The effects of thioperamide on extracellular levels of glutamate and GABA in the rat prefrontal cortex

Abstract

These data indicate that H3 receptors in the prefrontal cortex can enhance stimulated GABA release, but do not regulate basal levels of glutamate or GABA.

Differential Effects of the Histamine H3Receptor Agonist Methimepip on Dentate Granule Cell Excitability, Paired-Pulse Plasticity and Long-Term Potentiation in Prenatal Alcohol-Exposed Rats

“…This effect was accompanied by an increase in the fEPSP paired pulse ratio (Figure 2A), suggesting that methimepip reduced the probability of glutamate release in control rats. In agreement with this observation, several studies indicate a role for histamine H 3 receptors in modulating glutamate release in the medial frontal cortex (Welty and Shoblock, 2009), globus pallidus (Osorio-Espinoza et al, 2011), thalamus (Garduno-Torres et al, 2007), striatum (Molina-Hernandez et al, 2001) and dentate gyrus (Brown and Haas, 1999) of rats. Since no effects were observed in the PS paired-pulse ratio at stimulus intensities sufficient to elicit a large PS (Figure 3), it is not likely that the reductions in E-S coupling can be attributed to elevated GABA release.…”

“…The efficacy of a variety of so-called “procognitive agents” whose primary mechanism of action targets nerve terminals include histamine H 3 receptor antagonists or inverse agonists (Fox et al, 2005; Galici et al, 2009; Medhurst et al, 2007). Histamine H 3 receptors reside predominantly on nerve terminals (Fujimoto et al, 1991), and inhibit histamine release (Giannoni et al, 2010; Kitbunnadaj et al, 2005), as well as the release of acetylcholine (Bacciottini et al, 2002), GABA (Welty and Shoblock, 2009) and glutamate (Brown and Haas, 1999). Antagonists and inverse agonists of H 3 receptors have procognitive actions in a variety of animal models (Brioni et al, 2011; Esbenshade et al, 2008).…”

Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats

“…Notably, systemic co-injection with RAM failed to reverse the modulating effect of H3R antagonist E177 (5 mg/kg) on hippocampal GLU levels, suggesting that the hippocampal GLU modulating effect provided by H3R antagonist E177 was not only mediated through histaminergic transmission, but other possible mechanisms may have contributed ( Figure 6). It can be suggested from earlier findings that H3R antagonists may modify neurotransmitters release differently under normal or stimulated conditions [128], which explains the inhibitory effect of H3R antagonist E177 on the PTZ-induced high GLU release through H3 hetero-receptors. Accordingly, reducing the abnormal hippocampal GLU levels was at least partially involved in the anticonvulsant and memory-enhancing effect of H3R antagonist E177 in PTZ-kindled animals.…”

Tonic and phasic release of glutamate and acetylcholine neurotransmission in sub-regions of the rat prefrontal cortex using enzyme-based microelectrode arrays

“…In previous microdialysis studies that used KCl to evoke neurotransmitter release, the infusion of KCl into the mPFC resulted in an increase in glutamate levels of 90% (Frantz et al, 2002). KCl has also been reported to have no effect on glutamate levels (Welty and Shoblock, 2009). However, these studies were not specific to subregions of the mPFC, and they did not measure rapid changes in glutamate or ACh.…”