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Effects of chronic lead exposure on short-term and long-term depression in area CA1 of the rat hippocampus in vivo

CHEMOSPHERE 2000年第1-2期41卷 165-171页

作者： Ruan, DY Yan, KF Ge, SY Xu, YZ Chen, JT Wang, M Univ Sci & Technol China Sch Life Sci Anhua 230027 Peoples R China

Chronic developmental lead (Pb) exposure to the rat has been reported to impair the long-term potentiation (LTP) in area CAI and DG of the hippocampus. The present study was performed to investigate the effects of chronic Pb exposure on homosynaptic short-term depression (STD) and long-term depression (LTD) of population spikes (PS) in area CA1 of the rat hippocampus in vivo. Neonatal Wistar rats were exposed to Pb from parturition to weaning via the milk of dams fed with 0.2% lead acetate solution. The input/output (I/O) function, paired-pulse reaction (PPR), the PS were measured in the area CA1 in response to low frequency stimulation (LFS). The results showed that the home-STD amplitude of PS depotentiation in Pb-exposed rats (87.48 +/- 7.44%, n = 14) was less significant than that in control rats (72.34 +/- 6.05%, n = 18, P < 0.05), and the home-LTD amplitude of PS depotentiation in Pb-exposed rats (72.80 +/- 5.86%, n = 14) was even less significant than that in control rats (47.80 +/- 5.03%, n = 18, P < 0.01). The results suggest that chronic Pb exposure in neonatal rats caused impairments in the STD and LTD of area CAI of hippocampus. (C) 2000 Elsevier Science Ltd. All rights reserved.

关键词：动物新生电刺激脑电描记术诱发电位/药物作用海马/药物作用海马/生理学铅/副作用大鼠 Wistar 突触传递/药物作用动物女(雌)性男(雄)性大鼠

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Adenosine A1 and class II metabotropic glutamate receptors mediate shared presynaptic inhibition of retinotectal transmission

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JOURNAL OF NEUROPHYSIOLOGY 1999年第6期82卷 2947-2955页

作者： Zhang, CY Schmidt, JT SUNY Albany Neurobiol Res Ctr Albany NY 12222 USA SUNY Albany Dept Biol Sci Albany NY 12222 USA

Presynaptic inhibition is one of the major control mechanisms in the CNS. Previously we reported that adenosine Al receptors mediate presynaptic inhibition at the retinotectal synapse of goldfish. Here we extend these findings to metabotropic glutamate receptors (mGluRs) and report that presynaptic inhibition produced by both Al adenosine receptors and group II mGluRs is due to Gi protein coupling to inhibition of N-type calcium channels in the retinal ganglion cells. Adenosine (100 mu M) and an Al (but not A2) receptor agonist reduced calcium current (ICa2+) by 16-19% in cultured retinal ganglion cells, consistent with their inhibition of retinotectal synaptic transmission (-30% amplitude of field potentials). The general metabotropic glutamate receptor (mGluR) agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD, 50 mu M) and the selective group II mGluR receptor agonist (2S,2'R,3'R)-2-(2',3'-dicarboxy-cyclopropyl)glycine (DCG-IV, 300 nM) inhibited both synaptic transmission and ICa2+ whereas the group III mGluR agonist L-2-amino-4-phosphono-butyrate (L-AP4) inhibited neither synaptic transmission nor ICa2+. When the N-type calcium channels were blocked with omega-conotoxin GVIA, both adenosine and DCG-IV had much smaller percentage effects on the residual 20% of ICa2+ suggesting effects mainly on the N-type calcium channels. The inhibitory effects of A1 adenosine receptors and mGluRs were both blocked by pertussis toxin, indicating that they are mediated by either Gi or G(o). They were also inhibited by activation of protein kinase C (PKC), which is known to phosphorylate and inhibit G(i). Finally, when applied sequentially, inhibition by adenosine and DCG-IV were not additive but occluded each other. Together these results suggest that adenosine A1 receptors and group LT mGluRs mediate presynaptic inhibition of retinotectal synaptic transmission by sharing a pertussis toxin (PTX)-sensitive, PKC-regulated G(i) protein coupled to N-type calcium chan

