Chromosome 18 pairing behavior in human trisomic oocytes. Presence of an extra chromosome extends bouquet stage

Little is known about the first meiotic prophase stages in the human female because these occur during fetal life, and only a few studies have addressed aneuploid human oocytes. In this paper, the synaptic process in the meiotic prophase in three 47, XX + 18 cases is analyzed. A complete study of the dynamics of centromeres and telomeres, cohesin core and synapsis development in aneuploid female meiosis was performed. Investigation of chromosome dynamics in prophase of trisomy 18 oocytes show that these events follow the major patterns seen earlier in euploid oocytes. However, there is a significant delay in the resolution of bouquet topology which could relate to the presence of a surplus chromosome 18 axial element in zygotene oocytes. Pachytene oocytes displayed normal synapsis among the three chromosome 18s. However, in some oocytes the surplus chromosome 18 core was aligned to the bivalent 18. As ataxia telangiectasia and Rad3 related kinase (ATR) has been described as a marker for late-pairing chromosomes in mice, ATR distribution was analyzed in human meiocytes –spermatocytes, euploid oocytes and trisomic oocytes. In contrast to the observations made in mice, no preferential staining for late-pairing chromosomes was observed in humans. In the cases studied, bivalent synapses progressed as in a normal ovary, contrasting with the hypothesis that a surplus chromosome can modify pairing of other chromosomes.

LTP plays a distinct role in various brain structures

LTP is thought to be an experimental model for studying the cellular mechanism of learning and memory. Shors & Matzel review some contradictory data concerning the linkage between LTP and memory and suggest that LTP does not underlie learning and memory. LTP is a cellular and synaptic process and cannot be a memory mechanism. In fact, it is a cellular information storage mechanism.

Chiasma redistribution in the presence of different sized supernumerary segments in a grasshopper: dependence on nonhomologous synapsis

Eight different sized supernumerary segments located at distal ends of the long arms of chromosomes M4, M5, M6, and S8 of the grasshopper Stenobothrus festivus were studied in males with regard to the synaptic process and chiasma distribution in the bivalents that carry them. The M4, M5, and M6 bivalents heterozygous for extra segments were always monochiasmate, in contrast to their bichiasmate condition observed in basic homozygotes. Furthermore, the presence of any of these extra segments led to chiasma redistribution in the carrier bivalents, so that such chiasmata were formed preferentially further away from the extra segment. The intensity of this effect is dependent on the size of the segment. Not all heteromorphic bivalents exhibited synaptonemal complexes with equalized axes at pachytene, but there was always a variable proportion of heterosynapsis around the distal ends of the long arms that was dependent on both the size of the segment and the size of the carrier chromosome. It is proposed that the absence of chiasmata in nonhomologous synapsed regions is responsible for the results obtained. Length measurements of the different extra segments and their carrier chromosomes between pachytene and diplotene indicated that synaptonemal complex is underrepresented in supernumerary heterochromatin.Key words: chiasma distribution, grasshopper, heterosynapsis, supernumerary segment, synaptonemal complex.

Synaptonemal complex behavior in asynaptic maize

Synatonemal complexes were studied in silver-stained spread preparations of microsporocyte complements of asynaptic maize. Complexes were found predominantly in terminal regions of chromosome pairs. These tend to be aggregated in a common portion of the nucleus and to have polar orientation. As many as 19 of the 20 ends were found to be involved in relatively short paired segments. Intercalary regions of cores were not strongly organized and aligned, but some contained completed synaptonemal complex segments. The defect in asynaptic appears to represent stalling of the synaptic process at an early stage of synaptic progression.Key words: chromosome pairing, synaptonemal complex, synaptic defect.

Analysis of synaptic inputs to on-off amacrine cells of the carp retina.

To elucidate the synaptic transmission between bipolar cells and amacrine cells, the effect of polarization of a bipolar cell on an amacrine cell was examined by simultaneous intracellular recordings from both cells in the isolated carp retina. When either an ON or OFF bipolar cell was depolarized by an extrinsic current step, an ON-OFF amacrine cell was transiently depolarized at the onset of the current but no sustained polarization during the current was detected. The current hyperpolarizing the OFF bipolar cell also produced the transient depolarization of the amacrine cell at the termination of the current. These responses had a latency of approximately 10 ms. The amplitude of the current-evoked responses changed gradually with current intensity within the range used in these experiments. They were affected by polarization of the amacrine cell membrane; the amplitude of the current-evoked responses as well as the light-evoked responses was increased when the amacrine cell membrane was hyperpolarized, while the amplitude was decreased when the cell was depolarized. These results confirm directly that ON-OFF amacrine cells receive excitatory inputs from both ON and OFF bipolar cells: the ON transient is due to inputs from ON bipolar cells, and the OFF transient to inputs from OFF bipolar cells. The steady polarization of bipolar cells is converted into transient signals during the synaptic process.

Are there structural alterations in synapses related to functioning?

One would like to know whether synapses change structurally during learning or as a result of increased use, or disuse. The difficulties lie in deciding where learning takes place, how to produce a considerable increase in the amount of learning, or of use, or disuse, and how to produce such a change uniformly throughout a piece of tissue which can be examined anatomically. In recent years it has been found that exposure of light-reared animals to darkness, or of dark-reared animals to light, has effect on the cellular structure of the visual system that can be measured by light microscopy (see review by Riesen 1966). I have tried to extend this work by looking at synapses in the visual system with electron microscopy. This technique allows one to estimate the area of the synaptic profiles, to calculate the density of the axon terminals in the tissue, to measure the length of thickened apposition with the post-synaptic process and to look at the density and size of the synaptic vesicles within the synaptic profiles. Local variations in these parameters necessitate random sampling of the tissue, and this is provided by examination of several small blocks obtained by chopping the formalin-perfused tissue in osmium tetroxide solution. At all stages of the preparation from the living animal to the measurement of synapses it is essential to maintain strict pairing and identical treatment of the tissues to be compared. Sections from the light- and dark-exposed animals were mounted on opposite sides of finder grids, and batches of six plates were made from each kind of tissue alternately. The material was photographed and measured without knowing at the time whether it came from a light- or a dark-exposed animal.