Intraspecific variation of spectral sensitivity in threespine stickleback (Gasterosteus aculeatus) from different photic regimes

To examine the influence of the spectral characteristics of underwater light on spectral sensitivity of the ON and OFF visual pathways, compound action potential recordings were made from retinal ganglion cells of threespine stickleback from different photic regimes. In fish from a red-shifted photic regime (P₅₀ 680 nm for downwelling light at 1m), peak sensitivity of both the ON and OFF pathways was limited to long wavelength light (_max 600–620). In contrast, the ON pathway of fish from a comparatively blue-shifted (P₅₀ 566 nm) photic regime exhibited sensitivity to medium (_max 540–560) and long (_max 600 nm) wavelengths, while the OFF pathway exhibited peak sensitivity to only medium (_max 540 nm) wavelength light. In a third population, where the the ambient light is moderately red-shifted (P₅₀ 629 nm), the ON pathway once again exhibited only a long wavelength sensitivity peak at 620 nm, while the OFF pathway exhibited sensitivity to both medium (_max 560 nm) and long (_max 600–620 nm) wavelength light. These findings suggest that the photic environment plays an integral role in shaping spectral sensitivity of the ON and OFF pathways.     

电刺激兔肾脏传入神经对血压,心率及加压素释放的影响

本工作以兔为实验对象,观察电刺激肾脏传入神经（ＡＲＮ）对血压、心率、颈交感神经放电、以及加压素（ＡＶＰ）合成和释放的影响,并对ＡＲＮ进入中枢的通路作了观察。结果显示,电刺激ＡＲＮ可以引起血压下降、心率减慢、颈交感神经放电抑制等反应,ＡＲＮ的兴奋还可使下丘脑的视上核、室旁核中的ＡＶＰ含量增加,垂体中ＡＶＰ含量下降,血浆ＡＶＰ水平升高。硝普钠的降压实验和静脉注射ＡＶＰ受体阻断剂ＡＶＰａ的实验均证实了Ａ     

神经生长因子在6－OHDA化学性去交感神经中的保护作用

本实验用６－ＯＨＤＡ造成成年小白鼠领下腺化学性去交感神经,观察了神经生长因子对该神经的保护作用。６－ＯＨＤＡ（１５ｍｇ／ｋｇｉｐ）处理后２４ｈ腺体内去甲肾上腺素（ＮＥ）含量降至正常水平的２％以下。若在６－ＯＨＤＡ处理同时开始多次给予神经生长因子（ＮＧＦ）,则ＮＥ残留量明显提高。减小６－ＯＨＤＡ剂量至１０ｍｇ／ｋｇ,ＮＥ残留量增加,同时ＮＧＦ的作用亦较用６－ＯＨＤＡ１５ｍｇ／ｋｇ时更为显著。若提前２４ｈ给予ＮＧＦ,尽管仍显著提高ＮＥ残留量,但程度却显然低于与６－ＯＨＤＡ同时给予者。以上结果表明外源性ＮＧＦ对６－ＯＨＤＡ造成交感神经化学性损毁有保护作用,此作用与神经受损的严重程度以及ＮＧＦ处理时间有关。     

Genetic control of chalcone isomerase activity in anthers of Petunia hybrida

The gene Po in pollen of Petunia hybrida Vilm. controls a discrete step in flavonoid biosynthesis. In recessive genotypes, naringenin-chalcone (4, 2,4,6-tetrahydroxychalcone) is accumulated, whereas, under the influence of the wild-type allele flavonols and anthocyanins are formed. Enzymic investigations on anthers of four genetically defined lines with different pollen colouration revealed a clear correlation between accumulation of naringenin-chalcone and deficiency of chalcone isomerase (EC 5.5.1.6). The results allow the conclusion that chalcone is the first product of the flavanone synthase reaction in anthers of Petunia hybrida and that chalcone isomerase is essential for the formation of flavonols and anthocyanins. These results were similar to those previously obtained with Callistephus chinensis (L.) Nees.Abbreviations EGME ethylen glycol monomethyl ether - MeOH methanol - CI chalcone isomerase - HOAc acetic acid - TLC thinlayer chromatography     

