Glutamate, GABA and epilepsy

Bradford, H. F.

doi:10.1016/0301-0082(95)00030-5

Cited by 415 publications

(259 citation statements)

References 145 publications

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“…The extracellular GABA concentration is a function of release vs. metabolism or reuptake by GABA transporters located on the membrane of presynaptic terminals and on glial cells (10,15). Although postsynaptic CB 1 receptors have been suggested to exist in the brain (2,35,(42)(43)(44), there is no evidence that CB 1 receptors located postsynaptically influence GABA transporter function.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture modulates vlPAG release of GABA through presynaptic cannabinoid CB₁ receptors

Fu¹,

Longhurst²

2009

Journal of Applied Physiology

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Fu L-W, Longhurst JC. Electroacupuncture modulates vlPAG release of GABA through presynaptic cannabinoid CB1 receptors. J Appl Physiol 106: 1800 -1809, 2009. First published April 9, 2009 doi:10.1152/japplphysiol.91648.2008.-Previous studies have demonstrated that electroacupuncture (EA) attenuates sympathoexcitatory reflex responses by activating a long-loop pathway involving the hypothalamic arcuate nucleus (ARC), midbrain ventrolateral periaqueductal gray (vlPAG), and rostral ventrolateral medulla (rVLM). Neurons in the ARC provide excitatory input to the vlPAG, whereas the vlPAG inhibits neuronal activity in the rVLM. ␥-Aminobutyric acid (GABA) and glutamate (Glu) have been identified in the vlPAG. Endocannabinoids (ECs), acting as atypical neurotransmitters, inhibit the release of both neurotransmitters in the hypothalamus and midbrain through a presynaptic cannabinoid type 1 (CB1) receptor mechanism. The EC system has been observed in the dorsal but not in the vlPAG. Since it is uncertain whether ECs influence GABA and Glu in the vlPAG, the present study tested the hypothesis that EA modulates the release of these neurotransmitters in the vlPAG through a presynaptic CB1 receptor mechanism. We measured the release of GABA and Glu simultaneously by using HPLC to assess samples collected with microdialysis probes inserted unilaterally into the vlPAG of intact anesthetized rats. Twenty-eight min of EA (2 Hz, 2-4 mA, 0.5 ms) at the P5-6 acupoints reduced the release of GABA by 39% during EA and by 44% 15 min after EA. Thirty-five minutes after EA, GABA concentrations returned to pre-EA levels. In contrast, sham EA did not change the vlPAG GABA concentration. Blockade of CB1 receptors with AM251, a selective CB1 receptor antagonist, reversed the EA-modulated changes in GABA concentration, whereas microinjection of vehicle into the vlPAG did not alter EA-modulated GABA changes. In addition, we observed no changes in the vlPAG Glu concentrations during EA, although the baseline concentration of Glu was much higher than that of GABA (3,541 Ϯ 373 vs. 33.8 Ϯ 8.7 nM, Glu vs. GABA). These results suggest that EA modulates the sympathoexcitatory reflex responses by decreasing the release of GABA, but not Glu, in the vlPAG, most likely through a presynaptic CB1 receptor mechanism. somatic afferents; sympathoexcitatory reflex; cannabinoid type 1 receptor; microdialysis ELECTROACUPUNCTURE (EA), a potent alternative to manual acupuncture, has been suggested to be effective in treating certain cardiovascular diseases including hypertension, arrhythmias, and angina pectoris (5, 6, 41). Clinically, EA at the NeiguanJianshi (P5-6) acupoints has been used to treat cardiovascular diseases in Eastern and, more recently, Western countries (5, 21, 41). We and others have demonstrated that EA at P5-6 acupoints overlying the median nerve on the wrist modulate blood pressure elevation evoked by gastric distension (GD) in rats (27) or by gallbladder stimulation in cats (50) through a long-loop neural pathway, extending from the arcuate...

