Rotational behavior and electrophysiological effects induced by GABAB receptor activation in rat globus pallidus

Chen, L; Chan, C. Savio; Yung, Wing‐Ho

doi:10.1016/s0306-4522(02)00299-3

Cited by 40 publications

(44 citation statements)

References 51 publications

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“…Furthermore, both the antiepileptic drug tiagabine and the benzodiazepine type 1 receptor agonist zolpidem prolong the time course of decay of GABA-A receptor-mediated synaptic currents recorded from globus pallidus neurons [6,7]. Finally, administration of these compounds into the globus pallidus of behaving rats induced rotational behaviour [5][6][7]. These data provide the rationale for further investigating the involvement of globus pallidus in epileptic seizure, and the role of GABA neurotransmission in this process.…”

Section: Introductionmentioning

confidence: 77%

“…Several of our recent reports demonstrate that a number of compounds, well known for their interaction with the GABA system as well as the control of epilepsy, are neuroactive in the globus pallidus. For example, we have shown that the GABA-B receptor agonist baclofen inhibits the presynaptic release of glutamate onto globus pallidus neurons [5]. Furthermore, both the antiepileptic drug tiagabine and the benzodiazepine type 1 receptor agonist zolpidem prolong the time course of decay of GABA-A receptor-mediated synaptic currents recorded from globus pallidus neurons [6,7].…”

Section: Introductionmentioning

confidence: 99%

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GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

Chen

Chan²,

Yung

2004

J Biomed Sci

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To determine the involvement of the globus pallidus in mediating epilepsy, the effects of microinjection of a GABA uptake blocker (tiagabine), a benzodiazepine agonist (zolpidem) and a GABA-B receptor agonist (baclofen) on pentylenetetrazol (PTZ)-induced tonic seizure were examined in adult rats. Administration of PTZ induced tonic seizures in all control animals, accompanied with a 100% mortality rate. Pretreatment with bilateral intrapallidal microinjection of tiagabine (1 mM) suppressed the incidence of tonic seizures to 67.7% and reduced the mortality rate to 16.7%. Furthermore, the latency to tonic seizures was 1,275 ± 277 s, which was significantly longer than that of the corresponding control animals (319 ± 225 s). On the other hand, administration of zolpidem (1 mM) was without significant effects on the mortality rate, the incidence and latency of the tonic seizure. In sharp contrast, microinjection of baclofen (1mM) completely suppressed PTZ-induced tonic seizures and reduced the mortality rate to 0%. This effect was largely abolished by co-injection of the GABA-B receptor antagonist CGP55845. To elucidate the direct cellular action of baclofen, the excitability and membrane potential of globus pallidus neurons were studied by cell-attached and whole-cell patch-clamp recordings in the brain slice. Bath application of baclofen (50 µM) significantly reduced the firing of these neurons, and was often accompanied by a clear membrane hyperpolarization, in a CGP55845-sensitive manner. These data suggest that activation of GABA-B receptors in globus pallidus could significantly modulate PTZ-induced tonic seizures.

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Section: Introductionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

Chen

Chan²,

Yung

2004

J Biomed Sci

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“…In the striatum, presynaptic GABA B receptors are expressed in cortical and thalamic terminals, identified with vesicular glutamate transporters 1 and 2 (vGluT1 and vGluT2, respectively), indicating that the two main sources of excitatory inputs to striatal neurons can be regulated by GABA B receptors (Lacey et al, 2005). GABA B agonists, indeed, depress glutamate-mediated postsynaptic potentials in slices of rat striatum, GP and STN (Calabresi et al, 1990;Seabrook et al, 1990;Calabresi et al, 1991;Nisenbaum et al, 1992Nisenbaum et al, ,1993Shen and Johnson, 2001;Chen et al, 2002a).…”

Section: Gaba B Receptorsmentioning

confidence: 99%

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

2006

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GABA and glutamate, the main transmitters in the basal ganglia, exert their effects through ionotropic and metabotropic receptors. The dynamic activation of these receptors in response to released neurotransmitter depends, among other factors, on their precise localization in relation to corresponding synapses. The use of high resolution quantitative electron microscope immunocytochemical techniques has provided in-depth description of the subcellular and subsynaptic localization of these receptors in the CNS. In this article, we review recent findings on the ultrastructural localization of GABA and glutamate receptors and transporters in the basal ganglia, at synaptic, extrasynaptic and presynaptic sites. The anatomical evidence supports numerous potential locations for receptor-neurotransmitter interactions, and raises important questions regarding mechanisms of activation and function of synaptic versus extrasynaptic receptors in the basal ganglia.

