Synaptic plasticity promotion

Noradrenaline acts on three types of receptor. The ai receptors mediate the main excitatory effects of noradrenaline upon wake-active neurons in the dorsal raphe, basal forebrain, and elsewhere (Vandermaelen Aghajanian, 1983 Nicoll, 1988 Fort et al., 1995 Brown et al., 2002). The a2 receptors mediate inhibitory effects of noradrenaline, e.g. on noradrenaline neurons themselves and on cholinergic brainstem neurons (Williams et al., 1985 Williams Reiner, 1993). The (3-receptors modulate neurons in a more subtle fashion, increasing excitability via blockade of afterhyperpolarizations in hippocampal and cortical neurons (Haas Konnerth, 1983). Activation of (3-receptors also promotes synaptic plasticity via activation of the cyclic-AMP-dependent kinase (PKA) and cyclic AMP response element binding protein (CREB) signal transduction pathway (Stanton Sarvey, 1987 Cirelli et al., 1996). 

Omega-3 PUFAs are essential unsaturated fatty acids obtained from food sources or from supplements. Amongst nutritionally important polyunsaturated n-3 fatty acids, a-linolcnic acid (ALA), eicosapentae-noic acid (EPA), and docosahexaenoic acid (DHA) are highly concentrated in the brain and have antioxidative stress, anti-inflammatory and antiapoptotic effects. The exposure to n-3 fatty acids enhances adult hippocampal neurogenesis associated with cognitive and behavioral processes, promotes synaptic plasticity by increasing longterm potentiation, and modulates synaptic protein expression to stimulate the dendritic arborization and new spine formation [496]. 

In addition, exercise also upregulates the expression of the mitochondrial uncoupling protein 2, an energy-balancing factor concerned with ATP formation and free radical management (Vaynman et al., 2006), supporting the view that in brain tissue physical exercise promotes a fundamental mechanism by which key elements of energy metabolism may modulate the substrates of hippocampal synaptic plasticity. 

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