硝酸士的宁对刺激鲫鱼脊髓诱发的Mauthner细胞胞内电位变化的影响

目的探索肌注硝酸士的宁对刺激鲫鱼脊髓所诱发的M细胞胞内电位变化的影响。方法运用微电极穿刺技术记录M细胞的胞内电位变化。结果肌注硝酸士的宁后逆向动作电位后突触后电位（PSPs）的幅度升高,持续时间增加,并可在此基础上暴发动作电位。结论从脊髓到M细胞的传入通路中可能有抑制性递质甘氨酸的释放和相应受体的存在,其与兴奋性递质一起调节M细胞兴奋性,从而使M细胞的活动与整体一致。     

刺激迷走神经引起的鲫鱼Mauthner细胞顺向激活

目的 :研究迷走神经感觉传入信息对Mauthner细胞 (M细胞 )兴奋性的影响。方法 :刺激鲫鱼迷走神经 ,并运用微电极穿刺技术记录鲫鱼M细胞胞内电位变化。结果 :在M细胞胞内记录到分级的、复合的兴奋性突触后电位(EPSP) ,分为第一成分和第二成分。随着刺激强度的增大 ,EPSP的幅度增大 ,反应持续时间延长。当刺激强度足够大时 ,在第一成分或第二成分的基础上可爆发动作电位。结论 :①刺激迷走神经可引起M细胞顺向激活 ,这与以往的观点不同 ;②从迷走神经到M细胞的感觉传入通路可能由含有兴奋性和抑制性成分的不同种类的神经链构成 ,M细胞的兴奋性取决于兴奋和抑制之间的相互关系     

硝酸士的宁对鲫鱼皮肤刺激诱发Mauthner细胞电位的影响

目的:探讨硝酸士的宁对刺激皮肤激活鲫鱼Mauthner细胞产生胞内电位的影响.方法:运用微电极穿刺技术.结果:①直接刺激皮肤,可在同侧或者对侧的M细胞产生一种高幅度的复合性突触后电位(postsynaptic potentials,PSPs).此反应在不同的刺激频率下表现出不同的幅度.②肌注硝酸士的宁后皮肤刺激诱发的胞内反应的幅度增加,甚至在原有去极化的基础上爆发动作电位.③将逆向动作电位重合到胞内反应的不同时刻,观察到逆向动作电位在整个由皮肤刺激诱发的胞内反应期间都降低.④肌注硝酸士的宁后逆向动作电位衰减的逐渐幅度减小,峰值提前,时程缩短,直至不发生衰减.结论:从皮肤到M细胞的传入通路中既有兴奋性成分,又有抑制性成分,二者相互制约平衡,对M细胞的兴奋性进行精密的调节.     

刺激鲫鱼小脑腹外侧区诱发的Mauthner细胞兴奋性突触后电位

实验采用微电极胞内记录技术探查鲫鱼Mauthner细胞(M-细胞)对小脑刺激的电反应特征。电刺激鲫鱼小脑腹外侧部,可在双侧M-细胞胞体、腹侧树突和外侧树突近端记录到一种复合性兴奋性突触后电位(小脑诱发性EPSP)。小脑诱发性EPSP潜伏期较短(0.63±0.09 ms),持续时间较长(5.49±1.13 ms),幅度分级和刺激频率依从等特征。以较高强度刺激小脑常引起M-细胞顺向激活。多点胞内连续穿刺实验显示小脑诱发性EPSP起源于腹侧树突远端。实验结果提示,小脑-M-细胞通路可能包含一组长短不等的神经元链,它们根据链的短或长,由近及远依次投射在腹侧树突远端。     

甘氨酸对鲫鱼视网膜ERG b-波和ON型双极细胞活动的调制

本工作在分离灌流的鲫鱼视网膜上研究了甘氨酸对明,暗视视网膜电图（ＥＲＧ）ｂ－波和胞内记录的ＯＮ型双极细胞反应的作用。结果表明,甘氨酸能明显压抑ＥＲＧ ｂ－波和ＯＮ型双极细胞的反应,其作用能为士的宁所翻转;甘氨酸对用谷氨酸分离的ＥＲＧ ＰⅢ成分（光感受器电位）无明显影响。这些结果提示,甘氨酸可能直接作用于双极细胞的受体,从而调节视网膜ＯＮ通路的活动。     

