Clonidine and cortical plasticity: possible evidence for noradrenergic involvement.
In order to test the hypothesis that noradrenergic transmission modulates ocular dominance plasticity in kitten visual cortex, we monocularly deprived kittens while administering the alpha-2 adrenergic agonist clonidine (CLON). To avoid bias in testing the hypothesis, we included, with a single blind technique, saline-treated control kittens in the series. First, using high-pressure liquid chromatography, we demonstrated that CLON treatments resulted in an average decline in cerebrospinal fluid levels of the norepinephrine metabolite, 3-methoxy-4-hydroxy phenylethylene glyolol (MHPG) of 44%. Then, single-unit recording in area 17 revealed the expected ocular dominance (OD) shift in monocularly deprived saline controls, but recording failed to find a significant shift in CLON-treated kittens. Our results support the notion that CLON treatment interferes with ocular dominance plasticity by inhibiting noradrenergic transmission in visual cortex. We discuss side effects of CLON, concluding that CLON's sedative effect may contribute to the lack of OD shift.
D000818:Animals; D002415:Cats; D003000:Clonidine / Q000494:pharmacology*; D004292:Dominance, Cerebral / Q000502:physiology*; D008734:Methoxyhydroxyphenylglycol / Q000134:cerebrospinal fluid; D009473:Neuronal Plasticity; D009638:Norepinephrine / Q000502:physiology*; D009799:Ocular Physiological Phenomena; D012683:Sensory Deprivation; D014793:Visual Cortex / Q000187:drug effects / Q000254:growth & development / Q000502:physiology*
D008734:Methoxyhydroxyphenylglycol; D003000:Clonidine; D009638:Norepinephrine