Presynaptic inhibition of glutamatergic synaptic transmission to rat motoneurons by serotonin

1. In a brain stem slice preparation, we recorded glutamatergic excitatory postsynaptic currents (EPSCs) in hypoglossal motoneurons (HMs) evoked by extracellular stimulation in the reticular formation just ipsilateral to the hypoglossal motor nucleus (n. XII). Serotonin (5-HT) inhibited glutamatergic synaptic transmission in a dose-dependent fashion as indicated by a reduction in the evoked EPSC (eEPSC) peak amplitude to 46 +/- 2% (mean +/- SE, n = 26) of control (5-HT 10 microM). This effect was not voltage dependent, as the eEPSC reversal potential was not altered (n = 5). Additionally, 5-HT decreased the rate of rise of the eEPSC to 41 +/- 2% of control (n = 14). Blockade of N-methyl-D-aspartate-receptor-channels by D(-)-2-amino-5-phosphonopentanoic acid (50 microM) or of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptor-channels by 6,7-dinitro-quinoxaline (20 microM) did not alter the relative reduction of the eEPSC amplitude by 5-HT (n = 7 and 3, respectively). 2. In the presence of tetrodotoxin (1 microM), bath application of 5-HT did not reduce postsynaptic glutamate currents elicited by pressure ejection of L-glutamate (1 mM) onto HMs (n = 5), and it increased the median interevent interval of spontaneous miniature EPSCs (mEPSCs) to 178 +/- 12% of control (n = 4), suggesting that 5-HT acts presynaptically to reduce the probability of vesicle release. mEPSC amplitude was decreased slightly in three of four cells (median amplitude = 92 +/- 3% of control). 3. The specific 5-HT1B receptor agonist [3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one] (1 microM) mimicked 5-HT in its effect on eEPSCs (eEPSC amplitude reduced to 31 +/- 5% of control; rate of rise reduced to 40 +/- 4% of control, n = 10 and 5, respectively) and mEPSCs (median interevent interval increased to 231 +/- 36% of control; median mEPSC amplitude = 102 +/- 3% of control, n = 5). Additionally, 5-HT-mediated inhibition was not blocked by coapplication of 1-(2-methoxyphenyl)-4-[4-(2-phthalimido) butyl] piperazine hydrobromide (1 microM), a 5-HT1A antagonist, and 3-[2-[4-(4-flurobenzoyl)-1-piperdinyl]ethyl]-2,4(1H,3H)-quin azolinedione tartrate (1 microM), a 5-HT2A/2C antagonist (n = 4). These data indicate that the 5-HT effect is primarily 5-HT1B receptor mediated. 4. We conclude that 5-HT, acting through presynaptic 5-HT1B receptors, inhibits glutamatergic synaptic transmission by reducing the probability of vesicle release.

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Properties and Pharmacology of a TTX-insensitive Na+ Current in Neurones of the Jellyfish Cyanea Capillata

Journal of Experimental Biology ◽

10.1242/jeb.133.1.231 ◽

1987 ◽

Vol 133 (1) ◽

pp. 231-248 ◽

Cited By ~ 4

Author(s):

PETER A. V. ANDERSON

Keyword(s):

Synaptic Transmission ◽

Motor Nerve ◽

Reversal Potential ◽

Patch Clamp Technique ◽

Inward Current ◽

Outward Currents ◽

Voltage Dependent ◽

Negative Membrane Potential ◽

Sea Anemone Toxin ◽

Cyanea Capillata

Neurones of the motor nerve net of the jellyfish Cyanea capillata were axotomized, and voltage-clamped using the whole-cell configuration of the patch-clamp technique. Outward currents were blocked by a combination of extracellular 4-aminopyridine (4-AP) and intracellular Cs+, tetraethylammonium (TEA+) and 4-AP. Under normal conditions, the inward current consisted of a fast, transient current which could be abolished by removal of extracellular Na+ and whose reversal potential was dependent on the extracellular Na+ concentration. This current was completely insensitive to tetrodotoxin (TTX), saxitoxin (STX) and conotoxin GIIIA but could be blocked by extracellular Cd2+, lidocaine, W7 [N-(6 aminohexyl)-5-chloro-1-napthalenesulphonamide] and verapamil. Inactivation was voltage-dependent with a Vh of −15mV, and was unaffected by veratridine, batrachotoxin (BTX), sea anemone toxin and scorpion (Leiurus) venom. Reactivation required repolarization to a negative membrane potential for 12 ms for half-maximal reactivation. In the absence of extracellular Na+ no inward current was visible unless [Ca2+]o was elevated. In Na+-free, 95 mmoll−1 Ca2+ saline, a slightly slower, inward current was recorded. This current is believed to be the Ca2+ current that underlies synaptic transmission. 7. These findings are discussed with reference to synaptic transmission in these cells and the evolution of ion channels.