齿状回突触后电位和群峰电位的负相关现象

考察大鼠静卧状态下,相同强度刺激信号作用于前穿质通道时,海马齿状回颗粒细胞诱发电场电位的兴奋性突触后电位EPSP和群峰电位PS之间的一种负相关变化关系,即EPSP斜率减小时,PS幅值增加。采用同时记录齿状回诱发电位和大脑皮层ECoG电位的方法,分析诱发电位各成份和ECoG功率谱密度之间的关系,可见ECoG出现低频高幅慢波时,与ECoG出现高频低幅快波时比较,齿状回诱发响应的PS幅值较大,而EPSP斜率较小。这可能是因为：中脑网状结构上行激励系统通过丘脑－皮层回路使ECoG去同步化（出现低幅快波ECoG）时,同时也通过另一途径,即隔－海马连接,激活了作用于齿状回颗粒细胞胞体的抑制性神经通路,使得颗粒细胞兴奋性降低,从而使反应动作电位总和的PS幅值减小。在麻醉剂乌拉坦作用下,EPSP和PS的负相关变化减小或消失。这种负相关现象对于研究海马的生理功能具有重要的意义。     

大鼠背根节神经元后超极化中Ca~(2 )激活K~ 电流的蜂毒明肽敏感成分I_(AHP)

为了明确大鼠背根节（DRG）神经元中存在慢的Ca2 激活K 电流成分,本实验在新鲜分散的DRG神经元胞体上,采用全细胞电压箝技术,给予DRG神经元一定强度的去极化刺激,记录刺激结束后30ms时的尾电流幅度。结果发现：（1）随着去极化时间从1ms延长至180ms时,尾电流幅度由9．3±2．8pA逐渐增大至64.1±3．4pA（P＜0．001）;（2）当去极化结束后的复极化电位降低时,尾电流幅度先逐渐下降到零,然后改变方向,逆转电位约为-63mV;（3）细胞外施加500μmol／LCd2 或细胞内液中施加11mmol／LEGTA时尾电流明显减小甚至完全消失;（4）尾电流中慢成分的幅度在细胞外给与200nmol／L蜂毒明肽后,减小了约26.32±3。9％（P＜0。01）;（5）细胞外施加10mmol／LTEA,可明显降低尾电流中的快成分。结果提示,在DRG神经元启超极化中存在Ca2 激活K 电流的蜂毒明肽敏感成分──IAHP。     

瞬时外向钾电流的降低介导了慢性压迫背根神经节细胞兴奋性的升高

慢性压迫大鼠背根神经节（chronic compression of the dorsal root,ganglion,CCD）后,背根神经节细胞兴奋性升高,但引起神经元兴奋性改变的离子通道机制还需进一步探索。本实验采用胞内记录以及全细胞膜片钳记录方法,研究急性分离的大鼠背根神经节细胞兴奋性改变与瞬时外向钾电流（A-type potassium current,ⅠA）的关系。结果表明,CCD术后背根神经节细胞兴奋性升高,在急性分离的体外细胞中仍继续存在,表现为对辣椒素敏感的背根神经节细胞产生动作电位的最小电流刺激强度,即阈电流（current threshold）及阈电位（voltage threshold）降低;给予正常对照组神经元（未压迫损伤）瞬时外向钾通道阻断剂4-氨基吡啶,出现了类似CCD术后兴奋性升高的改变。进一步用两步电压钳方法分离ⅠA,研究CCD术后神经元ⅠA的变化,结果表明,CCD组神经元的ⅠA比对照组神经元ⅠA降低,并且与其阈电位的改变一致。以上结果提示,背根神经节压迫受损后,神经节细胞ⅠA降低可能参与介导了神经节细胞兴奋性的升高。     

