Does increasing the ratio of AMPA-to-NMDA receptor mediated neurotransmission engender antidepressant action? Studies in the mouse forced swim and tail suspension tests

Differential role of AMPA receptors in mouse tests of antidepressant and anxiolytic action

“…LY451646 produced antidepressantlike responses in both the mFST and mTST, in accordance with literature evidence suggesting a link between increased AMPAR-mediated neurotransmission and antidepressant efficacy (Andreasen et al, 2013;Li et al, 2001;Li et al, 2003). Our finding that GYKI-53655 produced a depressogenic-like response in the TST lends further support to this hypothesis.…”

“…Thus, increased AMPAR expression levels have been demonstrated after chronic treatment with monoamine-based antidepressants (Barbon et al, 2011;Martinez-Turrillas et al, 2002) or the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine (Tizabi et al, 2012). In accordance with this hypothesis, AMPAR positive allosteric modulators (PAMs) produce antidepressant-like responses in rodents (Li et al, 2001) and enhance the antidepressant-like effects of monoamine-based antidepressants (Andreasen et al, 2013;Li et al, 2003) as well as the NMDAR antagonist MK-801 (Andreasen et al, 2013).…”

Anxiety- and depression-like phenotype of hph-1 mice deficient in tetrahydrobiopterin

“…Despite their face value similarity, the FST and TST measure activity involving partially different neuronal mechanisms (Bai et al, 2001;Renard et al, 2003). These tests have shown differential sensitivities to drugs exploiting both monoamine (Bai et al, 2001;Renard et al, 2003) and non-monoamine mechanisms (Andreasen and Redrobe, 2009;Andreasen et al, 2013). Moreover, baseline and drug responses in these two tests depend on both genotype and sex (Andreasen and Redrobe, 2009).…”

Characterization of Senescence-Accelerated Mouse Prone 6 (SAMP6) as an Animal Model for Brain Research

“…Spontaneous genetic alteration (s) near these QTLs might have been co-fixed in SAMP6 through selective breeding, leading to the alterations in the dopamine, serotonin, and LTP-related-molecule systems as described above. Since neurotransmission systems of dopamine, serotonin, and glutamate are known to affect one another [1, 5, 16, 28, 33, 61, 62], a genetic alteration related to these neurotransmitter pathways might trigger the multiple molecular and behavioral alterations in SAMP6. Identifying QTLs for behavioral characteristics of SAMP6 is needed to elucidate the mechanisms involved.…”