中樞神經系統生理研究的一些新進展

大腦皮層的結構及高級神經活動 在本屆國際生理學大會上,蘇聯因病未能出席,但他有一篇書面報導,證明大腦皮層的結構與機能的相互關係。通過複杂的暫時聯繫的機制,即各種條件反射的形成,機體得以適應變化萬千的環境。在大腦皮層內,有三種細胞參加皮層活動的過程,即錐體細胞、星形細胞與梭形細胞。錐體舆梭形細胞的軸突,通常離開皮層,向外傳導衝動。在種族與個體發育中研究皮層的神經细胞舆神經細胞間的聯繫,發見星形細胞有三個特點:(1)星形細胞系統     

輔酶細胞色素還原酶系的研究——Ⅰ.還原輔酶Ⅰ与琥珀酸的同時氧化

(一)本報告提供了一個從輔酶Ⅰ,用酶還原法製備還原輔酶Ⅰ的方法。我們所製得的還原輔酶Ⅰ鈉鹽乾粉,可以在低温保存數月而不被氧化。 (二)與心肌製劑中顆粒相結合的輔酶Ⅰ細胞色素還原酶系,和用乙醇抽出的水溶性的輔酶Ⅰ細胞色素還原酶的性質頗不相同。其中比較重要的不同點是對於細胞色素c的親力,前者遠大於後者,其米氏常數僅約為後者的十二分之一。 (三)用一心肌顆粒製劑作為材料,無論用氧或過量之細胞色素c作為氫受體,還原輔酶Ⅰ與琥珀酸同時氧化時的總速度,不等於二者分別氧化時速度之和,而僅等於其中氧化較快者單獨氧化時之速度。但如用[2,6]二氯靛酚作為氫受體時,二者共同氧化時之總速度完全等於二者分別氧化時速度的和。 (四)當用氧或過量之細胞色素c作為氫受體時,琥珀酸與還原輔酶Ⅰ能彼此互相抑制對方氧化的速度。有足夠的實驗材料說明,還原輔酶Ⅰ對於琥珀酸氧化的抑制,不是由於草醯乙酸聚集的緣故。 (五)如果在反應混合物中同時含有琥珀酸脫氫酶的專一抑制劑,丙二酸,則琥珀酸對於還原輔酶Ⅰ氧化作用的抑制即被解除。 (六)根據以上的實驗結果,可以認為,還原輔酶Ⅰ及琥珀酸先通過一個共同的因子與細胞色素c作用。這個共同的因子在一般情形之下,也是這兩個酶系統的速度限制因子。應該指出在我們的實驗中,並未使用任何可能影響酶系統結構的條件,因此我們的結果是在一個比較接近於生理狀態的情形之下獲得的。 (七)應該着重指出,從本報告的結果可以看到,一個用人為的方法從複雜酶系上溶解下來的酶的性質,有時並不能代表這個酶在有組織的酶系統中的真實情况。 (八)我們相信,本報告所說明的兩酶系競爭一個共同因子的一些現象,將为研究複雜酶系之間的相互關係,提供一個新的方法。     

大腦皮層對胼胝體的逆行刺激的反應

摘除一侧大腦半球的一部分,等待足够時日使發源於這一部分大腦皮層的胼胝體纖維變質,然後刺激暴露出來的胼胝體就可以得到純粹的逆行衝動傳向對側大腦皮層的胼胝體神經原。用單極引出,這種逆行衝動在大腦皮層引起的反應首先是一個簡單的正電位,然後是一個時程較長的負電位。這負電位可被番木龞鹼大大增加,並伴有錐體束放射。這些表明,胼胝體神經原在接受逆行刺激時能通過其側枝引起突觸後的活動。在用接連兩次逆行刺激時,隨着所用刺激是弱或強,第一個反應的負電位部分可以增大或減小。由胼胝體的逆行刺激和錐體束的逆行刺激在皮層所引起的兩個反應之間有相互影響,當後者在先時,前者的負電位部分減少。就局部施加於大腦皮層表面的普魯卡因溶液對於它們的藥效發展的快慢而言,胼胝體逆行刺激在皮層引起的反應與胼胝體的順行及逆行混合刺激所引起的反應的各組成部分有其特異的差別。用微電極逐步插入皮層不同深度處記錄得到的胼胝體逆行刺激所引起的反應表現有系統的變化。這些結果從有關組織學資料可以得出自然的解釋。     