强直电刺激嗅内皮质—海马环路诱发CAI神经元的癫痫同步性膜电位振？…

目的和方法：４００－５００μｍ大鼠水平脑切片吸封闭的ＥＣ－海马环路。强直电刺激（６０Ｈｚ,２ｓ）海马Ｓｃｈａｅｆｆｅｒ侧支诱发癫痫放电,全细胞记录ＣＡ１胞体层单个神经元电活动,同步记录相应树突外场电位,探讨单个神经元膜电位振荡特性和细胞外癫痫电活动之间的关系。结果：（１）强直电刺激诱发ＣＡ１神经元膜电位后放性振呈宽频特征（３－１００ＨＺ）。以θ节律多见,跟随在刺激引起的膜电位去极化或超极化偏移之后     

延髓腹外侧区在降压反射中的作用

在各种心血管反射中,降压反射是最主要的,延髓腹外侧区在降压反射中起重要作用。目前认为降压反射中枢通路中至少有四种成分是最基本的：（１）孤束核中的神经元;（２）延髓腹外侧头端的交感前运动细胞;（３）延髓腹外侧尾端;（４）疑核或和迷走神经背运动核。此外,兴奋性与抑制性氨基酸受体和抑制性神经元也是中枢通路的关键成分。下丘脑视上核与室旁核的升压素分泌细胞也有一定作用     

Reticulospinal and propriospinal monosynaptic influences on motoneurons in frogs

Monosynaptic effects evoked by electrical stimulation of suprasegmental structures and the ventral and lateral columns were recorded intracellularly from motoneurons of the lumbar and cervical enlargements after isolation of the spinal cord and medulla in frogs. Reticulospinal fibers arising from cells of the medial reticular formation of the medulla and running in the ventro-lateral columns evoke monosynaptic excitation of cervical and lumbar motoneurons. The reticulo-motoneuronal E PSPs do not exceed 2–3 mV in amplitude and do not reach the threshold for action potential generation. Division of the spinal cord and interaction between all synaptic inputs tested in chronic experiments showed that monosynaptic E PSPs evoked by direct stimulation of the ventral and lateral columns are due to activation of the descending system of propriospinal fibers. By transmembrane polarization experiments the equilibrium potentials of the reticulo-motoneuronal and propriospinal monosynaptic E PSPs could be determined.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Leningrad. Translated from Neirofiziologiya, Vol. 5, No. 2, pp. 164–173, March–April, 1973.     

Influence of oxytocin on integration of postsynaptic potentials in molluscan neurons.

1. Intracellular recordings were made from identified and non-identified neurons in perioesophageal ganglionic ring with buccal ganglia of the mollusc, Helix pomatia. The influence of oxytocin (OXT) on neuronal integration: space and temporal summations of postsynaptic potentials (PSPs) in various neurons was investigated. The obtained data indicated that these PSPs were cholinergic PSPs. 2. Ten minute exposure to 10(-8) M OXT had no effects on the resting membranes, but triggered secondary mechanisms, which lead to enhancement of the excitatory PSP (EPSR) amplitudes and the decrease of the decay time constant (tau EPSR) obtained from the falling phase of the EPSP. 3. The enhancement of the EPSP amplitude and the decrease of tau EPSP after OXT application evoked the appearance of action potential under space summation of two spontaneous EPSPs and made easier the appearance of action potential under temporal summation of EPSPs produced by paired afferent stimuli, when the corresponding interstimuli interval was smaller than tau EPSP in the presence of OXT. 4. Ten minute exposure to 10(-8) M OXT made the integrated amplitude of the excitatory acetylcholine response and the inhibitory dopamine response in the neuron E5 more positive only when the interval between applications of these mediators was smaller than the time constant of desensitization of acetylcholine receptors in the presence of OXT. 5. The pharmacological studies showed that drugs, which elevate intracellular cyclic AMP levels, mimicked the influence of OXT on integration of PSPs in the investigated neurons.     