关键词：腺苷/药理学钙通道/药物作用钙通道/生理学细胞培养的环丙烷类/拮抗剂和抑制剂酶激活/生理学 GTP结合蛋白质α亚单位 Gi-Go/生理学甘氨酸/类似物和衍生物甘氨酸/拮抗剂和抑制剂金鱼膜电位/生理学百白咳毒素蛋白激酶C/代谢嘌呤能P1受体激动剂受体亲代谢性谷氨酸盐/拮抗剂和抑制剂受体亲代谢性谷氨酸盐/生理学受体突触前/药物作用受体突触前/生理学受体嘌呤能P1/生理学视网膜/生理学视网膜神经节细胞/生理学上丘/生理学突触/生理学突触传递/药物作用突触传递/生理学毒力因子鲍特菌属/药理学动物

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Effects of a naturally occurring neurosteroid on GABA_A IPSCs during development in rat hippocampal or cerebellar slices

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期521卷 437-449页

作者： Cooper, EJ Johnston, GAR Edwards, FA UCL Dept Physiol London WC1E 6BT England Univ Sydney Dept Pharmacol Sydney NSW 2006 Australia

1. The effects of the naturally occurring neurosteroid tetrahydrodeoxycorticosterone (THDOC) on GABA(A) receptor-mediated miniature, spontaneous and evoked IPSCs was tested using patch-clamp techniques in slices of hippocampus and cerebellum from rats at two developmental stages (similar to 10 and similar to 20 days postnatal). The cells studied were hippocampal granule cells and cerebellar Purkinje and granule cells. 2. Most miniature GABAergic currents (mIPSCs) decayed with two exponentials and neurosteroids caused a similar to 4-fold increase in the decay time constant of the second exponential at the highest concentration used (2 mu M). Similar effects were seen at high concentrations of THDOC (1-2 mu M) in all cell groups tested. No effects were seen on amplitude or rise time of mIPSCs. 3. The effects of THDOC (1 mu M) were shown to be stereoselective and rapidly reversible, indicating that the neurosteroid binds to the GABA(A) receptor, rather than acting genomically. 4. At concentrations of THDOC likely to occur physiologically (50-100 nM), the decay time of IPSCs was also enhanced (25-50%) in all cerebellar cell groups tested. In contrast, at 100 nM THDOC, seven of 11 hippocampal granule cells were sensitive from the 10 day group but the 20 day hippocampal granule cells showed no significant enhancement in the presence of these lower concentrations of THDOC. 5. The differences in sensitivity of hippocampal and cerebellar cells to THDOC are compared to data reported in the literature on regional development of expression of different receptor subunits in the brain and it is suggested that the progressive relative insensitivity of the 20 day hippocampal cells may depend on increasing expression of the delta subunit of the GABA(A) receptor and possibly an increase in the alpha 4 subunit.

关键词：抗焦虑药/化学抗焦虑药/药理学脱氧皮质酮/类似物和衍生物脱氧皮质酮/化学脱氧皮质酮/药理学剂量效应关系药物电刺激诱发电位/药物作用海马/化学海马/生理学膜电位/药物作用膜电位/生理学器官培养技术膜片钳术浦肯野细胞/化学浦肯野细胞/生理学大鼠 Wistar 受体 GABA-A/生理学立体异构现象突触传递/药物作用突触传递/生理学动物男(雄)性大鼠

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Presynaptic muscarinic facilitation of parasympathetic neurotransmission after sympathectomy in the rat choroid

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期294卷 627-632页

作者： Steinle, JJ Smith, PG Univ Kansas Med Ctr Dept Mol & Intergrat Physiol Kansas City KS 66160 USA Univ Kansas Med Ctr RL Smith Mental Retardat Res Ctr Kansas City KS 66160 USA