硫噴妥鈉和安密妥鈉及自然睡眠對於血液濃度的影響的初步觀察

和他的同工們的研究,已經肯定了各種內臟活動包括循環器官、脾臟、肝臟的活動及腺細胞的通透能等在內都能受大腦皮層的控制。對於血管的通透能,雖然我們没有看到進行條件反射研究的報導,但是在他所著的“大腦皮層與內臟”一書中,已經舉出了一些神經控制血管通透能的材料。Barbour等發現了由於冷熱水浴引起     

問題解答

問:达尔文主义基礎下册李森科論春化法後的結論中,指出個体发育与系統發育的統一;米丘林指出嫁接用的枝与芽必须採用树上部的枝芽,為什麼只有树上部的技芽才適合,在什么地方? 答:細胞內部的质变,引起對發育条件要求的更换,這种质变,也即阶段的改變,只是發生在嫩枝生長點的分生細胞中。這些細胞傳给所有起源於他們的子細胞。植物茎的下部在時間上是最初出現的,但就階段性來說,它是最幼龄的分生组织發育出來的,並且因為阶段的改變只能发生在未分化的分生細胞中,所以莖的整個下部,始終保持在產生它的分生細胞原來所具备的幼龄阶段狀態,而嫩枝上出現较晚的並形成其顶部的组织,就阶段性來說,起源於较老的分生组织,因而它     

內分泌學的新進展

近年來內分泌學有着很大的進步,在某些方面,甚至於可以說是有着驚人的進步。這些成績,無疑地是由生理學、生物化學、藥理學等各科工作者的密切配合而獲得的。代表着整個內分泌學發展方向的一項具有重大意義的成就,就是證明了作爲中樞神經系統一部分的丘腦下部對於垂體機能的管制作用。由於垂體對於多種其他內分泌腺具     

問題解答

問:農民們認為桃樹的樹幹上用刀剁很多的裂口,這樣它的果實就結得大,這種說法是否正確? 答:一般果樹樹幹或樹枝的外面部分,是植物的韌皮部及木栓層等,韌皮部裏有篩管,由許多管狀細胞連接而成的。這篩管是植物營養分運輸的道路。在植物的葉中由於光合作用,而生成的炭水化物(如糖類等);還有其他的有機物,都經過筛管由上端向下運輸的。如果把樹幹用刀剁很多的裂孔,韌皮部的許多篩管被切斷了,上端的營養分自然不能完全向樹幹的下部運輸,那末營養分都可供應植物的上面部分需用了,故在果實成長的時候,因爲得到更多的營養分,當可長得更大了。(黄宗甄答) 問:單子葉植物是否可以嫁接? 答:單子葉植物是可以嫁接的。嫁接也可分爲好幾種方法,如單取植物的幼芽,使癒合於與其他植物體;或取枝條插入其他植物的莖幹;也有用同樣大小的莖幹或枝條;也有用根如蘿蔔用來作為砧     

关於胰岛素作用问题的探讨

胰島素與真性糖尿病的關係雖早已在1890年爲Von Mehring舆Minkowski兩氏所確定,但晶體胰島素的正式用於臨症治療則僅有30年的歷史。遺慽的是,關於胰島素作用機制與其化学理論的研究却遠遠落後於其實踐知識的進展,以致常無法圓满地解說釋激素的種種代謝效應。近7年來,由於Sanger氏與Waugh氏兩學派的科學     

在出生後發育時期兔子大腦皮層電活動的變化

本工作觀察在出生後發育時期中小兔大腦皮層自發電位的成熟過程和被激起的電位的出現與變化。初生的小兔,用番木龞鹼溶液直接塗在大腦皮層土郎能引起番木龞鹼波,但是在出生後一週左右大腦皮層才開始有連續的電位變化。在出生後的第三週末第四週初時小兔大腦皮層的自發電位的圖形已與從大免得到的相仿。在大腦皮層各種被激起的電位變化中,直接刺激大腦皮層所引起的負電位出現得最早。通過胼胝體所引起的電位變化以及刺激錐體束在大腦皮層引起的電位變化都在小兔出生後一週內出現,這兩種電位初出現時都缺少相當於在成年兔得到的相應的反应中,由於突觸後反應所引起的那些部分。兔在出生後的12天左右睜眼。在出生後10天左右用光線刺激眼睛已能在大腦皮層視區引起反應,使眼睛不見光或摘除眼睛對視區電位變化的成熟看不出有影響。     