Axonal effects of capsaicin: an electrophysiological study

The effects of axonally applied capsaicin on the discharge activity and compound action potential of the cat vagus, saphenous and phrenic nerves and the cervical sympathetic trunk were studied under in vivo and in vitro conditions. Application of capsaicin (10(-4) M) to the vagus, saphenous and phrenic nerves resulted in the appearance of intense discharge activity which reached its maximum after 3-4 min and lasted for 15-20 min. Parallel with the increase in discharge activity, elicited by orthodromic activation induced by capsaicin, the amplitudes of the A delta and C components of an antidromically evoked compound action potential were significantly reduced. After the excitatory action of capsaicin vanished, an increase in the latency and duration and a decrease in the amplitudes of the components of the compound action potential were observed which might have led to the development of a local block of impulse propagation. These changes proved to be reversible after the removal of capsaicin from the nerve. Compound action potentials recorded from the saphenous or vagus nerves pretreated with capsaicin 3-5 days before the experiments failed to show any significant changes. It is concluded that upon direct axonal application capsaicin results in the excitation of both A delta and C fibres which is followed by a nonspecific but reversible blockade of impulse propagation. The possible significance of these transient effects of axonally applied capsaicin in term of the development of the highly specific functional impairment occurring a few days after perineural capsaicin treatment remains to be elucidated.     

Elementary polysynaptic potentials of hippocampal neurons

Synaptic connections of 26 pairs of hippocampal neurons were studied in nonanesthetized rabbits by spike-triggered averaging of intracellularly recorded activity. Synchronized activity was detected in 5 pairs and considered to represent common inputs to the neurons recorded. Hyperpolarizing or depolarizing potentials with 3--4 ms latency were revealed in 3 additional pairs. These potentials are considered to be individual postsynaptic potentials (PSPs) evoked in the target neuron by spikes of the adjacent (0.5--2 mm apart) neuron. A quantum analysis of the individual PSPs was performed. The mean quantum content (0.27--0.65) and quantum size (35--200 mkV) were found to be of the same order as those of the excitatory PSPs previously recorded after intracerebral stimulation. It is concluded that most hippocampal synapses are of low efficacy.     

A comparison of electrically evoked and channel rhodopsin-evoked postsynaptic potentials in the pharyngeal system of Caenorhabditis elegans

Dissecting the function of neural circuits requires the capability to stimulate and record from the component neurones. Optimally, the methods employed should enable precise activation of distinct elements within the circuit and high-fidelity readout of the neuronal response. Here we compare two methods for neural stimulation in the pharyngeal system of Caenorhabditis elegans by evoking postsynaptic potentials (PSPs) either by electrical stimulation or by expression of the channelrhodopsin [ChR2(gf)] in cholinergic neurones of the pharyngeal circuit. Using a dissection that isolates the pharynx and its embedded neural system of 20 neurones permits analysis of the neurotransmitter pathways within this microcircuit. We describe protocols for selective electrically evoked or ChR2-mediated cholinergic synaptic events in this circuit. The latter was achieved by generating strains, punc-17::ChR2(gf);yfp, that express ChR2(gf) in cholinergic neurones. PSPs evoked by both electrical and light stimulation exhibited a rapid time-course and were blocked by cholinergic receptor antagonists and rapidly reversed on cessation of the stimulus. Electrically evoked PSPs were also reduced in a hypomorphic mutant for the synaptic vesicle acetylcholine transporter, unc-17, further indicating they are nicotinic cholinergic PSPs. The pharyngeal nervous system is exquisitely sensitive to both electrical and light activation. For the latter, short light pulses of 200 μs delivered to punc-17::ChR2(gf);yfp are capable of generating full muscle action potentials. We conclude that the application of optogenetic approaches to the C. elegans isolated pharynx preparation opens the way for a precise molecular dissection of synaptic events in the pharyngeal microcircuit by providing a molecular and system level analysis of the synapses that control the feeding behaviour of C. elegans.     

Magnesium-resistant excitatory synaptic potentials in the leech Retzius cell.

