GABA release

GABA is the most prominent inhibitory neurotransmitter in the mammalian nervous system and acts via GABA receptors. Activation of GABAb receptors by GABA released from local spinal interneurons (Fig. 1) negatively modulates nociceptive transmission in the spinal cord. Agonists at GABAb receptors... 

Tetanus is a disease caused by the release of neurotoxins from the anaerobic, spore-forming rod Clostridium tetani. The clostridial protein, tetanus toxin, possesses a protease activity which selectively degrades the pre-synaptic vesicle protein synaptobrevin, resulting in a block of glycine and y-aminobutyric acid (GABA) release from presynaptic terminals. Consistent with the loss of neurogenic motor inhibition, symptoms of tetanus include muscular rigidity and hyperreflexia. The clinical course is characterized by increased muscle tone and spasms, which first affect the masseter muscle and the muscles of the throat, neck and shoulders. Death occurs by respiratory failure or heart failure. 

Cotter R, Williams C, Ryan L et al (2002) FractaUdne (CX3CL1) and brain inflammation impU-cations for HIV-l-associated dementia. J Neurovirol 8 585-598 Cunha-Reis D, Ribeiro JA, Sebastiao AM (2008) Al and A2A receptor activation by endogenous adenosine is required for VIP enhancement of K+-evoked [3H]-GABA release from rat hippocampal nerve terminals. Neurosci Lett 430 207-212 Davalos D, Grutzendler J, Yang G et al (2005) ATP mediates rapid microglial response to local brain injury in vivo. Nat Neurosci 8 752-758... 

Figure 4.13 GABA release by reversed uptake ( retrotransport ). Depolarization of a neuronal, or glial cell process by glutamate, with a concomitant rise in [Na+]i reverses the operation of the GABA uptake carrier, raising [GABA]o. (Modified from Attwell, Barbour and Szatkowski 1993, with permission from the publisher Cell Press)...

Figure 15.9 Peptide modulation of striatal input to the globus pollidus. Enkephalin released from axon terminals of neurons of the indirect pathway (see Fig. 15.2 for details) is thought to inhibit GABA release from the same terminals so that feedback (auto) inhibition is reduced. This will free the neurons to inhibit the subthalamic nucleus (SThN) and its drive to GPint and SNr which in turn will have less inhibitory effect on cortico-thalamic traffic and possibly reduce akinesia. Dynorphin released from terminals of neurons of the direct pathway may also reduce glutamate release and excitation in the internal globus pallidus and further depress its inhibition of the cortico-thalamic pathway. High concentrations of these peptides may, however, result in dyskinesias. (See Henry and Brotchie 1996 and Maneuf et al. 1995)...

Inhibition of glutamate release was thought to be the mode of action of lamotrigine. It reduces MBS and kindling and also glutamate (and to a lesser extent GABA) release induced in brain slices by veratridine, which opens sodium channels. But it now seems likely that the actual block of sodium channels is its primary action (see later). 

Reubi, J.-C. Iversen, L.L. and Jessell, T.M. Dopamine selectively increases H-GABA release from slices of rat substantia nigra in vitro. Nature 268 652-654, 1977. 

Santos, M. S., Ferreira, F., Faro, C. el al. (1994). The amount of GABA present in aqueous extracts of valerian is sufficient to account for [3H] GABA release in synaptosomes. Planta Med., 60, 475-6. 

GABA release and GABAergic control of arousal systems... 

Nitz, D. Siegel, J. M. (1996). GABA release in posterior hypothalamus across sleep-wake cycle. Am. J. Physiol. 271, R1707-12. 

Floran B., Floran L., Erlij D., Aceves J. (2004). Activation of dopamine D4 receptors modulates [3H]GABA release in slices of the rat thalamic reticular nucleus. Neuropharmacology 46, 497-503. 

Hong, Z. Y., Huang, Z. L., Qu, W. M. et al. (2005). An adenosine A receptor agonist induces sleep by increasing GABA release in the tuberomammillary nucleus to inhibit histaminergic systems in rats. J. Neurochem. 92 (6), 1542-9. 

We recently demonstrated that CGS21680, an adenosine A2aR agonist, inhibited histamine release in both the frontal cortex and medial POA in a dose-dependent manner, and increased GABA release specifically in the TMN but not... 

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