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Muscarinic depression of synaptic transmission at the hippocampal mossy fiber synapse

Journal of Neurophysiology ◽

10.1152/jn.1990.64.4.1089 ◽

1990 ◽

Vol 64 (4) ◽

pp. 1089-1097 ◽

Cited By ~ 46

Author(s):

S. Williams ◽

D. Johnston

Keyword(s):

Synaptic Transmission ◽

Mossy Fiber ◽

Reversal Potential ◽

Input Resistance ◽

Cesium Chloride ◽

Resting Potential ◽

Excitatory Postsynaptic Potential ◽

Bath Application ◽

Before And After ◽

Mossy Fiber Synapse

1. The action of muscarine was studied in the CA3 region of the rat hippocampal slice with single-electrode voltage-clamp techniques. 2. Bath application of 1 or 10 microM muscarine produced an increase in the input resistance of these cells and reduced the slow afterhyperpolarization (sAHP) response. Changes in input resistance were more pronounced around the resting potential of the cell (-50 to -60 mV), but in many cells an effect was also seen at -80 mV. These effects were absent when cesium chloride-containing microelectrodes were used. 3. At 1 microM, muscarine had little effect on synaptic transmission, causing a 0 +/- 7% (mean +/- SE, n = 19) change in excitatory postsynaptic potential (EPSP) and decreasing the excitatory postsynaptic current (EPSC) by 11 +/- 6% (n = 14); neither change was statistically significant. 4. In contrast, 10 microM muscarine produced a reliable depression of both the EPSP and EPSC. This effect was independent of the electrolyte used: with KCl the EPSP was depressed 23 +/- 4% (n = 5) and the EPSC 35 +/- 5% (n = 4); for CsCl the EPSP was depressed 23 +/- 10% (n = 7) and the EPSC 34 +/- 5% (n = 7). 5. Muscarine did not alter the reversal potential of the synaptic current but merely produced a decrease in slope conductance (37 +/- 5%, n = 6). 6. Muscarine did not significantly alter the shape of the EPSC waveform. This was assessed by comparing the 10-90% rise time and the half decay time of the current before and after muscarine.(ABSTRACT TRUNCATED AT 250 WORDS)

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GABAc receptor mediated modulation of glutamatergic synaptic transmission to amacrine cells in the mouse retina

Neuroscience Research ◽

10.1016/s0168-0102(00)81038-x ◽

2000 ◽

Vol 38 ◽

pp. S32

Author(s):

K Matsui

Keyword(s):

Synaptic Transmission ◽

Amacrine Cells ◽

Mouse Retina ◽

Glutamatergic Synaptic Transmission ◽

Gabac Receptor

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Spreading Depression (SD) Waves in the Brainstem of Immature Rats Propagate Independently of Glutamatergic Synaptic Transmission

Klinische Neurophysiologie ◽

10.1055/s-2004-832137 ◽

2004 ◽

Vol 35 (03) ◽

Author(s):

F Richter ◽

A Lehmenkuhler ◽

HG Schaible

Keyword(s):

Synaptic Transmission ◽

Spreading Depression ◽

Glutamatergic Synaptic Transmission ◽

Immature Rats

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Bidirectional modulation of glutamatergic synaptic transmission by mGlu7 receptors at Schaffer Collateral-CA1 hippocampal synapses

10.26226/morressier.5b31ec632afeeb001345a2fa ◽

2018 ◽

Author(s):

Ricardo Martín

Keyword(s):

