大鼠旁巨细胞外侧核呼吸神经元的型及其对某些递质类药物的反应

目的和方法：用细胞外记录法和多管微电极微电泳法在36只麻醉自主呼吸的SD大鼠,系统探查旁巨细胞外侧核尾兰侧（cPGCL）和呼吸神经元（RNs）的类型及该区的递质受体情况,结果：在14只大鼠系统探查,记录到39个RNs,包括吸气神经元24个、呼气神经元12个和跨时相神经元3个。在另22只大鼠,观察到微电泳谷氮酸钠（L－Glu)使12／14个RNs兴奋,γ－氨基丁酸（GABA）使全部受试RNs抑制(n=22);对NMDA受体拮抗剂DL－2－氨基－5－磷酸戊酸（AP5）、GABAA受体拮抗剂荷包牡丹碱（BIC）有兴奋、抑制和无作用三类效应;AP5部分阻断大部分受试神经元（6／9个）对L－Glu的兴奋反应,BIC部分或完全阻断大部分受试神经元（9／11个）,对GABA的抑制反应。结论：PGCL是呼吸调控的重要中枢部位之一,该区可能存在起神经递质作用的内源性L－Glu和GABA及兴雷性氨基酸（包括NMDA和非NMDA）受体和GABAA受体,它们可能介导PGCL对呼吸的调控。     

5－羟色胺对大鼠下丘脑脑片弓状核神经元自发电活动的影响

在７４张大鼠下丘脑脑片上,用玻璃微电极记录到弓状核自发放电单位１７６个,其放电形式有三种：慢不规则型（１１９个,６７．６％）;快连续型（４６个,２６．１％）;位相型（１１个,６．３％）。５－ＨＴ（１０－６ｍｏｌ／Ｌ,３ｍｉｎ）对不同形式放电单位的作用均以抑制为主：对部分慢不规则单位（９／１１９）则表现为先抑制后兴奋的双相性反应,对少数神经元有兴奋作用。１２个被５－ＨＴ抑制的单位,其抑制作用不能被噻庚啶（ＣＨＤ,１０－５ｍｏｌ／Ｌ）阻断,４个被５－ＨＴ抑制的的单位中,其抑制作用可被二甲基麦角新碱（ＭＳＧ１０－６ｍｏｌ／Ｌ）部分或完全阻断。７个被５－ＨＴ抑制的单位,其中４个单位中,５－ＨＴ的抑制作用可被特异性５－ＨＴ１Ａ受体阻断剂Ｐｉｎｄｏｂｉｎｄ－５－ＨＴ１Ａ部分阻断;但另外３个单位的阻断效果不明显。上述结果表明：５－ＨＴ对弓状核不同形式放电单位的作用均以抑制为主,其作用可能是通过５－羟色胺（５－ＨＴ１）受体介导的,部分还可能是通过５－ＨＴ１Ａ受体介导的。     

γ—氨基丁酸能抑制可镜化大棕蝠听皮层神经元频率调谐

本实验使用了9只成年健康的大棕蝠（Eptesicus fuscus）。采用双声刺激和多管电极电泳导入荷包牡丹碱（bicuculline,Bic）的方法,研究了γ－氨基丁酸（γ－aminobutyric,GABA）能抑制在锐化听皮层（primary auditory cortex,AC,即初级听皮层）神经元频率调谐中的作用。结果发现：正常AC神经元的频率调谐曲线表现出单峰开放式、多峰开放式和单峰封闭式2种类型;用双声刺激方法研究证实,至AC神经元的抑制性输入能被抑制性声刺激所激活,且这种神经抑制有自身的最佳频率,根据其对兴奋反应的影响程度和系统地改变抑制性声刺激的强度,可在兴奋性频率调谐曲线或兴奋区的高频边或／和低频边测出抑制性频率调谐曲线或抑制区;当这种抑制性输入被抑制性声刺激激活后,能降低阈上10fB声强引起的兴奋反应的发放率,抑制效率随抑制声刺激强度的增强而加强;电泳GABAa受体拮抗剂荷包牡丹碱Bic后,可不同程度地去GABA能抑制参与构成至AC神经元的抑制性输入,在正常情况下这种抑制有助于提高中枢听神经元的信号／噪声比和频率分析能力,并锐化频率调谐,因此本结果在正常情况下这种抑制有助于提高中枢听神经元的信号／噪声比和频率分析能力,并锐化频率调谐,因此本结果提示,声音的各参量中所包含的信息从外周传入中枢后,随着中枢的升级,逐级抽提整合成若干特征,直至在AC形成某种“声像（sound image)”,对大多数AC神经元而言,GABA能抑制在该过程中起关键作用。     

