Page 46 - 《运动与健康科学》(英文)2024年第2期

TaggedAPTARAEnd168 Y. Dai et al.
is one of the most studied activities that has been shown to dendritic plasticity. The neuromuscular junction is a specialized
positively influence adult neuroplasticity. 95 Neuroplasticity is synapse formed between motoneurons and skeletal muscle
an umbrella term that includes all the functional and structural fibers. Early studies have shown endurance training increases
changes occurring within a neural circuit, and it involves the synapse size of neuromuscular junctions in adult mice 109
various mechanisms, such as synaptic plasticity, dendritic and rats. 110,111 Exercise also induced hypertrophy of neuromus-
remodeling, and neurogenesis. 9698 Neurons are typically cular junctions of the extensor digitorum longus and gluteus
comprised of a cell body, an axon through which they transmit maximus in adult mice and rats. 112,113 TaggedAPTARAEnd
information to other neurons, and a dendritic arbor where TaggedAPTARAPChronic exercise also affects receptor expression in neurons
input from other neurons is primarily received. 99 Neurotrans- involved in sensory signal transmission of the dorsal root
mitter receptors are largely restricted to the surface of dendritic ganglion. These changes include an increase in opioid receptor
spines, which are small membranous protrusions whose struc- m subunit mRNA levels in conjunction with decreases in
tural geometry correlates with the strength of synaptic connec- 5-HT 1A , tyrosine-related kinase receptors A and B, and delta-type
tions. 100 Neuronal plasticity is correlated to the density and opioid receptor mRNA levels. 114 Furthermore, exercise also
morphology of the dendritic spines given they are the main promotes morphological and functional plasticity in astrocytes. 115
sites of synaptic input for neurons. 101 TaggedAPTARAEnd Recent studies have demonstrated that exercise induces various
TaggedAPTARAPExercise can modulate neuronal excitability by regulating changes in astrocytes, including increased proliferation, improved
various ion channels, which can in turn alter neuronal maintenance of basal levels of catecholamine, enhanced gluta-
115
morphology. Several studies have shown exercise causes the mate uptake, and increased trophic factor release. TaggedAPTARAEnd
regeneration of spinal cord neurons by increasing the length of
neuronal dendrites, causing the synthesis of nutritional factors TaggedAPTARAH17. Exercise increases nutritional factors and protein
inside neurons, and increasing the density of neuronal synthesisTaggedAPTARAEnd
synapses. 3,102104 Significant adaptations in neural
TaggedAPTARAPNeurotrophins are a group of soluble growth factors that
morphology, including changes in soma size and dendritic can modulate neuronal synaptic function, plasticity, and
3
number, as well as herald changes in functional properties. A 116
survival. Brain-derived neurotrophic factor plays a signifi-
previous study demonstrated endurance training increases the cant role in promoting dendritic plasticity, 117 and their
average soma diameter of rat soleus motoneurons. 105 Addi-
increased expression is associated with changes in neuronal
tional research has shown chronic exercise leads to an increase
morphology. Treadmill training has been shown to signifi-
in motoneuron membrane capacitance, an index of cell size, cantly increase brain-derived neurotrophic factor expression in
suggesting motoneuron size increases following exercise. 10
rat lumbar motoneurons in conjunction with an increase in
Exercise promotes dendritic spine formation and enhances 118
total neurite length. It has been known since the 1950s that
motor learning in the mouse hippocampus and motor motoneurons of treadmill-trained rats exhibit increased
cortex. 106 Recent research has revealed 3 weeks of treadmill
staining intensity for glucose-6-phosphate dehydrogenase,
exercise facilitates dendritic plasticity in midbrain 5-HT 119
which suggests heightened synthesis of that protein. More-
neurons of juvenile mice as evidenced by an increase in the
over, a study in mice has reported moderate-intensity treadmill
number of dendritic length, branches, and branch points within exercise leads to increased expression of several factors in the
16
a range of 50200 mm from the soma. These results matched motor cortex of a crushed spinal cord injury, including brain-
those of similar studies in spinal lamina X neurons. 15 Past
derived neurotrophic factor, insulin-like growth factor 1, phos-
studies have also confirmed that the distribution of the Cav1.3 120
33,73 phorylated ribosomal S6 protein, and protein kinase B.
is concentrated in neuronal dendrites. In fact, exercise can
15,16 These studies support the notion that chronic exercise can
increase PICs mediated by Cav1.3. Altogether, these
induce alterations in nutritional factors and protein synthesis
results illustrate a model for the cellular and ionic basis of
that ultimately facilitate neuronal plasticity.TaggedAPTARAEnd
exercise-induced dendritic plasticity.TaggedAPTARAEnd
TaggedAPTARAH18. ConclusionTaggedAPTARAEnd
TaggedAPTARAH16. Exercise modulates receptor expressionTaggedAPTARAEnd
TaggedAPTARAPVertebrate neurons possess an astounding ability to alter
TaggedAPTARAPExercise also alters synaptic density and structural formation. themselves at cellular and molecular scales in adaptation to
Previous studies have shown that passive cycling can increase their surroundings. Nowhere is this truer than in the case of the
synaptic density in rat lumbar motoneurons by increasing the neurons composing the locomotor system, which display
expression of 5-HT 2A ,5-HT 7 , and potassium-chloride cotrans- remarkable plasticity in response to increases or decreases in
porter 2 receptors in extensor motoneurons. 92,107 Conversely, muscle use, upstream or downstream motor injury, and aging.
exercise reduces the expression of 5HT 1A receptor and g amino- Research in various animal models from the past up to the
butyric acid receptor subunit a 2. 92 Furthermore, resistance present has shown that exercise induces significant alterations
training increases the number of excitatory synapses on spinal in the function and physiology of these neurons. Multiple
motoneurons while inhibitory synapses remain unaffected, mechanisms are involved in the plasticity and excitability of
suggesting motoneurons receive greater excitatory synaptic neurons, and the modulation of ion channels and facilitation of
input from chronic exercise. 108 This change in neurotransmitter dendritic plasticity are of particular importance to their adap-
receptor densities suggest exercise enhances spinal motoneuron tive response during/following chronic exercise. Exercise also