Enhancement of neuronal plasticity by activating the norepinephrine system in the brain: a remedy for amblyopia.
The norepinephrine hypothesis claims that an increase in the local availability of norepinephrine necessarily enhances neuronal plasticity in a given brain region. This claim had been successfully tested, and reviewed here briefly, in two experimental paradigms: 1) restoration of cortical plasticity by localized and continuous perfusion of the catecholamine-terminal-depleted visual cortex with exogenous norepinephrine and dibutyryl adenosine cyclic monophosphate, and 2) acceleration of cortical recovery from the effects of prior monocular lid suture by direct perfusion of the cortex with norepinephrine. Activation of the norepinephrine-beta-adrenergic receptor system in the visual cortex was discussed as a potential remedy for amblyopia.
D000550:Amblyopia / Q000188:drug therapy*; D000818:Animals; D003994:Bucladesine / Q000627:therapeutic use*; D002415:Cats; D006801:Humans; D007223:Infant; D008125:Locus Coeruleus / Q000502:physiology; D009414:Nerve Growth Factors / Q000494:pharmacology; D009473:Neuronal Plasticity / Q000187:drug effects*; D009638:Norepinephrine / Q000378:metabolism / Q000627:therapeutic use*; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D014793:Visual Cortex / Q000187:drug effects* / Q000502:physiology
D009414:Nerve Growth Factors; D011943:Receptors, Adrenergic, beta; D003994:Bucladesine; D009638:Norepinephrine