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Ursula V. Staubli, Natalie Rangel-Diaz, John Donello, Alan Foster, Dan Gil; Pharmacological Enhancement of LTP in Primary Visual Cortex via activation of Alpha 2a/c Adrenergic Receptors. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5722.
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Long-term potentiation (LTP) serves as a cellular model for visual cortex plasticity and has functional consequences on visual evoked responses. The visual cortex receives an intense axonal projection from noradrenergic locus coeruleus neurons. Noradrenaline released from the nerve terminals gates experience-dependent modification of visual responsiveness including ocular dominance shifts after monocular deprivation. To measure the contribution of alpha adrenergic receptor subtypes, the effect of alpha 2 pan agonist brimonidine on LTP was studied in visual cortex slices prepared from adult Sprague Dawley rats.
Extracellular field potentials evoked by layer 4 stimulation were recorded from layer 2/3, and LTP was induced by theta burst stimulation.
Brimonidine produced a marked and dose-dependent enhancement of LTP with a threshold dose of 3 nM. This facilitatory effect was fully suppressed by the alpha 2 pan antagonist atipamazole, but was unaffected by selective alpha 2B receptor blockade. These findings were confirmed and extended using alpha 2 subtype specific knockout (KO) mice where brimonidine at 30 nM dramatically enhanced LTP in wild type as well as 2B KO and 2C KO mice, but not in 2A KO mice. Moreover, when brimonidine was tested at a higher dose of 300 nM, a small yet significant LTP reduction was observed in the 2C KO mice compared to the wild type counterpart.
In summary, these data demonstrate that LTP in primary visual cortex can be facilitated via activation of alpha 2A/C receptors, with the Alpha2A receptor subtype being the major contributor.
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