Psychological responses to stress and exercise on students’ lives
Romain Meeusen, Sabine Schaefer, Phillip Tomporowski, Richard Bailey in Physical Activity and Educational Achievement, 2017
Exercise can change HPA function in different ways, for example, by reducing ACTH during the morning, increasing corticosterone levels during dark phase, and other responses (Droste et al., 2003). HPA axis response can also be changed when trained animals are faced with different kinds of stress (Droste et al., 2003). In summary, it is difficult to understand the complex adjustment of the HPA by chronic effects of exercise. In this context, it is very interesting to note that exercise activates the HPA axis in a similar way to other stressors. However, some stressors (i.e. social stress) have a negative impact on our body, while exercise can have a positive impact. The differentiation between these positive and negative effects is not clear. Stranahan, Lee, and Mattson (2008) discussed that exercise generates positive effects because it is predictable, controllable and a rewarding stimulus. The reward system is composed of many brain areas (for review, see Arias-Carrion et al., 2014) that when stimulated work to reinforce stimuli for a repetitive behaviour. Thus, exercise-activated reward system can be the key to stress management, because exercise will be tolerated and will generate positive effects in the organism.
Brain Motor Centers and Pathways
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
The basal ganglia have been implicated in a wide range of functions, as evidenced by the distribution of the inputs they receive. Practically all areas of the cerebral cortex project essentially topographically to the dorsal striatum, thence to other nuclei, and back through the feedback loops via the thalamus to the same cortical areas of origin of the given input to the basal ganglia. The dorsal striatum also receives: (i) feedback input from thalamic nuclei, (ii) dopaminergic input from the ventral tegmental area of the midbrain, which is believed to be part of the “reward” system in the brain, and (iii) serotonergic input from the raphe nuclei, which are a group of nuclei in the brainstem that are a major source of serotonin to the rest of the brain. Serotonin is a neurotransmitter that influences many brain functions, including mood, behavior, sleep, memory, and learning.
Appetite Control in C. elegans
Ruth B.S. Harris in Appetite and Food Intake, 2017
Song and Avery found that this preference toward familiar food is conserved in C. elegans. Using two equally good qualities of bacteria (let us name them A and B for convenience), they showed that C. elegans that had fed on bacteria A chose A but the C. elegans that had fed on B chose B, when they were given choices between A and B. Song and Avery further discovered that this behavior is mediated by a neuronal serotonin system. Serotonin has been implicated in mimicking food in C. elegans (Horvitz et al. 1982, Sze et al. 2000, Niacaris and Avery 2003), exerting several food-related behaviors such as promoting feeding motions and egg-laying and suppressing locomotion. In mammals, serotonin plays a critical role in controlling appetite and food choices by controlling dopamine pathway reward circuits. Song and Avery’s work suggests that a conserved reward circuit is used to promote feeding after recognizing familiar food.
Placebo and cultural responses*
Published in Nordic Journal of Psychiatry, 2018
Antonio Ventriglio, Giuseppe Magnifico, Luisa Borraccino, Angelo Rinaldi, Antonello Bellomo
Recent studies have demonstrated that different neurotransmitter systems are involved in the placebo response. The endogenous opioid anti-nociceptive system is undoubtedly involved in placebo analgesia. In 1978, Levine et al. [5] administered placebo as an analgesic for postoperative pain, observing a significant reduction in painful symptoms and a reversal of this response by the opioid antagonist naloxone. Moreover, it was found that β-endorphin levels were higher in the cerebrospinal fluid of placebo responders than non-responders [6]. In addition, the endocannabinoid system has been recently identified as a new non-opioid component of placebo analgesia [7]. It has been observed that the administration of placebo, proposed as an anti-Parkinsonian drug, can lead to an improvement in motor performances among patients with Parkinson’s disease. This effect may be mediated by the endogenous release of dopamine in the dorsal striatum, a critical component of the motor systems [8]. In fact, the ventral striatum, and in particular the nucleus accumbens, are involved in the reward circuit, mediating reinforcement and motivational responses. Activation of the ventral striatum should be present in any response to placebo and the release of dopamine would be linked to the expectation of reward rather than the reward itself [8,9].
Assessment of the relationship between food addiction and nutritional status in schizophrenic patients
Published in Nutritional Neuroscience, 2019
Özge Küçükerdönmez, Murat Urhan, Merve Altın, Özge Hacıraifoğlu, Burak Yıldız
It is known there are similar pathways in food addiction and substance addiction. A study found that when images of appetizing foods (foods containing fat and sugar at high levels) were shown to study participants, the reward area in their brains which is related to substance addiction became activated and dopamine was released automatically.45 The brain-reward system consists of the mesolimbic dopamine system (the ventral tegmental area, nucleus accumbens (NAc), prefrontal cortex, amygdala), lateral hippocampus, and medial forebrain. This system shows its effects mainly via dopamine. The dopaminergic system is in a continuous communication with opioid-mediated-gabaergic system, cholinergic system, and serotoninergic system. These systems can modulate the activation of the reward system and the release of dopamine.46,47 A study by Leigh and Morris48 showed that when a highly tasty diet is eaten, the expression of D1 dopamine receptor mRNA levels decreases, the striatal D2 dopamine receptor levels may be associated with obesity predisposition, and mu-opioid gene expression decreases in NAc.
Sexual dysfunction with major depressive disorder and antidepressant treatments: impact, assessment, and management
Published in Expert Opinion on Drug Safety, 2022
Joan Winter, Kimberly Curtis, Bo Hu, Anita H. Clayton
Serotonin binding at the post-synaptic 5-HT1A receptor produces antidepressant and anxiolytic effects, while increased binding at the 5-HT2A and 5-HT2C receptors leads to increased anxiety, insomnia, and sexual dysfunction. Multiple antidepressants (eg. mirtazapine, trazodone, several TCAs, and norquetiapine – the active metabolite of quetiapine) with fewer sexual side effects exhibit antagonism at 5-HT2. The release of dopamine and norepinephrine in the cortex is inhibited by stimulation of 5-HT2A and 5-HT2C receptors [9–10]. Norepinephrine and nitric oxide promote tumescence of sexual organs and lubrication. Dopamine is a key neurotransmitter of the reward system, which includes the nucleus accumbens/ventral striatum, ventral tegmental area (VTA), pre-frontal cortex, orbitofrontal cortex, anterior cingulate cortex, and amygdala. Dopamine promotes sexual function at varying concentrations at progressive stages of sexual engagement: from sexual desire to increased parasympathetic activation required for erections, and finally climax. Dopamine may also be involved in the medial preoptic area of the hypothalamus (mPOA) in the initial disinhibition of genital reflexes[12]. In addition to central effects, serotonin acts in the peripheral nervous system by directly suppressing spinal ejaculatory centers [10–11]. Thus, the increase of serotonin at the synaptic cleft as a result of antidepressant action can impact many levels of sexual functioning: decreased interest and arousal, inhibited/delayed orgasm, and diminished intensity and frequency of orgasm[13].
Related Knowledge Centers
- Classical Conditioning
- Emotion
- Operant Conditioning
- Valence
- Euphoria
- Motivational Salience
- Learning
- Reinforcement
- Pleasure
- Joy