“…It is possible that elevations in both carnosine and β-alanine may have influenced the results observed in this study. Recently, evidence has been presented indicating that β-alanine can act as a neurotransmitter in the brain (Tiedje et al 2010; Chesnoy-Marchais 2016). Specifically, it has been reported to interact with glial γ-aminobutyric acid (GABA) uptake transporter mechanisms (Tiedje et al 2010).…”
Section: Discussionmentioning
confidence: 99%
“…Specifically, it has been reported to interact with glial γ-aminobutyric acid (GABA) uptake transporter mechanisms (Tiedje et al 2010). A recent study demonstrated that β-alanine can reverse the blocking action of GABA receptors suggesting that β-alanine itself may have a neuroprotective role during damaging situations (Chesnoy-Marchais 2016). Although speculative, it is possible that the increased resiliency of mTBI-like behavior may have been the result of the combined effects of both increased carnosine and possibly β-alanine content in the hippocampus.…”
This study investigated the benefit of β-alanine (BA) supplementation on behavioral and cognitive responses relating to mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) in rats exposed to a low-pressure blast wave. Animals were fed a normal diet with or without (PL) BA supplementation (100 mg kg−1) for 30-day, prior to being exposed to a low-pressure blast wave. A third group of animals served as a control (CTL). These animals were fed a normal diet, but were not exposed to the blast. Validated cognitive-behavioral paradigms were used to assess both mTBI and PTSD-like behavior on days 7–14 following the blast. Brain-derived neurotrophic factor (BDNF), neuropeptide Y, glial fibrillary acidic protein (GFAP) and tau protein expressions were analyzed a day later. In addition, brain carnosine and histidine content was assessed as well. The prevalence of animals exhibiting mTBI-like behavior was significantly lower (p = 0.044) in BA than PL (26.5 and 46%, respectively), but no difference (p = 0.930) was noted in PTSD-like behavior between the groups (10.2 and 12.0%, respectively). Carnosine content in the cerebral cortex was higher (p = 0.048) for BA compared to PL, while a trend towards a difference was seen in the hippocampus (p = 0.058) and amygdala (p = 0.061). BDNF expression in the CA1 subregion of PL was lower than BA (p = 0.009) and CTL (p < 0.001), while GFAP expression in CA1 (p = 0.003) and CA3 (p = 0.040) subregions were higher in PL than other groups. Results indicated that BA supplementation for 30-day increased resiliency to mTBI in animals exposed to a low-pressure blast wave.
“…It is possible that elevations in both carnosine and β-alanine may have influenced the results observed in this study. Recently, evidence has been presented indicating that β-alanine can act as a neurotransmitter in the brain (Tiedje et al 2010; Chesnoy-Marchais 2016). Specifically, it has been reported to interact with glial γ-aminobutyric acid (GABA) uptake transporter mechanisms (Tiedje et al 2010).…”
Section: Discussionmentioning
confidence: 99%
“…Specifically, it has been reported to interact with glial γ-aminobutyric acid (GABA) uptake transporter mechanisms (Tiedje et al 2010). A recent study demonstrated that β-alanine can reverse the blocking action of GABA receptors suggesting that β-alanine itself may have a neuroprotective role during damaging situations (Chesnoy-Marchais 2016). Although speculative, it is possible that the increased resiliency of mTBI-like behavior may have been the result of the combined effects of both increased carnosine and possibly β-alanine content in the hippocampus.…”
This study investigated the benefit of β-alanine (BA) supplementation on behavioral and cognitive responses relating to mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) in rats exposed to a low-pressure blast wave. Animals were fed a normal diet with or without (PL) BA supplementation (100 mg kg−1) for 30-day, prior to being exposed to a low-pressure blast wave. A third group of animals served as a control (CTL). These animals were fed a normal diet, but were not exposed to the blast. Validated cognitive-behavioral paradigms were used to assess both mTBI and PTSD-like behavior on days 7–14 following the blast. Brain-derived neurotrophic factor (BDNF), neuropeptide Y, glial fibrillary acidic protein (GFAP) and tau protein expressions were analyzed a day later. In addition, brain carnosine and histidine content was assessed as well. The prevalence of animals exhibiting mTBI-like behavior was significantly lower (p = 0.044) in BA than PL (26.5 and 46%, respectively), but no difference (p = 0.930) was noted in PTSD-like behavior between the groups (10.2 and 12.0%, respectively). Carnosine content in the cerebral cortex was higher (p = 0.048) for BA compared to PL, while a trend towards a difference was seen in the hippocampus (p = 0.058) and amygdala (p = 0.061). BDNF expression in the CA1 subregion of PL was lower than BA (p = 0.009) and CTL (p < 0.001), while GFAP expression in CA1 (p = 0.003) and CA3 (p = 0.040) subregions were higher in PL than other groups. Results indicated that BA supplementation for 30-day increased resiliency to mTBI in animals exposed to a low-pressure blast wave.
