Effect of forced treadmill exercise on stimulation of BDNF expression, depression symptoms, tactile memory and working memory in LPS-treated rats

2021 ◽  
pp. 113645
Author(s):  
Moosavi Sohroforouzani Azam ◽  
Shakerian Saeed ◽  
Ghanbarzadeh Mohsen ◽  
Alaei Hojjatallah
Keyword(s):  
Working Memory ◽  
Treadmill Exercise ◽  
Depression Symptoms ◽  
Bdnf Expression ◽  
Tactile Memory ◽  
Stimulation Of

Stimulation of GABAB receptors in thebasal forebrain selectively impairs working memory of rats in the double Y-maze

1994 ◽  
Vol 641 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Norberto J. DeSousa ◽  
Richard J. Beninger ◽  
Khem Jhamandas ◽  
Roland J. Boegman
Keyword(s):  
Working Memory ◽  
Gabab Receptors ◽  
Y Maze ◽  
Stimulation Of

scholarly journals Neurocognitive effects of six ketamine infusions and the association with antidepressant effects in treatment-resistant bipolar depression: a preliminary study

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10208
Author(s):  
Wei Zheng ◽  
Yan-Ling Zhou ◽  
Cheng-Yu Wang ◽  
Xiao-Feng Lan ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Working Memory ◽  
Bipolar Depression ◽  
Visual Learning ◽  
Verbal Learning ◽  
Depression Symptoms ◽  
Speed Of Processing ◽  
Treatment Resistant ◽  
Observational Period ◽  
Preliminary Study ◽  
Over Time

Objective The N-methyl-D-aspartate subtype glutamate receptor antagonist ketamine has rapid antidepressant and antisuicidal effects in treating treatment-resistant bipolar depression (TRBD). The neurocognitive effects of repeated ketamine infusions in TRBD are not known. Methods Six intravenous infusions of ketamine (0.5 mg/kg over 40 min) were administered on a Monday–Wednesday–Friday schedule during a 12-day period on 16 patients with TRBD followed by a 2-week observational period. The assessment of neurocognitive function was conducted using the MATRICS Consensus Cognitive Battery at baseline, 13 and 26 days. Tasks were designed to test speed of processing, working memory, visual learning and verbal learning. Results A significant improvement was found only in scores of speed of processing (F = 9.9, p = 0.001) after a 2-week observational period, which was accounted for by the improvement of depression symptoms. There were no significant changes over time in terms of working memory, visual learning and verbal learning. Pearson correlation analysis showed that the improvement of depression symptoms through six ketamine infusions was greater among TRBD patients with lower working memory at baseline (r = 0.54, p = 0.03). In multiple regression analysis, the significant correlation was still maintained (beta = 0.67, t = 2.2, p = 0.04). Conclusion This preliminary study indicated that six ketamine infusions were not harmful but were slightly beneficial for speed of processing in TRBD. However, this change was mainly accounted for the improvement of depression symptoms over time. Lower baseline working memory appears to be associated with greater antidepressant response after completion of six ketamine infusions in patients with TRBD.

scholarly journals Muscle injury, impaired muscle function and insulin resistance in Chromogranin A-knockout mice

2017 ◽  
Vol 232 (2) ◽  
pp. 137-153 ◽  
Author(s):  
Kechun Tang ◽  
Teresa Pasqua ◽  
Angshuman Biswas ◽  
Sumana Mahata ◽  
Jennifer Tang ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Muscle Function ◽  
Chromogranin A ◽  
Secretory Pathway ◽  
Treadmill Exercise ◽  
Tubular Aggregates ◽  
Skeletal Muscle Function ◽  
Regulated Secretory Pathway ◽  
Exercise Induced ◽  
Stimulation Of

Chromogranin A (CgA) is widely expressed in endocrine and neuroendocrine tissues as well as in the central nervous system. We observed CgA expression (mRNA and protein) in the gastrocnemius (GAS) muscle and found that performance of CgA-deficient Chga-KO mice in treadmill exercise was impaired. Supplementation with CgA in Chga-KO mice restored exercise ability suggesting a novel role for endogenous CgA in skeletal muscle function. Chga-KO mice display (i) lack of exercise-induced stimulation of pAKT, pTBC1D1 and phospho-p38 kinase signaling, (ii) loss of GAS muscle mass, (iii) extensive formation of tubular aggregates (TA), (iv) disorganized cristae architecture in mitochondria, (v) increased expression of the inflammatory cytokines Tnfα, Il6 and Ifnγ, and fibrosis. The impaired maximum running speed and endurance in the treadmill exercise in Chga-KO mice correlated with decreased glucose uptake and glycolysis, defects in glucose oxidation and decreased mitochondrial cytochrome C oxidase activity. The lack of adaptation to endurance training correlated with the lack of stimulation of p38MAPK that is known to mediate the response to tissue damage. As CgA sorts proteins to the regulated secretory pathway, we speculate that lack of CgA could cause misfolding of membrane proteins inducing aggregation of sarcoplasmic reticulum (SR) membranes and formation of tubular aggregates that is observed in Chga-KO mice. In conclusion, CgA deficiency renders the muscle energy deficient, impairs performance in treadmill exercise and prevents regeneration after exercise-induced tissue damage.

scholarly journals Corticostriatal stimulation compensates for medial frontal inactivation during interval timing

2019 ◽  
Author(s):  
Eric B. Emmons ◽  
Morgan Kennedy ◽  
Youngcho Kim ◽  
Nandakumar S. Narayanan
Keyword(s):  
Working Memory ◽  
Temporal Processing ◽  
Response Times ◽  
Interval Timing ◽  
Brain Diseases ◽  
Axon Terminals ◽  
Optogenetic Stimulation ◽  
Prefrontal Dysfunction ◽  
Timing Task ◽  
Stimulation Of

AbstractPrefrontal dysfunction is a common feature of brain diseases such as schizophrenia and contributes to deficits in executive functions, including working memory, attention, flexibility, inhibitory control, and timing of behaviors. Currently, few interventions can compensate for impaired prefrontal function. Here, we tested whether stimulating the axons of prefrontal neurons in the striatum could compensate for deficits in temporal processing related to prefrontal dysfunction. We used an interval-timing task that requires working memory for temporal rules and attention to the passage of time. Our previous work showed that inactivation of the medial frontal cortex (MFC) impairs interval timing and attenuates ramping activity, a key form of temporal processing in the dorsomedial striatum (DMS). We found that 20-Hz optogenetic stimulation of MFC axon terminals in the DMS shifted response times and improved interval-timing behavior. Furthermore, optogenetic stimulation of terminals modulated time-related ramping of medium spiny neurons in the striatum. These data suggest that corticostriatal stimulation can compensate for deficits caused by MFC inactivation and they imply that frontostriatal projections are sufficient for controlling responses in time.

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