γ-氨基丁酸能抑制对大棕蝠听皮层神经元声反应特性的影响

为了探讨γ－氨基丁酸（γ-aminobutyric acid,GABA)能抑制对大棕蝠(Eptesicus fuscus)听皮层(auditory cortex,AC)神经元声反应特性的影响,采用多管微电极电泳方法,观察了8只大棕蝠AC神经元去ABA能抑制前后声刺激诱发的反应。结果显示,微电泳GABAa受体拮抗剂荷包牡丹碱(bicuculline,Bic)去ABA能抑制可改变声刺激诱发的反应模式;极大地增加神经元冲动发放率,缩短反应的潜伏期和降低反应的最小阈值;不同程度地改变强度－发放率和强度－潜伏期函数。结果提示：1、GABA能抑制对AC神经元声信号处理起重要作用;2、GABA能抑制可改变AC神经元兴奋性支配或输入的效应,并因此定型AC神经元的声反应性质,即发放模式、阈值、强度－发放率和强度－潜伏期函数;3、GABA能抑制为AC神经元的声诱发活动提供一种调制性抑制。     

GABA介导杏仁外侧核对皮层A Ⅰ区神经元声反应的抑制:在体微电泳研究

在SD大鼠上应用多顺利完成微电极方法,观察微电泳CABA及其受体的拮抗剂或激动剂对杏仁外侧核（LA）抑制皮层AⅠ神经元声反应效应的影响。结果显示,电泳GABA能抑制皮层AⅠ区神经元的电活动,电泳GABAA受体拮抗剂bicuculline（BIC）则能易化其反应;电刺激LA能抑制皮层AⅠ区听神经元声反应,电泳GABA产生类拟于刺激LA的抑制效应;LA对皮层AⅠ区神经的抑制效应能被BIC所翻转,而不能被什氨酸受体拮抗剂strychnine所翻转,电泳GABAB型受体例激动剂baclofen对神经元声反应无影响。上术结果表明,GABA可能是介民LA抑制皮层AⅠ区神经元声反应的最终递质,并且是通过GABAA受体作用的。     

γ-氨基丁酸对离体大鼠延髓头端腹外侧区神经元单位放电的抑制作用

在７３张脑片上观察了γ－氨基丁酸（ＧＡＢＡ）对１０６个延髓头端腹外侧区（ＲＶＬＭ）神经元单位放电的影响。外源性的ＧＡＢＡ（０．１￣３．０ｍｍｏｌ／Ｌ）抑制了１０６神经元中的８４个神经元的电活动,这些抑制效应呈剂量－反应关系。ＧＡＢＡ的抑制效应大部分可被ＧＡＢＡＡ受体选择性拮抗剂荷苞牡丹碱甲基碘化物（ＢＭＩ）和Ｃｌ＾－通道阻断剂印防己毒素（ＰＴＸ）所阻断,而单独灌流ＢＭＩ和ＰＴＸ对ＲＶＬＭ神经元主要     

P物质抑制培养大鼠海马大锥体细胞GABA—激活电流

研究主要探讨P物质（SP）对GABA－激活电流的调制。实验在培养的新生大鼠海马大锥体细胞上进行。应用全细胞膜片箝技术记录GABA激活的内向电流。在被检的大锥体细胞中,有72％（66／92）的神经元对GABA和SP同时敏感,预后SP后,GABA激活电流明显地被抑制,此抑制作用是呈剂量依赖性的。在预加10^-8,10^-7,10^-6,10^-5mol/LSP后,GABA的激活电流分别降低18％,24．8％,25．9％和28％,用SP的拮抗剂 spantide能阻断此种抑制作用,在电极中灌注H7（PKC抑制剂）能取消此抑制作用,上述结果提示：SP对GABA激活电流的抑制作用是SP作用于SP受体,通过胞内第二信使,使GABAA受体通道复合体胞内磷酸化所致。     