The effect of sympathectomy on parasympathetic regulation of ocular perfusion was investigated. Uveal blood flow through the vortex veins was measured by laser Doppler flowmetry during electrical stimulation of the superior salivatory nucleus, which activates ocular parasympathetic nerves, in adult rats with intact innervation and 2 days or 6 weeks after excision of the ipsilateral superior cervical ganglion. In all groups, parasympathetic stimulation produced comparable increases in flux, which were abolished by the selective neuronal nitric-oxide synthetase inhibitor, 1-(2-trifluoromethylphenyl) imidazole. Atropine had no effect in control and acutely sympathectomized rats but abolished the flux increase in four of six chronically sympathectomized animals, and 1-(2-trifluoromethylphenyl) imidazole eliminated the residual response. The muscarinic receptor agonist bethanechol did not affect basal flow in control or sympathectomized rats. However, bethanechol enhanced parasympathetically mediated vasodilation, but only in rats studied at 6 weeks after sympathectomy, a finding consistent with the appearance of muscarinic prejunctional facilitation of nitrergic transmission. In chronically sympathectomized rats, the M-2 and M-4 receptor antagonists methoctramine and tropicamide did not affect choroidal flow during parasympathetic activation. However, pirenzepine increased flux, implying the presence of M-1 inhibitory autoreceptors on these nerves. Parasympathetically mediated increased flux was partially blocked by the M-3 antagonist 4-diphenylacetoxy-N-methylpiperdine, and the remaining vasodilation was blocked by atropine. We conclude that parasympathetic prejunctional facilitatory M-3 and probably M-5 receptors adopt a crucial role after chronic sympathectomy in maintaining nitrergic vasodilatory ocular neurotransmission in the face of down-regulated nitric oxide transmitter mechanisms.

关键词：氯贝胆碱/药理学脉络膜/血液供给脉络膜/药物作用脉络膜/神经支配电刺激酶抑制剂/药理学神经节切除术咪唑类/药理学毒蕈碱激动剂/药理学毒蕈碱拮抗剂/药理学一氧化氮/生理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶Ⅰ型副交感神经系统/药物作用副交感神经系统/生理学哌啶类/药理学大鼠 Sprague-Dawley 受体毒蕈碱/分类受体毒蕈碱/生理学受体突触前/生理学局部血流/药物作用局部血流/生理学涎腺/神经支配颈上神经节/生理学颈上神经节/外科学突触传递/药物作用突触传递/生理学时间因素动物女(雌)性大鼠

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Effects of antidepressants in adrenergic neurotransmission of human vas deferens

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UROLOGY 2000年第4期55卷 592-597页

作者： Medina, P Segarra, G Ballester, R Chuan, P Domenech, C Vila, JM Lluch, S Univ Valencia Fac Med & Odontol Dept Fisiol Valencia 46010 Spain Univ Valencia Dept Cirugia Valencia 46010 Spain

Objectives. To evaluate the effects of sertraline, fluoxetine, and amitriptyline on the contractile responses of the human vas deferens muscle elicited by norepinephrine, electrical field stimulation, and KCl, because the therapeutic action of antidepressants may be accompanied by sexual dysfunction related to the contractility of the vas deferens smooth muscle. Methods, Ring segments of the epididymal part of the vas deferens were taken from 32 elective vasectomies and mounted in organ baths for isometric recording of tension. We then studied the effects of sertraline, fluoxetine, and amitriptyline on the neurogenic and agonist-induced contractile responses. Results. Amitriptyline caused concentration-dependent inhibition of neurogenic and norepinephrine-induced contractions. In contrast, only the highest concentration (10(-5) M) of sertraline and fluoxetine reduced the adrenergic contractions. The dihydropyridine calcium antagonist nifedipine (10(-6) M) completely prevented the inhibitory effect of sertraline and fluoxetine on neurogenic and norepinephrine-induced contractions but did not change the inhibition caused by amitriptyline. Sertraline, fluoxetine, and amitriptyline (all at 10(-5) M) attenuated contractions elicited by KCl and reduced contractions induced by CaCl2 in KCl-depolarized preparations, Conclusions. The results indicate that sertraline and fluoxetine inhibit vas deferens motility through inhibition of Ca2+ entry, with no effect on the adrenergic receptors, and amitriptyline acts as an adrenoceptor antagonist and inhibitor of the entry of calcium. UROLOGY 55: 592-597, 2000, (C) 2000, Elsevier Science Inc.

