Different effects of α-chloralose on spontaneous and evoked GABA release in rat hippocampal CA1 neurons

Matsuura, Takahiro; Iwata, Satomi; Shin, Min Chul; Wakita, Masahito; Ogawa, Shuji; Akaike, Norio

doi:10.1016/j.brainresbull.2011.03.022

Cited by 4 publications

(10 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A small depolarization of presynaptic terminals results in facilitation of both spontaneous and evoked release, presumably by enhancing action potential firing probability and Ca 2ϩ influx and vesicle exocytosis. In contrast, a larger depolarization of presynaptic terminals results in a reduction of action potential firing by inactivation of Na ϩ channels and/or a shunt of the membrane conductance of nerve terminals (Jang et al, 2006;Matsuura et al, 2011;Yamamoto et al, 2011). However, a large depolarization induces more Ca 2ϩ influx through Ca 2ϩ channels, resulting in the increase of sIPSCs and sEPSCs frequency, but an inhibition of eEPSCs and eEPSCs with an increase in their Rf.…”

Section: Gaba a Receptors On Inhibitory And Excitatory Nerve Terminalmentioning

confidence: 99%

“…A small depolarization of presynaptic terminals by the activation of presynaptic GABA A receptors enhances excitability by bringing the membrane potential closer to the firing threshold. However, a large depolarization of presynaptic terminals reduces excitability by a depolarization block of Na ϩ channels (inactivation of Na ϩ channels) and/or a shunt of the membrane conductance of nerve terminals (Jang et al, 2006;Matsuura et al, 2011;Yamamoto et al, 2011). Consequently, the coapplication of EtOH and muscimol induces a presynaptic depolarization sufficient to decrease evoked transmitter release with a reduced P 1 amplitude and an increase of Rf and PPR.…”

Section: ؉mentioning

confidence: 99%

“…Depolarization of presynaptic nerve terminals in isolated CA1 and CA3 pyramidal neurons enhances spontaneous transmitter release (Jang et al, 2006;Matsuura et al, 2011;Yamamoto et al, 2011). Hence as a test of whether muscimol and EtOH was depolarizing presynaptic nerve terminals via activation Glutamatergic eEPSCs elicited by focal paired-pulse electrical stimuli of single glutamatergic boutons in neurons isolated from 30-and 31-day-old rats.…”

Section: Cont Mus Mus +Etohmentioning

confidence: 99%

“…GABAergic eIPSCs were isolated from the glutamatergic ones by using 6-cyano-7-nitroquinoxaline-2,3-dione and D-(Ϫ)-2-amino-5-phosphonovaleric acid, and recording them at a V H of 0 mV, close to the reversal potential of glutamate response (Matsuura et al, 2011). Likewise, glutamatergic eEPSCs were isolated from GABAergic eIPSCs by recording them at a V H of Ϫ65 mV, close to the Cl Ϫ equilibrium potential (E Cl ) (Yamamoto et al, 2011).…”

Section: Methodsmentioning

confidence: 99%

“…This preparation involves mechanically dissociated neurons with adherent functional presynaptic terminals (Akaike and Moorhouse, 2003) and offers advantages for determining the locus of action of a neuromodulator such as EtOH because surrounding tissues, such as adjacent neurons and glia cells, are absent. We have identified presynaptic GABA A receptors on both GABAergic and glutamatergic nerve terminals projecting to hippocampal CA1 and CA3 neurons and spinal sacral dorsal commissural nucleus neurons that can modulate GABA and glutamate release evoked by focal electrical stimulation (Matsuura et al, 2011;Yamamoto et al, 2011). To clarify more precisely EtOH's actions on excitatory and inhibitory transmission, we report here the effects of EtOH on presynaptic GABA A receptors at single GABAergic and glutamatergic synapses in rat hippocampal CA1 and CA3 pyramidal neurons, using this synaptic bouton preparation.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Wakita¹,