Synaptic Transmission ◽

Schaffer Collateral ◽

Glutamatergic Synaptic Transmission ◽

Hippocampal Synapses ◽

Bidirectional Modulation

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Citalopram reduces glutamatergic synaptic transmission in the auditory cortex via activation of 5-HT1A receptors

Neuroreport ◽

10.1097/wnr.0000000000001366 ◽

2019 ◽

Vol 30 (18) ◽

pp. 1316-1322 ◽

Cited By ~ 2

Author(s):

Víctor Cervantes-Ramírez ◽

Martha Canto-Bustos ◽

Diana Aguilar-Magaña ◽

Elsy Arlene Pérez-Padilla ◽

José Luis Góngora-Alfaro ◽

...

Keyword(s):

Synaptic Transmission ◽

Auditory Cortex ◽

Glutamatergic Synaptic Transmission

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Nitric Oxide Activates Leak K+ Currents in the Presumed Cholinergic Neuron of Basal Forebrain

Journal of Neurophysiology ◽

10.1152/jn.00536.2007 ◽

2007 ◽

Vol 98 (6) ◽

pp. 3397-3410 ◽

Cited By ~ 21

Author(s):

Youngnam Kang ◽

Yoshie Dempo ◽

Atsuko Ohashi ◽

Mitsuru Saito ◽

Hiroki Toyoda ◽

...

Keyword(s):

Nitric Oxide ◽

Basal Forebrain ◽

Reversal Potential ◽

Soluble Guanylyl Cyclase ◽

Outward Current ◽

Pump Current ◽

Atp Depletion ◽

Equilibrium Potential ◽

No Donor ◽

Bath Application

Learning and memory are critically dependent on basal forebrain cholinergic (BFC) neuron excitability, which is modulated profoundly by leak K+ channels. Many neuromodulators closing leak K+ channels have been reported, whereas their endogenous opener remained unknown. We here demonstrate that nitric oxide (NO) can be the endogenous opener of leak K+ channels in the presumed BFC neurons. Bath application of 1 mM S-nitroso- N-acetylpenicillamine (SNAP), an NO donor, induced a long-lasting hyperpolarization, which was often interrupted by a transient depolarization. Soluble guanylyl cyclase inhibitors prevented SNAP from inducing hyperpolarization but allowed SNAP to cause depolarization, whereas bath application of 0.2 mM 8-bromoguanosine-3′,5′-cyclomonophosphate (8-Br-cGMP) induced a similar long-lasting hyperpolarization alone. These observations indicate that the SNAP-induced hyperpolarization and depolarization are mediated by the cGMP-dependent and -independent processes, respectively. When examined with the ramp command pulse applied at –70 mV under the voltage-clamp condition, 8-Br-cGMP application induced the outward current that reversed at K+ equilibrium potential ( EK) and displayed Goldman-Hodgkin-Katz rectification, indicating the involvement of voltage-independent K+ current. By contrast, SNAP application in the presumed BFC neurons either dialyzed with the GTP-free internal solution or in the presence of 10 μM Rp-8-bromo-β-phenyl-1,N2-ethenoguanosine 3′,5′-cyclic monophosphorothioate sodium salt, a protein kinase G (PKG) inhibitor, induced the inward current that reversed at potentials much more negative than EK and close to the reversal potential of Na+-K+ pump current. These observations strongly suggest that NO activates leak K+ channels through cGMP-PKG-dependent pathway to markedly decrease the excitability in BFC neurons, while NO simultaneously causes depolarization by the inhibition of Na+-K+ pump through ATP depletion.

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NMDA Receptor-Dependent Synaptic Activity in Dorsal Motor Nucleus of Vagus Mediates the Enhancement of Gastric Motility by Stimulating ST36

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2012/438460 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 9

Author(s):

Xinyan Gao ◽

Yongfa Qiao ◽

Baohui Jia ◽

Xianghong Jing ◽

Bin Cheng ◽

...

Keyword(s):

Synaptic Transmission ◽

Gastric Motility ◽

Low Frequency ◽

Synaptic Activity ◽

Motor Nucleus ◽

Dorsal Motor Nucleus ◽

Vagal Reflex ◽

Precise Molecular Mechanism ◽

Lines Of Evidence

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.

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