关键词：阿米替林/药理学抗抑郁药/药理学钙/代谢钙通道阻滞药/药理学培养技术剂量效应关系药物氟西汀/药理学肌收缩/药物作用硝苯地平/药理学受体肾上腺素能/药物作用舍曲林/药理学突触传递/药物作用输精管/神经支配人类男(雄)性

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Synaptic transmission at nicotinic acetylcholine receptors in rat hippocampal organotypic cultures and slices

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第3期515卷 769-776页

作者： Hefft, S Hulo, S Bertrand, D Muller, D Ctr Med Univ Geneva Dept Physiol CH-1211 Geneva 4 Switzerland

1. Whole-cell clamp recordings of the compound synaptic current elicited by afferent stimulation of Schaffer collaterals showed that blockade of the NMDA, AMPA. and GABA, receptor-mediated components by 6-nitro-7-sulphamoyl-benzo(f)quinoxaline-2,3-dione (NBQX), 3-((R)2-carboxypiperazine-4-yl)propyl-1-phosphonate (R-CPP) and picrotoxin, respectively, left a small residual current in 39 out of 41 CA1 pyramidal neurones in organotypic cultures and 9 out of 16 CA1 cells in acutely prepared slices. 2. This current represented 2.9 +/- 0.1% of the compound evoked synaptic response in organoypic cultures and 1.4 +/- 0.5% in slices. It was characterized by a slightly rectifying I-V curve and a reversal potential of 3.4 +/- 5.1 mV. 3. This residual current was insensitive to blockers of GABA(B), purinergic, muscarinic and 5-HT3 receptors, but it was essentially blocked by the nicotinic receptor antagonist d-tubocurarine (91 +/- 4% blockade;20 mu M), and partly blocked by alpha-bungarotoxin (200 nM) and methyllycaconitine (10 nM), two antagonists with a higher selectivity for alpha 7 subunit-containing nicotinic receptors (48 +/- 3% and 55 +/- 11% blockade, respectively). 4. The residual current was of synaptic origin, since it occurred after a small delay;its amplitude depended upon the stimulation intensity and it was calcium dependent and blocked by the sodium channel antagonist tetrodotoxin. 5. We conclude that afferent stimulation applied in the stratum radiatum evokes in some hippocampal neurones a small synaptic current mediated by activation of neuronal nicotinic receptors.

关键词：乌头碱/类似物和衍生物乌头碱/药理学环蛇毒素类/药理学诱发电位/药物作用兴奋性氨基酸拮抗剂/药理学 GABA拮抗剂/药理学海马/生理学烟碱拮抗剂/药理学器官培养技术印防己毒素/药理学哌嗪类/药理学锥体细胞/药物作用锥体细胞/生理学喹恶啉类/药理学大鼠 Sprague-Dawley 受体烟碱/生理学突触传递/药物作用突触传递/生理学筒箭毒碱/药理学动物大鼠

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Actin-dependent regulation of neurotransmitter release at central synapses

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NEURON 2000年第3期27卷 539-550页

作者： Morales, M Colicos, MA Goda, Y Univ Calif San Diego Div Biol La Jolla CA 92093 USA

Depolymerization of actin by latrunculin A transiently promotes neurotransmitter release. The mean rate of mEPSCs increases by a Ca2+-independent process, without a concomitant change in the mean amplitude. The readily releasable vesicle pool size and the rate of refilling of the readily releasable pool remain unaltered by latrunculin treatment. Evoked neurotransmitter release also increases in a manner consistent with an increase in vesicle release probability. The observed enhancement of neurotransmitter release is specific to actin depolymerization mediated by latrunculin A and is not caused by cytochalasin D. Our findings indicate that actin participates in a regulatory mechanism that restrains fusion of synaptic vesicles at the active zone.