Microtubules in myelinated and unmyelinated axons of rat sciatic nerve

Summary Tannic acid in glutaraldehyde was used to stain microtubules in myelinated and unmyelinated axons of rat sciatic nerve. In the majority of areas the tannic acid failed to penetrate the unmyelinated axons whilst penetrating neighbouring myelinated axons, suggesting a difference in the ability of the two types of nerves to exclude tannic acid. Where tannic acid had penetrated the unmyelinated axons the 13 protofilament substructure and size of the microtubules appeared identical to those seen in the myelinated axons.     

刺激兔皮层感觉运动区和静注士的宁引起的肋间神经放电效应

在30例清醒,肌肉麻痹、切断迷走神经的家兔,观察到刺激对侧皮层感觉运动区时,胁间神经的放电效应包括两种成分。在呼气相电刺激,肋间外神经的第一效应表现为短暂的放电,肋间内神经表现为呼气放电的抑制;在吸气相电刺激,肋间外神经的第一效应表现为吸气放电的抑制,肋间内神经表现为短暂的放电。肋间外神经的第二效应表现为吸气放电的提前出现,吸气时程和呼气时程的缩短;肋间内神经的第二效应表现为吸气时程的缩短和呼气时程的延长,呼气放电的幅度明显增加。上述结果说明,皮层直接控制脊髓的通路既能兴奋也能抑制肋间吸气或呼气运动神经元的活动,且吸气与呼气运动神经元之间表现交互抑制。静注士的宁引起肋间神经梭形放电的发生过程和放电频率,与膈神经上表现相同;但恢复过程不同,膈神经上吸气放电恢复早,肋间神经上呼吸性放电恢复迟。此外,肋间神经的呼吸性放电不具有高频振荡现象。     

Endopeptidase-24.11, a Cell-Surface Peptidace of Central Nervous System Neurons, Is Expressed by Schwann Cells in the Pig Peripheral Nervous System

Endopeptidase-24.11 is a 90-kDa surface glycoprotein with the ability to hydrolyze a variety of biologically active peptides. Interest in this enzyme is based on the consensus that it may play a role in the termination of peptide signals in the central nervous system. In the present study, we have investigated the distribution of endopeptidase-24.11 in two nerves of the peripheral nervous system of newborn pigs: the sciatic, composed of a mixture of myelinated and nonmyelinated axons, and cervical sympathetic trunk in which greater than 99% of the axons are nonmyelinated. The endopeptidase was monitored enzymatically, as well as by immunoblotting and immunocytochemistry using mono- and polyclonal anti-endopeptidase antibodies. Endopeptidase-24.11 was detected in both the sciatic nerve and the cervical sympathetic trunk. Membrane preparations from sciatic nerve hydrolyzed 125I-insulin B-chain, and more than 50% of the activity was inhibited by phosphoramidon with an IC50 concentration of 3.2 nM. Moreover, a 90-kDa polypeptide was detected by immunoblotting of sciatic nerve membranes. The type of cells expressing the endopeptidase was determined by immunohistochemistry. In teased nerve preparations, these cells were identified morphologically as myelin- and non-myelin-forming Schwann cells. Endopeptidase-24.11 was also expressed by cultured Schwann cells from sciatic nerve and cervical sympathetic trunk maintained for 3 h in vitro. The presence of endopeptidase-24.11 on the Schwann cell surface raises the possibility of a potential role for the enzyme in nerve development and/or regeneration.     