刺激中缝背核对大鼠小脑皮层下核团神经元电活动的影响

我们首次观察了电刺激大鼠中缝背核（ＤＲ）对小脑核团（ＤＣＮ）──内侧核（ＭＮ）,间位核（ＩＮ）和外侧核（ＬＮ）神经元电活动的影响。结果表明：刺激ＤＲ可引起ＤＣＮ神经元的抑制、兴奋和双相（兴奋－抑制、抑制－兴奋）三种不同类型的反应,其中以抑制性反应为主（７６％－９０％）;反应的潜伏期为１０—８４ｍｓ,但大多数细胞呈现小于３０ｍｓ的短潜伏期反应;ＤＣＮ细胞的自发放电频率为５－１２０Ｈｚ,自发放电频率高的神经元群体对ＤＲ刺激的反应比率却比自发放电频率低的群体低;静脉注射５－ＨＴ２／１ｃ受体阻断剂ｍｅｔｈｙｓｅｒｇｉｄｅ可以阻断ＤＣＮ细胞对ＤＲ刺激的抑制性反应（６６．７％－８３．３％）。这些结果提示中缝－小脑５－ＨＴ能纤维传入系统可能通过对ＤＣＮ细胞电活动的调制作用参予小脑的感觉运动整合过程。     

吗啡对培养海马神经元钙离子作用的机制研究

目的：研究吗啡对海马神经元[Ca^2 ]i影响的机制,为探索吗啡成瘾的神经生物学机制与可能的治疗途径。方法：荧光探针Fluo-4标记细胞内游离钙后,用激光共聚焦显微镜检测吗啡对大鼠原代培养海马神经元[Ca^2 ]i的影响。结果：吗啡急性刺激引起海马神经元[Ca^2 ]i升高,CTOP不能阻断吗啡引起的细胞内[Ca^2 ]i增加,而naltrindole能阻断吗啡引起的细胞内[Ca^2 ]i反应;Thapsigargin预处理阻断吗啡诱导的细胞内[Ca^2 ]i增加,Verapamil预处理不能完全抑制吗啡引起的细胞内[Ca^2 ]i增加;吗啡长时程作用后,海马神经元[Ca^2 ]i升高,加入纳络酮急性戒断后,不能阻断吗啡引起的细胞内[Ca^2 ]i升高,反而引起[Ca^2 ]i异常升高。结论：吗啡急性刺激引起的海马神经元内游离钙增加主要来源于δ2阿片受体介导的IP3敏感的钙库释放。     

刺激中缝背核调制小脑间位核神经元电活动

刺激中缝背核（ｄｏｒｓａｌｒａｐｈｅｎｕｃｌｅｕｓ,ＤＲ）可以引起小脑间位核（ｉｎｔｅｒｐｏｓｅｄｎｕｃｌｅｕｓ,ＩＮ）神经元抑制,兴奋和双相（抑制－兴奋和兴奋－抑制）３种不同类型的反应,其中以抑制反应为主（７６．０％）,多数细胞的反应潜伏期〈３０ｍｓ。ＩＮ细胞的自发放电频率为５－１２０Ｈｚ,自发放电频率高的神经元群体对ＤＲ刺激的反应率却比自发放电频率低的群体低。静脉注射５－ＨＴ２／１ｃ受体阻断剂     

Ca2+ influx into identified leech neurons induced by 5-hydroxytryptamine

The role of 5-hydroxytryptamine (5-HT, serotonin) in the control of leech behavior is well established and has been analyzed extensively on the cellular level; however, hitherto little is known about the effect of 5-HT on the cytosolic free calcium concentration ([Ca(2+)](i)) in leech neurons. As [Ca(2+)](i) plays a pivotal role in numerous cellular processes, we investigated the effect of 5-HT on [Ca(2+)](i) (measured by Fura-2) in identified leech neurons under different experimental conditions, such as changed extracellular ion composition and blockade of excitatory synaptic transmission. In pressure (P), lateral nociceptive (N1), and Leydig neurons, 5-HT induced a [Ca(2+)](i) increase which was predominantly due to Ca(2+) influx since it was abolished in Ca(2+)-free solution. The 5-HT-induced Ca(2+) influx occurred only if the cells depolarized sufficiently, indicating that it was mediated by voltage-dependent Ca(2+) channels. In P and N1 neurons, the membrane depolarization was due to Na(+) influx through cation channels coupled to 5-HT receptors, whereby the dose-dependency suggests an involvement in excitatory synaptic transmission. In Leydig neurons, 5-HT receptor-coupled cation channels seem to be absent. In these cells, the membrane depolarization activating the voltage-dependent Ca(2+) channels was evoked by 5-HT-triggered excitatory glutamatergic input. In Retzius, anterior pagoda (AP), annulus erector (AE), and median nociceptive (N2) neurons, 5-HT had no effect on [Ca(2+)](i).     