关键词：肌动蛋白类/分析肌动蛋白类/药物作用肌动蛋白类/代谢钙/代谢细胞培养的细胞松弛素D/药理学缩肽类依他酸/类似物和衍生物兴奋性突触后电位荧光抗体技术绿色荧光蛋白质类海马/代谢发光蛋白质类/遗传学海生毒素类/药理学神经组织蛋白质类/代谢神经递质药/代谢肽类环/药理学突触前末梢/代谢重组融合蛋白质类/生物合成重组融合蛋白质类/遗传学突触/代谢突触传递/药物作用突触小泡/代谢噻唑类/代谢噻唑类/药理学噻唑烷类动物小鼠大鼠

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Dopamine depresses excitatory synaptic transmission onto rat subicular neurons via presynaptic D1-like dopamine receptors

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JOURNAL OF NEUROPHYSIOLOGY 2000年第1期84卷 112-119页

作者： Behr, J Gloveli, T Schmitz, D Heinemann, U Humboldt Univ Univ Hosp Charite Inst Physiol Dept Neurophysiol D-10117 Berlin Germany Univ Calif San Francisco Dept Mol & Cellular Pharmacol San Francisco CA 94141 USA

Schizophrenia is considered to be associated with an abnormal functioning of the hippocampal output. The high clinical potency of antipsychotics that act as antagonists at dopamine (DA) receptors indicate a hyperfunction of the dopaminergic system. The subiculum obtains information from area CA1 and the entorhinal cortex and represents the major output region of the hippocampal complex. To clarify whether an enhanced dopaminergic activity alters the hippocampal output, the effect of DA on alveus- and perforant path-evoked excitatory postsynaptic currents (EPSCs) in subicular neurons was examined using conventional intracellular and whole cell voltage-clamp recordings. Dopamine (100 mu M) depressed alveus- elicited (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated EPSCs to 56 +/- 8% of control while perforant path-evoked EPSCs were attenuated to only 76 +/- 7% of control. Dopamine had no effect on the EPSC kinetics. Dopamine reduced the frequency of spontaneous miniature EPSCs without affecting their amplitudes. The sensitivity of subicular neurons to the glutamate receptor agonist (S)-alpha-amino-3-hydoxy-5-methyl-4-isoxazolepropionic acid was unchanged by DA pretreatment, excluding a postsynaptic mechanism for the observed reduction of excitatory synaptic transmission. The effect of DA on evoked EPSCs was mimicked by the D1 receptor agonist SFK 38393 and partially antagonized by the D1 receptor antagonist SCH 23390. While the D2 receptor agonist quinelorane failed to reduce the EPSCs, the D2 receptor antagonist sulpiride did not block the action of DA. The results indicate that DA strongly depresses the hippocampal and the entorhinal excitatory input onto subicular neurons by decreasing the glutamate release following activation of presynaptic D1-like DA receptors.

关键词： 2 3 4 5-四氢-7 8-二羟基-1-苯基-1H-3-苯骈吖庚因/药理学苯丙氮|艹卓|类/药理学多巴胺/药理学多巴胺激动剂/药理学多巴胺拮抗剂/药理学内嗅皮层/细胞学内嗅皮层/生理学兴奋性氨基酸激动剂/药理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学谷氨酸/生理学海马/细胞学海马/生理学神经元/化学神经元/生理学膜片钳术穿通通路/细胞学穿通通路/生理学突触前末梢/生理学喹啉类/药理学大鼠 Wistar 受体多巴胺D1/生理学舒必利/药理学突触传递/药物作用突触传递/生理学 α-氨基-3-羟基-5-甲基-4-异唑丙酸/药理学动物女(雌)性大鼠

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THE REGULATION OF OXYTOCIN RECEPTOR-BINDING IN THE VENTROMEDIAL HYPOTHALAMIC NUCLEUS BY GONADAL-STEROIDS

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES-SERIES 1992年第1期652卷 357-373页

