene double‐side MSC fabricated by the series connection of 12 spiral pattern MXene MSC units with interdigital electrodes of 10 μm width interspace can output a large working voltage of 7.2 V. Additionally, femtosecond laser etching brings the transformation of MXene into titania near‐etched edges with a lateral distance less than 1 µm. Such a small laser‐affected area has little influence on the capacitive performance, which is one of advantages for femtosecond laser over conventional lasers. This research is valuable for one‐step manufacturing of highly integrated MSCs in the field of miniaturized energy storage systems.     

Does phenotypic plasticity initiate developmental bias?

The generation of variation is paramount for the action of natural selection. Although biologists are now moving beyond the idea that random mutation provides the sole source of variation for adaptive evolution, we still assume that variation occurs randomly. In this review, we discuss an alternative view for how phenotypic plasticity, which has become well accepted as a source of phenotypic variation within evolutionary biology, can generate nonrandom variation. Although phenotypic plasticity is often defined as a property of a genotype, we argue that it needs to be considered more explicitly as a property of developmental systems involving more than the genotype. We provide examples of where plasticity could be initiating developmental bias, either through direct active responses to similar stimuli across populations or as the result of programmed variation within developmental systems. Such biased variation can echo past adaptations that reflect the evolutionary history of a lineage but can also serve to initiate evolution when environments change. Such adaptive programs can remain latent for millions of years and allow development to harbor an array of complex adaptations that can initiate new bouts of evolution. Specifically, we address how ideas such as the flexible stem hypothesis and cryptic genetic variation overlap, how modularity among traits can direct the outcomes of plasticity, and how the structure of developmental signaling pathways is limited to a few outcomes. We highlight key questions throughout and conclude by providing suggestions for future research that can address how plasticity initiates and harbors developmental bias.