Effects of 5-hydroxytryptamine on the neuronal firing rate of bulbar reticular neurons

The effects of 5-hydroxytryptamine (5-HT) on neuronal firing rate were studied in the reticular gigantocellular nucleus (GRN) and, for a comparison, in the interstitial (IRN), the parvicellular (PRN) and the lateral (LRN) nuclei, sharing some of GRN functional characteristics. Unitary extracellular recordings performed in anesthetized rats demonstrated that microiontophoretic application of 5-HT modulated the background firing rate in 92% of GRN, in 100% of IRN and LRN, and in 77% of PRN tested neurons. In GRN, 5-HT application induced excitatory responses in 49% of the neurons tested and inhibitions in 43% of them. Both types of effects were dose dependent and appeared scattered throughout the nucleus. Enhancements and decreases of firing rate in response to 5-HT application were also recorded in IRN (58% and 42% respectively), LRN (43% and 57%) and PRN (36% and 41%). The 5-HT(1A) receptor agonist 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT) mimicked 5-HT evoked inhibitions in all the nuclei tested and induced weak inhibitory responses also in neurons excited by 5-HT. The 5-HT2A receptor agonist alphamethyl-5-hydroxytryptamine (alpha-me-5-HT) mimicked excitatory as well as inhibitory responses to 5-HT, the former prevailing in GRN and the latter in the remaining reticular nuclei. Both excitatory and inhibitory responses to 5-HT were partially or totally blocked by the application of 5-HT2 receptor antagonist ketanserin. It is concluded that an extended, strong and differentiated control is exerted by 5-HT on the electrical activity of bulbar reticular neurons. Both 5-HT(1A) and 5-HT(2A) receptors mediate these effects, but the involvement of other receptors appears probable.     

Attenuation of the serotonin-induced increase in intracellular calcium in rat aortic smooth muscle cells by sarpogrelate

Although serotonin (5-HT) induced proliferation of vascular smooth muscle cells is considered to involve changes in intracellular Ca2+ ([Ca2+]i), the mechanism of Ca2+ mobilization by 5-HT is not well defined. In this study, we examined the effect of 5-HT on rat aortic smooth muscle cells (RASMCs) by Fura-2 microfluorometry for [Ca2+]i measurements. 5-HT was observed to increase the [Ca2+]i in a concentration- and time-dependent manner. This action of 5-HT was dependent upon the extracellular concentration of Ca2+ ([Ca2+]e) and was inhibited by both Ca2+ channel antagonists (verapamil and diltiazem) and inhibitors of sarcoplasmic reticular Ca2+ pumps (thapsigargin and cyclopia zonic acid). The 5-HT-induced increase in [Ca2+]i was blocked by sarpogrelate, a 5-HT2A-receptor antagonist, but not by different agents known to block other receptor sites. 5-HT-receptor antagonists such as ketanserin, cinanserin, and mianserin, unlike methysergide, were also found to inhibit the 5-HT-induced Ca2+ mobilization, but these agents were less effective in comparison to sarpogrelate. On the other hand, the increase in [Ca2+]i in RASMCs by ATP, angiotensin II, endothelin-1, or phorbol ester was not affected by sarpogrelate. These results indicate that Ca2+ mobilization in RASMCs by 5-HT is mediated through the activation of 5-HT2A receptors and support the view that the 5-HT-induced increase in [Ca2+]i involves both the extracellular and intracellular sources of Ca2+.     

Receptor-induced Ca(2+) signaling in cultured myenteric neurons

We studied the effect of excitatory neurotransmitters (10(-5) M) on the intracellular Ca(2+) concentration ([Ca(2+)](i)) of cultured myenteric neurons. ACh evoked a response in 48.6% of the neurons. This response consisted of a fast and a slow component, respectively mediated by nicotinic and muscarinic receptors, as revealed by specific agonists and antagonists. Substance P evoked a [Ca(2+)](i) rise in 68.2% of the neurons, which was highly dependent on Ca(2+) release from intracellular stores, since after thapsigargin (5 microM) pretreatment only 8% responded. The responses to serotonin, present in 90.7%, were completely blocked by ondansetron (10(-5) M), a 5-HT(3) receptor antagonist. Specific agonists of other serotonin receptors were not able to induce a [Ca(2+)](i) rise. Removing extracellular Ca(2+) abolished all serotonin and fast ACh responses, whereas substance P and slow ACh responses were more persistent. We conclude that ACh-induced signaling involves both nicotinic and muscarinic receptors responsible for a fast and a more delayed component, respectively. Substance P-induced signaling requires functional intracellular Ca(2+) stores, and the 5-HT(3) receptor mediates the serotonin-induced Ca(2+) signaling in cultured myenteric neurons.     