从条件反射与非条件反射看皮层与皮层下的相互关系

巴甫洛夫把外在動因与有機體對其回答性活動之間的固定聯系叫做非條件反射,而把它們之間的暫時聯系叫做條件反射,他認為皮層下神經節是最重要的非條件反射或本能的中樞——食物反射、防禦反射、性反射等的中樞;而條件反射則是高級神經活動,它代表着大腦兩半球以及位於其下的皮層下神經節的活動。同時他叉認為,從皮層与皮層下相互作用的觀点來看,高級神經活動雖不僅是皮層的活動,但是以大腦皮層的活動為其主要組成。貝科夫曾寫道:“在實驗條件下對所有器官都能形成暫時性聯     

Protection from radiation-induced male germ cell loss by sphingosine-1-phosphate

Male germ cells are susceptible to radiation-induced injury, and infertility is a common problem after total-body irradiation. Here we investigated, first, the effects of irradiation on germ cells in mouse testis and, second, the role of sphingosine-1-phosphate (S1P) treatment in radiation-induced male germ cell loss. Irradiation of mouse testes mainly damaged the early developmental stages of spermatogonia. The damage was seen by means of DNA flow cytometry 21 days after irradiation as decreasing numbers of spermatocytes and spermatids with increasing amounts of ionizing radiation (0.1-2.0 Gy). Intratesticular injections of S1P given 1-2 h before irradiation (0.5 Gy) did not protect against short-term germ cell loss as measured by in situ end labeling of DNA fragmentation 16 h after irradiation. However, after 21 days, in the S1P-treated testes, the numbers of primary spermatocytes and spermatogonia at G2 (4C peak as measured by flow cytometry) were higher at all stages of spermatogenesis compared with vehicle-treated testes, indicating protection of early spermatogonia by S1P, whereas the spermatid (1C) populations were similar. In conclusion, S1P appears to protect partially (16%-47%) testicular germ cells against radiation-induced cell death. This warrants further studies aimed at development of therapeutic agents capable of blocking sphingomyelin-induced pathways of germ cell loss.     

Temperature dependence of the electron spin-lattice relaxation rate from pulsed EPR of CUA and heme a in cytochrome c oxidase

This work shows the feasibility of using pulsed, saturation recovery EPR to study directly the magnetic relaxation properties of metal centers in cytochrome c oxidase in the 1.5-20 K range. Heme a and CuA both showed remarkably similar Tn temperature dependences in their spin-lattice relaxation rates. Either both are in environments with very similar protein backbone configurations (Stapleton, H.J., J.P. Allen, C.P. Flynn, D.G. Stinson, and S.R. Kurtz, 1980, Phys. Rev. Lett., 45:1456-1459; Allen, J.P., J.T. Colvin, D.G. Stinson, C.P. Flynn, and H.J. Stapleton, 1982, Biophys. J., 38:299-310), or the CuA is relaxed by nearby heme a. Spin-lattice relaxation of the nitrosylferrocytochrome a3 center in mixed valence oxidase showed enhancement of relaxation by a nearby paramagnetic center, most likely heme a.     

Cyp26b1 Expression in Murine Sertoli Cells Is Required to Maintain Male Germ Cells in an Undifferentiated State during Embryogenesis

In mammals, germ cells within the developing gonad follow a sexually dimorphic pathway. Germ cells in the murine ovary enter meiotic prophase during embryogenesis, whereas germ cells in the embryonic testis arrest in G0 of mitotic cell cycle and do not enter meiosis until after birth. In mice, retinoic acid (RA) signaling has been implicated in controlling entry into meiosis in germ cells, as meiosis in male embryonic germ cells is blocked by the activity of a RA-catabolizing enzyme, CYP26B1. However, the mechanisms regulating mitotic arrest in male germ cells are not well understood. Cyp26b1 expression in the testes begins in somatic cells at embryonic day (E) 11.5, prior to mitotic arrest, and persists throughout fetal development. Here, we show that Sertoli cell-specific loss of CYP26B1 activity between E15.5 and E16.5, several days after germ cell sex determination, causes male germ cells to exit from G0, re-enter the mitotic cell cycle and initiate meiotic prophase. These results suggest that male germ cells retain the developmental potential to differentiate in meiosis until at least at E15.5. CYP26B1 in Sertoli cells acts as a masculinizing factor to arrest male germ cells in the G0 phase of the cell cycle and prevents them from entering meiosis, and thus is essential for the maintenance of the undifferentiated state of male germ cells during embryonic development.     