“…5 mM, Ochoa-de la Paz et al, 2008 ). However, ρ subunit-containing hybrid ionotropic GABA receptors (which combine properties of GABA A and GABA C receptors) seem to be more sensitive to taurine and mediate considerable tonic currents at submillimolar taurine concentrations ( Chesnoy-Marchais, 2016 ). An interesting observation is that micromolar taurine concentrations can massively enhance tonic GABAergic currents, which suggest that extrasynaptic GABA and taurine may act synergistically ( Ochoa-de la Paz et al, 2008 ).…”
Section: Taurine Release Mechanisms and Taurine Receptorsmentioning
A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurodevelopmental events and the regulation of neuronal activity during early developmental epochs. The current knowledge is that taurine lacks a synaptic release mechanism but is released by volume-sensitive organic anion channels and/or a reversal of the taurine transporter. Extracellular taurine affects neurons and neuronal progenitor cells mainly via glycine, GABA(A), and GABA(B) receptors with considerable receptor and subtype-specific affinities. Taurine has been shown to directly influence neurogenesis in vitro as well as neuronal migration in vitro and in vivo. It provides a depolarizing signal for a variety of neuronal population in the immature central nervous system, thereby directly influencing neuronal activity. While in the neocortex, taurine probably enhance neuronal activity, in the immature hippocampus, a tonic taurinergic tone might be necessary to attenuate activity. In summary, taurine must be considered as an essential modulator of neurodevelopmental events, and possible adverse consequences on fetal and/or early postnatal development should be evaluated for pharmacological therapies affecting taurinergic functions.
“…In the case of GABA A receptors formed by the ρ subunit (GABA A -ρ), taurine activates the native GABA A -ρ1 and GABA A -ρ2 receptors in white perch bipolar cells [6] and modulates human cloned GABA A -ρ1 receptors heterologously expressed in Xenopus laevis oocytes [7]. However, the receptors that include the ρ subunit in their conformation apparently are more sensitive to taurine and, in some cases, regulate the tonic current at sub-millimolar concentrations of taurine [8]. Interestingly, micromolar concentrations of taurine regulate the GABA-induced current, suggesting that both GABA and taurine act synergistically in extra-synaptic GABA receptors [7].…”
Section: Interaction Of Taurine With Gaba Receptorsmentioning
Taurine is a β-amino acid present in high concentrations in different areas of the mammalian central nervous system (CNS). It participates in different physiological processes such as osmoregulation, signal transduction, antioxidant activity, trophic factor activity, modulation of calcium movements and neurotransmission. It is known that taurine is an agonist of GABA A receptors, and their affinity depends of the subunits that conform this receptor. GABA is the main inhibitory neurotransmitter of the CNS and exerts its effect through the activation of two types of specific receptors, called GABA A and GABA B. In the last years, changes in the expression pattern of the GABA A receptors subunits has been related to pathologies, such as epilepsy, depression and alcoholism, among others. This changes in the GABA A receptors conformation might be responsible of the loss in the effectiveness of the different drugs used in clinic protocols. Therefore, considering the physiological properties of taurine and the capacity to interact with GABA A receptors conformed by different subunits combinations, it is clear their great potential for the design of new pharmacological strategies aimed to treat the pathologies where GABA has shown a relevant participation.
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