Calcium influx into dendrites of the leech Retzius neuron evoked by 5-hydroxytryptamine

5-Hydroxytryptamine (5-HT) is a ubiquitous neurotransmitter and neuromodulator that affects neural circuits and behaviours in vertebrates and invertebrates. In the present study, we have investigated 5-HT-induced Ca(2+) transients in subcellular compartments of Retzius neurons in the leech central nervous system using confocal laser scanning microscopy, and studied the effect of 5-HT on the electrical coupling between the Retzius neurons. Bath application of 5-HT (50mM) induced a Ca(2+) transient in axon, dendrites and cell body of the Retzius neuron. This Ca(2+) transient was significantly faster and larger in dendrites than in axon and cell body, and was half-maximal at a 5-HT concentration of 5-12mM. The Ca(2+) transient was suppressed in the absence of extracellular Ca(2+) and by methysergide (100mM), a non-specific antagonist of metabotropic 5-HT receptors, and was strongly reduced by bath application of the Ca(2+) channel blocker Co(2+) (2mM). Injection of the non-hydrolysable GTP analogue GTPgammaS increased and prolonged the dendritic 5-HT-induced Ca(2+) transient. The non-selective protein kinase inhibitor H7 (100mM) and the adenylate cyclase inhibitor SQ22536 (500 mM) did not affect the Ca(2+) transient, and the membrane-permeable cAMP analogue dibutyryl-cAMP (500 mM) did not mimic the effect of 5-HT application. 5-HT reduced the apparent electrical coupling between the two Retzius neurons, whereas suppression of the Ca(2+) influx by removal of external Ca(2+) improved the transmission of action potentials at the electrical synapses which are located between the dendrites of the adjacent Retzius neurons. The results indicate that 5-HT induces a Ca(2+) influx through calcium channels located primarily in the dendrites, and presumably activated by a G protein-coupled 5-HT receptor. The dendritic Ca(2+) increase appears to modulate the excitability of, and the synchronization between, the two Retzius neurons.     

Opposite effects of presynaptic 5-HT3 receptor activation on spontaneous and action potential-evoked GABA release at hippocampal synapses

5-HT(3) (serotonin type 3) receptors are targets of antiemetics, antipsychotics, and antidepressants and are believed to play a role in cognition. Nevertheless, contrasting results have been obtained with respect to their functions in the CNS and in the control of transmitter release. We used rat hippocampal neurons in single-neuron microcultures to identify the roles of presynaptic 5-HT(3) receptors at central synapses. 5-HT (10 microm) caused a transient > 10-fold increase in the frequency of miniature inhibitory postsynaptic currents without affecting amplitudes or kinetics. This effect was abolished by tropisetron (30 nm) and when Ca(2+) channels were blocked by 100 microm Cd(2+) it was mimicked and occluded when neurons were depolarized by 20 mm, but not 10 mm, K(+). Thus, activation of presynaptic 5-HT(3) receptors increased spontaneous GABA release by causing depolarization and opening of voltage-gated Ca(2+) channels. In microculture neurons, 5-HT transiently reduced action potential-evoked inhibitory autaptic currents by > 50%; this effect was blocked by tropisetron and mimicked by 20 mm, but not 10 mm, K(+). Miniature excitatory postsynaptic currents were not altered by 5-HT. Excitatory autaptic currents were tonically reduced, an effect attenuated by 5-HT(1A) antagonists. Thus, presynaptic 5-HT(3) receptors control GABA, but not glutamate, release and mediate opposite effects on spontaneous and action potential-dependent release.     