作者： JOHNSON, AE KAROLINSKA INST HUDDINGE HOSP MED RES CTR S-14186 HUDDINGE SWEDEN

In the previous sections, data were presented on the regulation of OT receptor binding by gonadal hormones. However, it is important to emphasize that gonadal steroids and E2 in particular also regulate other facets of OT transmission. For example, OT peptide levels as indicated by mRNA levels and OT immunoreactivity are enhanced by gonadal steroids. Similarly, OT release is also influenced by circulating steroids. By focusing on data collected in female rats and combining these different factors, the following relationships emerge. Within the ventromedial hypothalamus, OT peptide levels are virtually undetectable and OT receptor binding is negligible in the absence of E2. As circulating levels of E2 rise, increases in OT immunoreactivity and OT-receptor binding in the ventromedial hypothalamus and in the VMN itself can be detected. Under these conditions, OT receptor binding in and around the vl-VMN is markedly increased, rendering cells in the vl-VMN responsive to OT stimulation. Significantly, this increased responsivity is most evident at low concentrations of OT. With further increases in E2, P4 is released from the ovary, resulting in a number of biochemical changes in the central nervous system, including a potentiation of the effects of E2 on hypothalamic OT-receptor binding. Within a few hours after the initiation of P4 release, sexual receptivity can be elicited. At this time, sexual contact by the male enhances OT-peptide levels in the ventromedial hypothalamus of steroid-primed female rats, which in turn potentiates the display of sexual receptivity. The model outlined above not only summarizes a large portion of the data on steroid regulation of hypothalamic OT receptors, but more importantly, serves to highlight areas that require additional study. One important question that remains to be resolved is the source of OT receptors in the ventromedial hypothalamus. While the lesion studies discussed above indicate that the majority of fibers in the ventrol

关键词：双氢睾酮/药理学雌二醇/药理学雌二醇/生理学动情期/代谢催产素/类似物和衍生物催产素/代谢孕酮/药理学受体血管紧张素/代谢受体催产素突触传递/药物作用时间因素下丘脑腹内侧核/代谢动物女(雌)性大鼠

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Phosphorylation regulates spontaneous and evoked transmitter release at a giant terminal in the rat auditory brainstem

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第2期526卷 349-357页

作者： Oleskevich, S Walmsley, B Australian Natl Univ John Curtin Sch Med Res Div Neurosci Synapt Struct & Funct Grp Canberra ACT 2601 Australia

1. The role of phosphorylation in synaptic transmission was investigated at a large glutamatergic terminal, the endbulb of Held, on bushy cells in the rat anteroventral cochlear nucleus (AVCN). 2. Whole-cell recordings of excitatory postsynaptic currents (EPSCs) were used to examine the effects of kinase inhibitors and activators on low-frequency (baseline) evoked release, spontaneous release, paired-pulse facilitation (PPF) or depression (PPD), repetitive stimuli and recovery from depression. 3. Application of the kinase inhibitor H7 (100 mu M) reduced low-frequency evoked EPSC amplitude (by 15 %) and simultaneously increased PPF (or reduced PPD), with no significant change in other aspects of transmission. H7 did not affect the amplitude or frequency of spontaneous miniature EPSCs. 4. Phorbol esters increased EPSC amplitude (by 50 %) with a concomitant decrease in PPF (or increase in PPD), and reduced the final EPSC amplitude during repetitive stimuli. The effect of phorbol esters was due exclusively to protein kinase C (PKC) activation, as the specific PKC inhibitor bis-indolylmaleimide (Bis) completely blocked the potentiating effect of phorbol esters on EPSC amplitude. 5. Significantly, phorbol esters did not increase the evoked EPSC amplitude at connections in which release was maximized using high extracellular calcium concentrations (4-6 mM). 6. Phorbol esters increased the frequency of spontaneous miniature EPSCs in physiological calcium (by 275 %), and in high extracellular calcium (by 210 %) when phorbol esters did not increase the evoked EPSC amplitude. 7. Our results are most consistent with the actions of H7 to decrease levy-frequency release probability and phorbol esters to increase law-frequency release probability at the endbulb-busy cell synaptic connection in the AVCN. The effects of H7 and phorbol esters on paired-pulse responses and tetanic depression appear to be largely consequential to these changes in low-frequency release probability.

关键词： 1-(5-异喹啉磺酰基)-2-甲基哌嗪/药理学 2-氨基-5-膦酰基戊酸盐/药理学蜗神经核/生理学酶抑制剂/药理学诱发电位/药物作用诱发电位/生理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学吲哚类/药理学马来酰亚胺类/药理学佛波醇12 13-二丁酸盐/药理学磷酰化突触前末梢/生理学蛋白激酶C/代谢大鼠 Wistar 突触传递/药物作用突触传递/生理学十四酰佛波乙酯/药理学动物大鼠

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