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“…The neurons were voltageclamped at -80 mV in ACSF containing gabazine. (Chen et al 2002(Chen et al , 2004. Thus functional GABA B receptors might exist at the glutamatergic synapses.…”

Section: Presynaptic Gaba B Responsesmentioning

confidence: 99%

“…In other brain areas, activation of postsynaptic GABA B receptors induces a slow hyperpolarization through the opening of potassium conductances and activation of receptors located at presynaptic terminals inhibits neurotransmitter release (Misgeld et al 1995). In spite of these findings, electrophysiological studies investigating the functional roles of GABA B receptors in the GP are scarce (Chen and Yung 2003;Chen et al 2002;Stefani et al 1999). Because previous studies were performed using the exogenous application of the GABA B receptor agonist baclofen, it remains to be determined whether synaptically released GABA can activate GABA B receptors in the GP.…”

Section: Introductionmentioning

confidence: 99%

Synaptically Released GABA Activates Both Pre- and Postsynaptic GABA_B Receptors in the Rat Globus Pallidus

Kaneda¹,

Kita²

2005

Journal of Neurophysiology

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Kaneda, Katsuyuki and Hitoshi Kita. Synaptically released GABA activates both pre-and postsynaptic GABA B receptors in the rat globus pallidus. J Neurophysiol 94: 1104 -1114, 2005; doi:10.1152/jn.00255.2005. The globus pallidus (GP) contains abundant GABAergic synapses and GABA B receptors. To investigate whether synaptically released GABA can activate pre-and postsynaptic GABA B receptors in the GP, physiological recordings were performed using rat brain slice preparations. Cell-attached recordings from GABA A antagonist-treated preparations revealed that repetitive local stimulation induced a GABA B antagonist-sensitive pause in spontaneous firings of GP neurons. Whole cell recordings revealed that the repetitive stimulation evoked fast excitatory postsynaptic potentials followed by a slow inhibitory postsynaptic potential (IPSP) in GP neurons. The slow IPSP was insensitive to a GABA A receptor antagonist, increased in amplitude with the application of ionotropic glutamate receptor antagonists, and was suppressed by the GABA B antagonist CGP55845. The reversal potential of the slow IPSP was close to the potassium equilibrium potential. These results suggest that synaptically released GABA activated postsynaptic GABA B receptors and induced the pause and the slow IPSP. On the other hand, in the neurons that were treated to block postsynaptic GABA B responses, CGP55845 increased the amplitudes of repetitive local stimulationinduced GABA A -mediated inhibitory postsynaptic currents (IPSCs) but not the ionotropic glutamate-mediated excitatory postsynaptic currents. Moreover, the GABA B receptor specific agonist baclofen reduced the frequency of miniature IPSCs without altering their amplitude distributions. These results suggest that synaptically released GABA also activated presynaptic GABA B autoreceptors, resulting in decreased GABA release in the GP. Together, we infer that both pre-and postsynaptic GABA B receptors may play crucial roles in the control of GP neuronal activity.

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Rotational behavior and electrophysiological effects induced by GABAB receptor activation in rat globus pallidus

Cited by 40 publications

References 51 publications

GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

Synaptically Released GABA Activates Both Pre- and Postsynaptic GABA_B Receptors in the Rat Globus Pallidus

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Rotational behavior and electrophysiological effects induced by GABAB receptor activation in rat globus pallidus

Cited by 40 publications

References 51 publications

GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

GABA-B Receptor Activation in the Rat Globus pallidus Potently Suppresses Pentylenetetrazol-Induced Tonic Seizures

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

Synaptically Released GABA Activates Both Pre- and Postsynaptic GABAB Receptors in the Rat Globus Pallidus

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Synaptically Released GABA Activates Both Pre- and Postsynaptic GABA_B Receptors in the Rat Globus Pallidus