Physiological and pharmacological properties of responses to GABA and ACh by abdominal motor neurons in Manduca sexta

1. GABA, ACh, and other agents were applied by pressure ejection to the neuropil of the third abdominal ganglion in the isolated nerve cord of Manduca sexta. Intersegmental muscle motor neurons with dendritic arborizations in the same hemiganglion were inhibited by GABA (Fig. 2) and excited by ACh (Fig. 5).
2. Picrotoxin was a potent antagonist of GABA (Fig. 4A). Bicuculline reduced GABA responses in some motor neurons (Fig. 4C), but had no effect on many other motor neurons. Curare reduced ACh responses (Fig. 6A). Bicuculline was an effective ACh antagonist in most motor neurons tested (Fig. 6B).
3. Motor neurons with dendrites across the ganglion from the ejection pipette exhibited different responses to GABA and ACh. Contralateral motor neurons often showed smaller, delayed hyperpolarizing GABA responses (Fig. 7). On two occasions, contralateral motor neurons had excitatory responses (Fig. 8). Contralateral motor neurons were hyperpolarized by ACh (Fig. 9). The inhibitory responses had only slightly longer latencies than ipsilateral excitatory ACh responses (Fig. 10A). The contralateral inhibitory ACh responses, but not the ipsilateral excitatory ACh responses, were eliminated by TTX (Fig. 10B).
4. A model, which includes inhibitory interneurons that cross the ganglionic midline to inhibit their contralateral homologs and motor neurons (Fig. 11), is proposed to account for contralateral responses to GABA and ACh and antagonistic patterns of activity of motor neurons during mechanosensory reflex responses.

     

5-Hydroxytryptamine stimulates net Ca2+ flux in the ventricular muscle of a mollusc (Busycon canaliculatum) during cardioexcitation.

Noninvasive, self-referencing calcium (Ca2+) electrodes were used to study the mechanisms by which 5-hydroxytryptamine (5-HT) affects net Ca2+ flux across the sarcolemma of myocytes from ventricular trabeculae (from a marine gastropod, Busycon canaliculatum). Treatment of isolated trabeculae with 5-HT causes a net Ca2+ efflux, which is 30% blocked by verapamil. These findings suggest that the efflux is in part the result of a previous Ca2+ influx through L-type Ca2+ channels and is due to a rapid Ca2+ extrusion mechanism inherent to the sarcolemma of these myocytes. 5-HT-induced net Ca2+ efflux is also reduced by about 40% by treatment with a sodium (Na+)-free, lithium (Li+)-substituted saline, which shuts down the Na-Ca exchanger during Ca2+ extrusion. Cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ ATPase, almost completely abolishes the 5-HT-induced net Ca2+ efflux, suggesting that the SR rather than the extracellular pool is the primary Ca2+ reservoir serving 5-HT-induced excitation.     

Studies on the stereoselective effects of a novel 5-HT2 receptor antagonist on contractile responses of rat aorta

The effect of the enantiomers of a novel 5-HT2 receptor antagonist, (+/-)-(1R,3S)-1-[2-[4-[3-(p-fluorophenyl)-1-indanyl]-piperazinyl] ethyl]-2-imidazolidinone, was studied on serotonin (5-HT), noradrenaline (NA), potassium (K+), and calcium (Ca2+)-induced contractions in isolated rat thoracic aorta. The enantiomers shifted the 5-HT, NA, K+, and Ca2+ concentration-response curves to the right in a concentration-dependent manner and depressed the maximal contractile responses. The (+)-enantiomer was a far more potent inhibitor of 5-HT-induced contractions than the (-)-enantiomer. The (+)-enantiomer and phentolamine, both at 10(-6) M, had equal inhibitory effects on NA-evoked contractions. The (+)-enantiomer was again more potent inhibiting NA-induced contractions than the (-)-enantiomer. Both enantiomers had an equieffective inhibitory effect on K+ and Ca2(+)-induced contractions. The results show that the 5-HT and alpha-adrenoceptor antagonism of the two enantiomers is stereoselective, the (+)-enantiomer being more potent than the (-)-enantiomer. In contrast the enantiomers had equal, nonstereoselective inhibitory effects on K+ and Ca2(+)-evoked contractions.     

Effect of antagonists of serotonin receptors on modulation with serotonin of synaptic activity of projectional neurons of rat amygdala dorsolateral nucleus

The work studies role of different receptor types of serotonin (5-hydroxytryptamine; 5-HT) in the process of synaptic activity modulation with 5-HT of rat dorsolateral amygdala projection neurons. The selective antagonist of 5-HT_1,2 receptors methylsergid maleate was shown to suppress the 5-HT inhibitory action on amplitude of the postsynaptic currents evoked by glutamate and GABA, whereas the antagonist of 5-HT_3,4 receptors SDZ202-557 produced no effect on the above-mentioned 5-HT action. The obtained action indicates that the 5-HT modulatory effect on the projectional neuron synaptic inputs is mediated by 5-HT receptors of the 1 and 2 types.