Postsynaptic potentials (PSPs) recorded from leech Retzius cells in response to stimulation of interganglionic connective could not be reversed by soma depolarization or abolished by 40 mM Mg ion, nor could input resistance changes be detected during them. Alteration of external Cl and K over a tenfold range provided no clear evidence that the PSPs involved a conductance change to either ion. The method of extrapolation yielded an apparent PSP equilibrium potential of about -20 mV. The steep portion of the relationship between Retzius cell action potential amplitude and membrane potential extrapolated to an apparent reversal potential of -13 mV. It is likely that the connective-to-Retzius cell PSPs were principally electrical events. Their apparent reversal potentials could have been in the range associated with chemical synapses because they traversed an electrical synapse with a variable coupling resistance, or because the polarizing currents, passing "backwards" across electrical synapses, changed the amplitude of the presynaptic action potentials.     

Magnesium-resistant excitatory synaptic potentials in the leech retzius cell

Postsynaptic potentials (PSPs) recorded from leech Retzius cells in response to stimulation of interganglionic connective could not be reversed by soma depolarization or abolished by 40 mM Mg ion, nor could input resistance changes be detected during them. Alteration of external Cl and K over a tenfold range provided no clear evidence that the PSPs involved a conductance change to either ion. The method of extrapolation yielded an apparent PSP equilibrium potential of about ?20 mV. The steep portion of the relationship between Retzius cell action potential amplitude and membrane potential extrapolated to an apparent reversal potential of ?13 mV. It is likely that the connective-to-Retzius cell PSPs were principally electrical events. Their apparent reversal potentials could have been in the range associated with chemical synapses because they traversed an electrical synapse with a variable coupling resistance, or because the polarizing currents, passing “backwards” across electrical synapses, changed the amplitude of the presynaptic action potentials.     

Spike-timing-dependent potentiation of sensory surround in the somatosensory cortex is facilitated by deprivation-mediated disinhibition

Functional maps in the cerebral cortex reorganize in response to changes in experience, but the synaptic underpinnings remain uncertain. Here, we demonstrate that layer (L) 2/3 pyramidal cell synapses in mouse barrel cortex can be potentiated upon pairing of whisker-evoked postsynaptic potentials (PSPs) with action potentials (APs). This spike-timing-dependent long-term potentiation (STD-LTP) was only effective for PSPs evoked by deflections of a whisker in the neuron's receptive field center, and not its surround. Trimming of all except two whiskers rapidly opened the possibility to drive STD-LTP by the spared surround whisker. This facilitated STD-LTP was associated with a strong decrease in the surrounding whisker-evoked inhibitory conductance and partially occluded picrotoxin-mediated LTP facilitation. Taken together, our data demonstrate that sensory deprivation-mediated disinhibition facilitates STD-LTP from the sensory surround, which may promote correlation- and experience-dependent expansion of receptive fields.     

Pre-junctional inhibitory action of prostaglandin E2 on excitatory neuro-effector transmission in the human bronchus

The effects of prostaglandin E2 (PGE2) and indomethacin on excitatory neuro-effector transmission in the human bronchus were investigated by tension recording and microelectrode methods. PGE2 (10(-10)-10(-9)M) suppressed the amplitude of twitch contractions and excitatory junction potentials (e.j.ps) evoked by field stimulation at a steady level of basal tension obtained by the combined application of indomethacin (10(-5) M) and FPL55712 (10(-6) M). In doses over 10(-8)M, PGE2 reduced the muscle tone and dose-dependently suppressed the amplitude of twitch contractions. Indomethacin (10(-5) or 5 x 10(-5) M) reduced the muscle tone and enhanced the amplitude of twitch contractions and e.j.ps evoked by field stimulation in the presence of FPL55712. PGE2 (10(-9) M) had no effect on the post-junctional response of smooth muscle cells to exogenously applied acetylcholine (ACh) (4 x 10(-7) M). However, indomethacin (10(-5) M) significantly enhanced the ACh-induced contraction of the human bronchus. These results indicate that PGE2 in low concentrations has a pre-junctional action to inhibit excitatory neuro-effector transmission in addition to a post-junctional action, presumably by suppressing transmitter release from the vagus nerve terminals in the human bronchial tissues.