Effects of long-lasting voluntary running on the cerebral levels of dopamine, serotonin and their metabolites in the spontaneously hypertensive rat

Hoffmann, Pavel; Elam, Mikael; Thorén, Peter; Hjorth, S

doi:10.1016/0024-3205(94)00622-9

Cited by 24 publications

(14 citation statements)

References 30 publications

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“…For example, some studies in laboratory rodents and humans suggest that physical exercise increases serotonin levels (Chaouloff, 1997) and that low levels of exercise correlate with aggressive behavior (Jagoe and Serpell, 1996;Tsatsoulis and Fountoulakis, 2006); however, other studies have failed to find such an effect (Acworth et al, 1986;Hoffmann et al, 1994). Preliminary findings suggest that aggressive dogs exercise less than nonaggressive dogs ).…”

Section: Discussionmentioning

confidence: 85%

Differences in serotonin serum concentration between aggressive English cocker spaniels and aggressive dogs of other breeds

Amat

Brech

Camps

et al. 2013

Journal of Veterinary Behavior

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Section: Discussionmentioning

confidence: 85%

Differences in serotonin serum concentration between aggressive English cocker spaniels and aggressive dogs of other breeds

Amat

Brech

Camps

et al. 2013

Journal of Veterinary Behavior

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“…However, in that study which compared five inbred rats, Bedford et al [2] demonstrated an inter-strain VO 2max difference with a decreased VO 2max in SHR compared with Sprague-Dawley rats, so in our study SHR may have been overtrained compared with Lewis rats. Alternatively, SHR have been shown to run long distances in another exercise paradigm, e.g., spontaneous wheel running [17], indicating that SHR display significant endurance capacities. Moreover, increases in basal CORT values have been reported in overtrained subjects, e.g., an observation that differs from ours where a significant decrease in plasma CORT values after 8 weeks of forced exercise was observed in SHR compared with Lewis rats.…”

Section: Discussionmentioning

confidence: 99%

Relationships between muscle mitochondrial metabolism and stress-induced corticosterone variations in rats

Duclos

Martin

Malgat

et al. 2001

Pflügers Arch - Eur J Physiol

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In order to determine the effect of chronic and acute stress on muscle mitochondrial metabolism, two strains of rats were selected on the basis of their different hypothalamo-pituitary-adrenal (HPA) axis responses to different stressors [Spontaneous Hypertensive Rats (SHR) and Lewis rats]. For 8 weeks animals were stressed by daily exposure to either a novel environment (SHR: n=16, Lewis: n=16) or forced exercise (SHR: n=16, Lewis: n=16). An unstressed group was left undisturbed (SHR: n=5, Lewis: n=5). Half of the stressed animals (n=32) were submitted to an acute stress (1-h immobilization). The mitochondrial responses of plantaris muscle [cytochrome-c-oxidase (COX), citrate synthase and succinate dehydrogenase activities, the latter two being measured as indices of functional mitochondrial amount] in the presence of different physiological plasma corticosterone (CORT) concentrations were analyzed. The novel environment and forced exercise stress induced different levels of plasma CORT which were negatively correlated with the amount of functional mitochondria in the plantaris muscle. Therefore, a chronic intermittent stress is able to induce an increase in plasma CORT which may be related to deleterious changes in muscle mitochondrial metabolism. Lastly, the acute stress was not associated with a decrease in functional mitochondria but with an increase in COX activity. This suggests that the relationship between CORT and muscle mitochondrial metabolism depends both on the level and duration of endogenous glucocorticoids exposure.

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“…The increase in DA content and release during physical activity was later restricted to areas rich in DA innervation including the striatum (Bailey et al 1992, 1993b, Freed and Yamamoto 1985Hattori et al 1994;Heyes et al 1988;MacRae et al 1987;Meeusen et al 1997b;Sabol et al 1990;Speciale et al 1986;Wilson and Marsden 1995), midbrain (Bailey et al 1992, 1993b, Chaouloff et al 1987, hippocampus (Bailey et al 1992, Chaouloff et al 1987), brain stem (Blomstrand et al 1989;Heyes et al 1988), hypothalamus (Bailey et al 1993b;Blomstrand et al 1989;Chaouloff et al, 1987;Hasegawa et al 2000;Heyes et al 1988), spinal cord (Gerin et al 1995;Gerin and Privat 1998), and cerebrospinal fluid (Chaouloff et al 1986). Interestingly, the increase in DA during exercise is dependent on the speed and postural direction of the animal (Freed and Yamamoto 1985;Hattori et al 1994), yet is increased independent of training status (trained versus untrained) (Blomstrand et al 1989, Chaouloff et al 1987Lim et al 2001;Meeusen et al 1997b;Sabol et al 1990), mode of exercise (swim versus treadmill versus wheel run) (Bliss and Ailion 1971;Elam et al 1987;Hoffmann et al 1994;Speciale et al 1986), duration of...…”

Section: Dopamine Neurotransmission During Physical Activity and The mentioning

confidence: 97%

Neuroplasticity of Dopamine Circuits After Exercise: Implications for Central Fatigue

2008

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Habitual exercise increases plasticity in a variety of neurotransmitter systems. The current review focuses on the effects of habitual physical activity on monoamine dopamine (DA) neurotransmission and the potential implication of these changes to exercise-induced fatigue. Although it is clear that peripheral adaptations in muscle and energy substrate utilization contribute to this effect, more recently it has been suggested that central nervous system pathways "upstream" of the motor cortex, which initiate activation of skeletal muscles, are also important. The contribution of the brain to exercise-induced fatigue has been termed "central fatigue." Given the well-defined role of DA in the initiation of movement, it is likely that adaptations in DA systems influence exercise capacity. A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could impair activation of the basal ganglia and reduce stimulation of the motor cortex leading to central fatigue. Here we present evidence that habitual wheel running produces changes in DA systems. Using in situ hybridization techniques, we report that 6 weeks of wheel running was sufficient to increase tyrosine hydroxylase mRNA expression and reduce D2 autoreceptor mRNA in the SNpc. Additionally, 6 weeks of wheel running increased D2 postsynaptic receptor mRNA in the caudate putamen, a major projection site of the SNpc. These results are consistent with prior data suggesting that habitually physically active animals may have an enhanced ability to increase DA synthesis and reduce D2 autoreceptor-mediated inhibition of DA neurons in the SNpc compared to sedentary animals. Furthermore, habitually physically active animals, compared to sedentary controls, may be better able to increase D2 receptor-mediated inhibition of the indirect pathway of the basal ganglia. Results from these studies are discussed in light of our understanding of the role of DA in the neurobiological mechanisms of central fatigue.

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Effects of long-lasting voluntary running on the cerebral levels of dopamine, serotonin and their metabolites in the spontaneously hypertensive rat

Cited by 24 publications

References 30 publications

Differences in serotonin serum concentration between aggressive English cocker spaniels and aggressive dogs of other breeds

Differences in serotonin serum concentration between aggressive English cocker spaniels and aggressive dogs of other breeds

Relationships between muscle mitochondrial metabolism and stress-induced corticosterone variations in rats

Neuroplasticity of Dopamine Circuits After Exercise: Implications for Central Fatigue

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