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Assessment of Second Messenger Function in the Hippocampus of Aged Rats with Cognitive Impairment
Published in David R. Riddle, Brain Aging, 2007
Michelle M. Nicolle, Hai-Yan Zhang, Jennifer L. Bizon
Another technical consideration in GTP binding assays involves the specifics of the buffer composition across neurotransmitter systems. In our laboratory, we noted that the magnitude of the metabotropic glutamate receptor-stimulated response was much lower than the muscarinic receptor-stimulated response. After optimization of the ion composition of the buffers, however, we were able to obtain an optimal signal using the mGluR Type 1 agonist 3,5-dihydroxyphenylglycine (DHPG). The differences in the buffer compositions are shown in Table 9.3, and such considerations are important when examining a variety of transmitter systems.
Nonclassical Ion Channels in Learning and Memory
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ze-Jie Lin, Xue Gu, Tian-Le Xu, Wei-Guang Li
Incapacity of aversive memory extinction is one of the common causes for brain diseases such as anxiety disorder and anorexia nervosa. For instance, if the conditioned memory of taste aversion cannot be extinguished effectively, it will easily lead to refractory feeding difficulties during the growth and development of children, which will irreversibly have adverse effects on the physical and intellectual welfare of young children. The insular cortex is well known for its critical role in encoding taste learning (Rosenblum et al. 1997) and processing aversively motivated learning tasks, such as conditioned taste aversion (CTA) (Garcia, Kimeldorf, and Koelling 1955; Chambers 1990; Elkobi et al. 2008; Adaikkan and Rosenblum 2015), a form of associative learning where the subject associates a novel taste with a subsequent transient visceral illness. At the synaptic level, LTP in insular cortex is demonstrated to contribute to the acquisition of CTA (Escobar, Alcocer, and Chao 1998; Jones et al. 1999). However, the molecular and synaptic mechanisms underlying CTA memory extinction (Berman and Dudai 2001; Eisenberg et al. 2003) remain undetermined. To answer this question, we reported the involvement of ASIC1a in mediating long-term depression (LTD) through a mechanism that requires glycogen synthase kinase-3β (GSK3β) at mouse insular synapses and extinction of CTA memory (Figure 7.3) (Li et al. 2016). Genetic ablation or pharmacological inhibition of ASIC1a reduces the induction probability of LTD by either low-frequency stimulation (LFS) or bath application of the group I metabotropic glutamate receptor agonist, 3,5-dihydroxyphenylglycine (DHPG), but without affecting the LTP induction in the insular cortex. Interestingly, aversive taste extinction learning leads to reduced synaptic efficacy in the insular cortex, which precludes further LTD induction, implicating the eligibility of LTP and LTD at insular synapses for bidirectional modulation of the CTA memory (Rodriguez-Duran, Martinez-Moreno, and Escobar 2017). Behaviorally, disruption of ASIC1a also attenuates the extinction of established taste aversion memory without altering the initial associative taste learning or its long-term retention. Moreover, the impaired insular LTD and extinction learning in Asic1a-null mice can be restored by virus-mediated expression of wild-type ASIC1a, but not its ion-impermeable mutant, in the insular cortices. These data thus demonstrate the involvement of an ASIC1a-mediated insular synaptic depression mechanism in CTA memory extinction.
Loss of mGluR1-LTD following cocaine exposure accumulates Ca2+-permeable AMPA receptors and facilitates synaptic potentiation in the prefrontal cortex
Published in Journal of Neurogenetics, 2021
The following drugs were used: cocaine (Sigma-Aldrich), (S)-3,5-Dihydroxyphenylglycine (DHPG, Tocris Bioscience), LY367385 (Tocris Bioscience), 3-((2-Methyl-1,3-thiazol-4-yl)ethynyl)pyridine hydrochloride (MTEP, Tocris Bioscience), 1-Naphthyl acetyl spermine trihydrochloride (Naspm, Sigma-Aldrich), picrotoxin (Sigma-Aldrich), PKI6-22 (Sigma-Aldrich), QX-314 (Sigma-Aldrich), rapamycin (Sigma-Aldrich), Ro67-7476 (Tocris Bioscience), SCH23390 (Tocris Bioscience), SKF81297 (Sigma-Aldrich), tetrodotoxin (Sigma-Aldrich), and U73122 (Tocris Bioscience). Picrotoxin was dissolved directly in the ACSF used for perfusion. LY367385 and MTEP were dissolved in DMSO with a 1:1000 ratio as stock solutions, which were added directly to ASCF to a desired final concentration during experiments. All other drugs were dissolved in distilled water with a 1:1000 ratio as stock solutions. Drugs were delivered to the recording chamber through a perfusion system (Harvard Apparatus).
The role of glutamate and its receptors in central nervous system in stress-induced hyperalgesia
Published in International Journal of Neuroscience, 2018
Yan-Na Lian, Qi Lu, Jin-Long Chang, Ying Zhang
Group I mGluRs have been shown to facilitate hyperalgesia [58,59]. Importantly, activation of group I mGluRs plays a crucial role in the development and maintenance of inflammatory hyperalgesia in spinal cord [60]. For example, activation of group I mGluRs can activate extracellular signal-regulated kinases (ERKs) ERK1 and ERK2 in mice, which work on the elevation of inflammation pain sensitivity [61]. Moreover, activation of mGluR1 and mGluR5 in the spinal cord with the Group I agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) can also cause mechanical and thermal hyperalgesia [62]. In contrast, blockade of mGlu1 is an effective treatment for hyperalgesia [63]. Pharmacological studies have suggested that antagonist blockade of mGlu5 or genetic disruption of mGlu5 can reduce peripheral hypersensitivity induced by DHPG in the central nucleus of the amygdala (CeA) of mice [64]. Amygdala is one neural substrate of SIH [2], playing a key role in the modulation of anxiety and fear. In addition, there is a research finding that the coupled cascade of group I mGluR and NMDA receptor can cause phosphorylation of the NMDA receptors and appears responsible for the initiation of spinal dorsal horn sensitization and behavioral hyperalgesia after inflammation [65]. So, group I mGluRs are closely related to NMDA receptors in hyperalgesia effect.