Juvenile spermatogonial depletion (jsd) mutant seminiferous tubules are capable of supporting transplanted spermatogenesis

In mice, the juvenile spermatogonial depletion (jsd) mutation results in a single wave of spermatogenesis followed by failure of type A spermatogonial stem cells to repopulate the testis, rendering male animals sterile. It is not clear whether the defect in jsd resides in a failure of the somatic component to support spermatogenesis or in a failure that is intrinsic to the mutant's germ cells. To determine if the jsd intratesticular environment is capable of supporting spermatogenesis, germ cell transplantation experiments were performed in which C57BL/6 ROSA germ cells were transplanted into jsd recipients. To determine if jsd spermatogonia are able to develop in a permissive seminiferous environment, jsd germ cells were transplanted into W/W(v) and busulfan-treated C57BL/6 animals. The data demonstrate that up to 7 mo after transplantation of normal germ cells, jsd seminiferous tubules are capable of supporting spermatogenesis. In contrast, when jsd germ cells were transplanted into busulfan-treated C57BL/6 testis, or into testis of W/W(v) mice, no jsd-derived spermatogenesis was observed. The data support the hypothesis that the jsd phenotype is due to a defect in the germ cells themselves, and not in the intratubular environment.     

A novel function for the Sm proteins in germ granule localization during C. elegans embryogenesis

General mRNA processing factors are traditionally thought to function only in the control of global gene expression. Here we show that the Sm proteins, core components of the splicesome, also regulate germ granules during early C. elegans development. Germ granules are large cytoplasmic particles that localize to germ cells and their precursors during embryogenesis of diverse organisms. In C. elegans, germ granules, called P granules, are segregated to the germline precursor cells during embryogenesis by asymmetric cell division, and they remain in germ cells at all stages of development. We found that at least some Sm proteins are components of P granules. Moreover, disruption of Sm activity caused defects in P granule localization to the germ cell precursors during early embryogenesis. In contrast, loss of other splicing factor activities had no effect on germ granule control in the embryo. These observations suggest that the Sm proteins control germ granule integrity and localization in the early C. elegans embryo and that this role is independent of pre-mRNA splicing. Thus, a highly conserved splicing factor may have been adapted to control both snRNP biogenesis and the localization of components important for germ cell function.     

Expression of heat shock proteins by isolated mouse spermatogenic cells.

Proteins of the hsp70 family are abundant in mouse spermatogenic cells. These cells also synthesize relatively large amounts of a 70,000-molecular-weight protein (P70) that appears to be a cell-specific isoform of hsp70, the major heat-inducible protein (R.L. Allen, D.A. O'Brien, and E.M. Eddy, Mol. Cell. Biol. 8:828-832, 1988). In this study, proteins of unstressed and heat-stressed spermatogenic cells consisting of purified preparations of preleptotene, leptotene-zygotene, pachytene spermatocytes, and round spermatids were analyzed by two-dimensional polyacrylamide gel electrophoresis. Unstressed preleptotene and leptotene-zygotene spermatocytes contained little P70, whereas relatively large amounts of P70 were present in pachytene spermatocytes and round spermatids. Labeling studies showed that P70 was synthesized primarily in pachytene spermatocytes and that little synthesis occurred in round spermatids or in preleptotene and leptotene-zygotene stages of spermatogenesis. Synthesis of hsp70 was not detectable in unstressed cells but was induced in all stages of isolated germ cells following heat stress. These results indicate that P70 is expressed in a stage-specific manner during cell differentiation, whereas hsp70 is synthesized in response to stress in all populations of isolated spermatogenic cells examined.     

Depletion of the cap-associated isoform of translation factor eIF4G induces germline apoptosis in C. elegans

During mammalian programmed cell death, cleavage of the translation initiation factor 4G proteins (eIF4GI and eIF4GII) by caspase-3 induces the cap-independent synthesis of pro-apoptotic proteins. Apoptosis occurs naturally in the gonad to remove germ cells that are not selected to grow as oocytes and mature into eggs. Here, we describe two major isoforms of Caenorhabditis elegans eIF4G that are derived from a single gene (ifg-1) and their separate roles in germline homeostasis. Full length IFG-1 protein (170 kDa isoform) differs from the shorter isoform (130 kDa) by the inclusion of the N-terminal domain containing the putative eIF4E-binding site required for mRNA cap recognition. Depletion of the cap-associated p170 isoform induced CED-4 expression in oocytes and markedly increased germline apoptotic events, but did not prevent early mitotic germ cell proliferation. Loss of both p170 and p130 suppressed germ cell proliferation and arrested larval development. Evidence suggests that eIF4G isoforms are differentially utilized during oogenesis to regulate germ cell apoptosis. We propose that an alternative mechanism to eIF4G cleavage may be employed in germ cells by changing the availability of the p170 isoform.