Cholesterol from Degenerating Nerve Myelin Becomes Associated with Lipoproteins Containing Apolipoprotein E

Apolipoprotein E is synthesized and secreted by rat sciatic nerve consequent to several types of injury. It has been proposed that endoneurial apolipoprotein E, in analogy to its role in systemic cholesterol transport, is involved in the salvage and reutilization of myelin cholesterol during degeneration and regeneration. To test this hypothesis, nerve lipids were prelabeled via intraneural injection of [3H]acetate. Four weeks later the nerves were crushed. From 1 to 12 weeks later, crushed nerves were examined for extracellular lipoprotein-bound cholesterol label. By 2 weeks after injury, 10% of the endoneurial lipid label was in a soluble form that was releasable into incubation medium. This released fraction was enriched in labeled cholesterol, and its labeled lipid composition was constant, in contrast to the changing distribution of label in the nerve with time after injury. On a KBr gradient, the released lipid label cofractionated with the released apolipoprotein E at densities similar to that of lipoproteins. These data indicate that at least some myelin cholesterol in injured nerve becomes associated with apolipoprotein E-containing lipoproteins and thus is available for reutilization via the hypothesized model.     

Effects of Muscarinic Agonists and Depolarizing Agents on Inositol Monophosphate Accumulation in the Rabbit Vagus Nerve

The effects of muscarinic agonists and depolarizing agents on inositol phospholipid hydrolysis in the rabbit vagus nerve were assessed by the measurement of [3H]inositol monophosphate production in nerves that had been preincubated with [3H]inositol. After 1 h of drug action, carbachol, oxotremorine, and arecoline increased the inositol monophosphate accumulation, though the maximal increase induced by these agonists differed. Addition of the muscarinic antagonists atropine or pirenzepine shifted the carbachol dose-response curves to the right, without decreasing the carbachol maximal stimulatory effects. The KB for pirenzepine was 35 nM, which is characteristic of muscarinic high-affinity binding sites coupled to phosphoinositide turnover and often associated with the M1 receptor subtype. On the other hand, agents known to depolarize or to increase the intracellular Ca2+ concentration, e.g., elevated extracellular K+, ouabain, Ca2+, and the Ca2+ ionophore A23187, also increased inositol monophosphate accumulation. These effects were not mediated by the release of acetylcholine, as suggested by the fact that they could not be potentiated by the addition of physostigmine nor inhibited by the addition of atropine. The Ca(2+)-channel antagonist Cd2+, also known to inhibit the Na+/Ca2+ exchanger, was able to block the effects of K+ and ouabain, but did not alter those of carbachol. These results suggest that depolarizing agents increase inositol monophosphate accumulation in part through elevation of the intracellular Ca2+ concentration and that muscarinic receptors coupled to phosphoinositide turnover are present along the trunk of the rabbit vagus nerve.     

Target-Dependent Regulation of Retinal Nicotinic Acetylcholine Receptor and Tubulin RNAs During Optic Nerve Regeneration in Goldfish

A fundamental issue in central nervous system development regards the effect of target tissue on the differentiation of innervating neurons. We address this issue by characterizing the role the retinal ganglion cell target, i.e., the optic tectum, plays in regulating expression of tubulin and nicotinic acetylcholine receptor genes in regenerating retinal ganglion cells. Tubulins are involved in axonal growth, whereas nicotinic acetylcholine receptors mediate communication across synapses. Retinal ganglion cell axons were induced to regenerate by crushing the optic nerve. Following crush, there was a rapid increase in alpha-tubulin RNAs (3 days), which preceded the increase in nicotinic acetylcholine receptor RNAs (10-15 days). Both classes of RNAs approached control levels by the time retinotectal synapses and functional recovery were restored (4-6 weeks). If the optic nerve was repeatedly crushed or its target ablated, tubulin RNAs remained elevated, and the increase in receptor RNAs that would otherwise be seen 2 weeks after a single nerve crush did not occur. The interaction of retinal ganglion cell axons with their targets in the optic tectum appears, then, to exert a suppressive effect on the RNA encoding a cytoskeletal protein, tubulin, and an inductive effect on RNAs encoding nicotinic acetylcholine receptors involved in synaptic communication.