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture modulates vlPAG release of GABA through presynaptic cannabinoid CB₁ receptors

Fu¹,

Longhurst²

2009

Journal of Applied Physiology

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“…2c). To investigate the underlying mechanisms of the functional changes after stimulation (RF enlargement and increase of the cortical representation), brain tissue from stimulated and shamoperated animals was evaluated with Nissl stain (we counted in the ROI the number of cells to get an overview about the total number of cortical cells and to rule out cell loss as a possible reason for changes in protein expression) and immunohistochemical markers indicative for neuronal activity and the state of the glutamatergic and GABAergic transmitter systems (Bradford, 1995;MacDermott, 2001).…”

Section: Peripheral Representation (Receptive Field) Of the Icms Sitementioning

confidence: 99%

Excitation and Inhibition Jointly Regulate Cortical Reorganization in Adult Rats

Benali¹,

Weiler²,

Benali³

et al. 2008

J. Neurosci.

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The primary somatosensory cortex (SI) retains its capability for cortical reorganization after injury or differential use into adulthood. The plastic response of SI cells to peripheral stimulation is characterized by extension of cortical representations accompanied by changes of the receptive field size of neurons. We used intracortical microstimulation that is known to enforce local, intracortical synchronous activity, to induce cortical reorganization and applied immunohistochemical methods in the same individual animals to investigate how plasticity in the cortical topographic maps is linked to changes in the spatial layout of the inhibitory and excitatory neurotransmitter systems. The results reveal a differential spatiotemporal pattern of upregulation and downregulation of specific factors for an excitatory (glutamatergic) and an inhibitory (GABAergic) system, associated with changes of receptive field size and reorganization of the somatotopic map in the rat SI. Predominantly local mechanisms are the specific reduction of the calcium-binding protein parvalbumin in inhibitory neurons and the low expression of the activity marker c-Fos. Reorganization in the hindpaw representation and in the adjacent SI cortical areas (motor cortex and parietal cortex) is accompanied by a major increase of the excitatory transmitter glutamate and c-Fos. The spatial extent of the reorganization appears to be limited by an increase of glutamic acid decarboxylase and the inhibitory transmitter GABA. The local and medium-range net effects are excitatory and can facilitate receptive field enlargements and cortical map expansion. The longer-range increase of inhibition appears suited to limit these effects and to prevent neurons from pathological hyperexcitability.

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“…It is known that the lack of inhibitory GABA A -mediated responses in BMI-treated hippocampal slices markedly increases neuronal excitability and glutamate release, which in turn produces epileptogenesis (Bradford, 1995). We analyzed the contribution of ionotropic glutamate receptors in the generation of astrocytic network correlation in the BMI-induced epilepsy model.…”

Section: Activation Of Ionotropic Glutamate Receptors Is Required Formentioning

confidence: 99%

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

et al. 2002

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Spontaneous neuronal activity is essential to neural development. Until recently, neurons were believed to be the only excitable cells to display spontaneous activity. However, cultured astrocytes and, more recently, astrocytes in situ are now known to exhibit spontaneous Ca 2ϩ transients. Here we used Ca 2ϩ imaging of astrocytes from transgenic mice for the simultaneous monitoring of [Ca 2ϩ ] i changes in large numbers of astrocytes. We found that spontaneous activity is a common property of most brain astrocytes that is lost in response to a lesion. These spontaneous [Ca 2ϩ ] i oscillations require extracellular and intracellular Ca 2ϩ . Moreover, network analysis revealed that most astrocytes formed correlated networks of dozens of these cells, which were synchronous with both astrocytes and neurons. We found that decreasing spontaneous [Ca 2ϩ ] i transients in neurons by TTX does not alter the number of active astrocytes, although it impairs their synchronous network activity. Conversely, bicuculline-induced epileptic patterns of [Ca 2ϩ ] i transients in neurons cause an increase in the number of active astrocytes and in their network synchrony. Furthermore, activation of non-NMDA and NMDA ionotropic glutamate receptors is required to correlate astrocytic networks. These results show that spontaneous activity in astrocytes and neurons is patterned into correlated neuronal/astrocytic networks in which neuronal activity regulates the network properties of astrocytes. This network activity may be essential for neural development and synaptic plasticity.

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Glutamate, GABA and epilepsy

Cited by 415 publications

References 145 publications

Electroacupuncture modulates vlPAG release of GABA through presynaptic cannabinoid CB₁ receptors

Electroacupuncture modulates vlPAG release of GABA through presynaptic cannabinoid CB₁ receptors

Excitation and Inhibition Jointly Regulate Cortical Reorganization in Adult Rats

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

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