One single physical exercise session improves memory persistence by hippocampal activation of D1 dopamine receptors and PKA signaling in rats

Lima, Karine Ramires; Rosa, Ana Carolina de Souza da; Picua, Steffanie Severo; Silva, Shara Souza e; Soares, Náthaly Marks; Mello‐Carpes, Pâmela Billig

doi:10.1016/j.brainres.2021.147439

Cited by 6 publications

(4 citation statements)

References 37 publications

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“…Specifically, four studies that used Barnes maze and/or novel object recognition tests to assess learning and memory in control mice with or without exercise were identified. One study showed that adult control rats with one episode of exercise that was at 60–70% maximal indirect oxygen uptake for 30 min immediately after the training session of novel object recognition test had better memory performance assessed 7 days but not at 1 day or 14 days after the training session [ 43 ]. The second study showed that voluntary exercise for 4 weeks did not affect the learning and memory assessed by Barnes maze and novel object recognition tests in control rats [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice

Lai

Shan

et al. 2021

Mol Psychiatry

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Postoperative cognitive dysfunction (POCD) affects the outcome of millions of patients each year. Aging is a risk factor for POCD. Here, we showed that surgery induced learning and memory dysfunction in adult mice. Transplantation of feces from surgery mice but not from control mice led to learning and memory impairment in non-surgery mice. Low intensity exercise improved learning and memory in surgery mice. Exercise attenuated surgery-induced neuroinflammation and decrease of gut microbiota diversity. These exercise effects were present in non-exercise mice receiving feces from exercise mice. Exercise reduced valeric acid, a gut microbiota product, in the blood. Valeric acid worsened neuroinflammation, learning and memory in exercise mice with surgery. The downstream effects of exercise included attenuating growth factor decrease, maintaining astrocytes in the A2 phenotypical form possibly via decreasing C3 signaling and improving neuroplasticity. Similar to these results from adult mice, exercise attenuated learning and memory impairment in old mice with surgery. Old mice receiving feces from old exercise mice had better learning and memory than those receiving control old mouse feces. Surgery increased blood valeric acid. Valeric acid blocked exercise effects on learning and memory in old surgery mice. Exercise stabilized gut microbiota, reduced neuroinflammation, attenuated growth factor decrease and preserved neuroplasticity in old mice with surgery. These results provide direct evidence that gut microbiota alteration contributes to POCD development. Valeric acid is a mediator for this effect and a potential target for brain health. Low intensity exercise stabilizes gut microbiota in the presence of insult, such as surgery.

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Section: Discussionmentioning

confidence: 99%

Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice

Lai

Shan

et al. 2021

Mol Psychiatry

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“…We compared the percentage of total time spent exploring the familiar and novel object/food within each group in the training and test sessions using paired Student's t ‐tests. To perform comparisons between groups in the test session, we calculated a discrimination index (DI) for the novel object/food: DI = [(T novel—T familiar)/(T novel + T familiar) × 100 (%) (Ramires Lima et al., 2021) and compared the DI by two‐way ANOVA. Two‐way ANOVAs were used to compare adipose tissue depots (calculated as a percentage of body weight), Search for Food and Open Field Test, BioDAQ® food monitoring measures, and all biochemical measurements between groups.…”

Section: Methodsmentioning

confidence: 99%

The impact of poor fetal growth and chronic hyperpalatable diet exposure in adulthood on hippocampal function and feeding patterns in male rats

Mucellini,

Laureano,

Alves

et al. 2024

Developmental Psychobiology

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Poor fetal growth affects eating behavior and the mesocorticolimbic system; however, its influence on the hippocampus has been less explored. Brain insulin sensitivity has been linked to developmental plasticity in response to fetal adversity and to cognitive performance following high‐fat diet intake. We investigated whether poor fetal growth and exposure to chronic hyperpalatable food in adulthood could influence the recognition of environmental and food cues, eating behavior patterns, and hippocampal insulin signaling. At 60 days of life, we assigned male offspring from a prenatal animal model of 50% food restriction (FR) to receive either a high‐fat and ‐sugar (HFS) diet or standard chow (CON) diet. Behavioral tests were conducted at 140 days, then tissues were collected. HFS groups showed a diminished hippocampal pAkt/Akt ratio. FR‐CON and FR‐HFS groups had higher levels of suppressor of cytokine signaling 3, compared to control groups. FR groups showed increased exploration of a novel hyperpalatable food, independent of their diet, and HFS groups exhibited overall lower entropy (less random, more predictable eating behavior) when the environment changed. Poor fetal growth and chronic HFS diet in adulthood altered hippocampal insulin signaling and eating patterns, diminishing the flexibility associated with eating behavior in response to extrinsic changes in food availability in the environment.

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“…Male BALB/c mice injected with quetiapine every other day and pretreated with the D1 receptor antagonist SKF-35866 in the following experiments found a significant increase in the preference to the quetiapine-paired chamber in mice treated with 120 mg/kg quetiapine, and this effect was blocked by pretreatment with SKF-35866, suggesting that the antidepressant-like effects of quetiapine may be modulated by D1 receptors ( Althobaiti, 2021 ). Recent experimental studies have shown that activation of the DRD1 receptor and PKA is involved in the memory-improving effect of acute physical exercise ( Ramires Lima et al, 2021 ).…”

Section: Dopamine Receptors and Depressionmentioning

confidence: 99%

Dopamine Receptors: Is It Possible to Become a Therapeutic Target for Depression?

et al. 2022

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Dopamine and its receptors are currently recognized targets for the treatment of several neuropsychiatric disorders, including Parkinson’s disease, schizophrenia, some drug use addictions, as well as depression. Dopamine receptors are widely distributed in various regions of the brain, but their role and exact contribution to neuropsychiatric diseases has not yet been thoroughly studied. Based on the types of dopamine receptors and their distribution in different brain regions, this paper reviews the current research status of the molecular, cellular and circuit mechanisms of dopamine and its receptors involved in depression. Multiple lines of investigation of these mechanisms provide a new future direction for understanding the etiology and treatment of depression and potential new targets for antidepressant treatments.

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One single physical exercise session improves memory persistence by hippocampal activation of D1 dopamine receptors and PKA signaling in rats

Cited by 6 publications

References 37 publications

Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice

Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice

The impact of poor fetal growth and chronic hyperpalatable diet exposure in adulthood on hippocampal function and feeding patterns in male rats

Dopamine Receptors: Is It Possible to Become a Therapeutic Target for Depression?

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