Shin²,

Iwata³

et al. 2012

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

Ethanol (EtOH) has a number of behavioral effects, including intoxication, amnesia, and/or sedation, that are thought to relate to the activation of GABA A receptors. However, GABA A receptors at different cellular locations have different sensitivities to EtOH. The present study used the "synaptic bouton" preparation where we could stimulate nerve endings on mechanically dissociated single rat hippocampal CA1 and CA3 pyramidal neurons and investigate the effects of EtOH on presynaptic and postsynaptic GABA A receptors. Low concentrations of EtOH (10 mM) had no effect on postsynaptic GABA A and glutamate receptors or voltage-dependent Na ϩ and Ca 2ϩ channels. Higher concentrations (Ն100 mM) could significantly inhibit these current responses. EtOH at 10 mM had no direct effect on inhibitory postsynaptic currents (IPSCs) and excitatory postsynaptic currents (EPSCs) evoked by focal stimulation of single boutons [evoked IPSCs (eIPSCs) and evoked EPSCs (eEPSCs)]. However, coapplication of 10 mM EtOH with muscimol decreased the amplitude of eIPSCs and eEPSCs and increased their paired-pulse ratio. The effects on eEPSCs were reversed by bicuculline. Coapplication of muscimol and EtOH significantly increased the frequency of spontaneous IPSCs and EPSCs. The EtOH effects on the postsynaptic responses and eEPSCs were similar in neurons from neonatal and mature rats. These results revealed that low concentrations of EtOH can potentiate the activation of presynaptic GABA A receptors to inhibit evoked GABA and glutamate release. These results indicate a high sensitivity of presynaptic GABA A receptor to EtOH, which needs to be accounted for when considering the cellular mechanisms of EtOH's physiological responses.

show abstract

Section: Gaba a Receptors On Inhibitory And Excitatory Nerve Terminalmentioning

confidence: 99%

Section: ؉mentioning

confidence: 99%

Section: Cont Mus Mus +Etohmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Wakita¹,

Shin²,

Iwata³

et al. 2012

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

show abstract

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Yang

Chang

2020

Neurourology and Urodynamics

View full text Add to dashboard Cite

Aims The aim of this study is to investigate whether ketamine could relieve the social stress (SS)‐related bladder dysfunction in mice. Materials and Methods The FVB mice were randomly assigned to either undergo SS exposure for 60 minutes per day on seven consecutive days for 4 weeks (SS1) or control without SS (SS0). The SS0 were then allocated to single or no injection of ketamine (SS0K1 and SS0K0). In the group of SS1, the SS1 mice were allocated to receive single injection of saline (SS1K0), single dose (SS1K1) or five daily dose of (SS1K5) ketamine injection (25 mg/kg/day/ip) since day 22. In vivo cystometry and tissue bath wire myography were performed on day 29. Serum and urine level of brain‐derived neurotrophic factor (BDNF) were measured with enzyme‐linked immunosorbent assay. Results In mice without social stress exposure, ketamine administration did not significantly affect voiding frequency (P > .05). SS1K0, SS1K1, and SS1K5 had significantly lower voiding frequency than that of control (SS1K0) (each n = 15, P < .05). Ketamine administration reversed the trend of decreased voiding frequency in SS1 mice. Stressed mice had significant higher serum level of BDNF that reduced by short‐term ketamine. Stressed mice had detrusor overactivity and impaired detrusor contractility which were not reversed by short‐term ketamine. Conclusions Social stress leads to elevated serum BDNF, infrequent voiding, detrusor overactivity, and impaired contractility. Short‐term administration of ketamine may improve SS‐related infrequent voiding and elevated serum BDNF level. However, ketamine did not improve SS‐related bladder dysfunction on urodynamic and myography studies.

show abstract

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment

Wakita¹,

Nagami²,

Takase³

et al. 2015

Brain Research Bulletin

Self Cite

View full text Add to dashboard Cite

Different effects of α-chloralose on spontaneous and evoked GABA release in rat hippocampal CA1 neurons

Cited by 4 publications

References 42 publications

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment

Contact Info

Product

Resources

About

Different effects of α-chloralose on spontaneous and evoked GABA release in rat hippocampal CA1 neurons

Cited by 4 publications

References 42 publications

Effects of Ethanol on GABAA Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Effects of Ethanol on GABAA Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment

Contact Info

Product

Resources

About

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

Effects of Ethanol on GABA_A Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals