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Adrenergic modulation of glutamate induced calcium mobilization in cultured rat visual cortical neurons Yang, Benduan


Since Wiesel and Hubel first discovered that the responsiveness of the cortical neurons in the striate cortex to visual stimuli via either eye was subject to postnatal developmental manipulation, three decades have passed in strenuous efforts to unravel the mechanism underlying this ocular dominance plasticity. Among these studies, a variety of neurotransmitters/neuromodulators, including noradrenalin, acetylcholine and serotonin, have been implicated at both system and cellular levels. In view of the facts that noradrenalin changes neuronal excitability and the N-Methyl-D-aspartate (NMDA) receptor plays a crucial role in neuroplasticity, this study was designed to obtain evidence whether adrenergic modification worked through interacting with glutamergic system in terms of calcium dynamics and how this process occurred. In primary neuronal cultures derived from the visual cortex of embryonic day 16-18 rats, intracellular free calcium concentration, [Ca²⁺]i, was increased by bath application of glutamate in a dose dependent manner. Noradrenalin applied alone had relatively small effects. However, when glutamate concentrations eliciting modest increases in [Ca²⁺]i were applied together with 1 µM noradrenalin, the increase in [Ca²⁺]i could be enhanced by a factor of up to eight in 147 neurons out of a total of 215 cells observed in 54 experiments. The observed enhancement was much more obvious at low doses of glutamate than with higher doses, augmenting all submaximal calcium responses to similar asymptotic levels. 2-Amino-5-phosphonovalerate (APV), the NMDA receptor antagonist, completely blocked the adrenergic enhancing effect (29/29 cells in 8 experiments). Among the antagonists specific to άl , ά2 and ϐ subtypes of adrenoceptors, the ϐ antagonist propranolol most completely blocked the enhancing effect (13/14 cells in 4 experiments, by an amplitude of 90%). The involvement of the ϐ receptor pathway was further supported by the ability of a cAMP analog to mimic the enhancing effect of noradrenalin. These results suggest that receptors for noradrenalin and glutamate colocalize on postsynaptic cortical cells and that adrenergic modulation of glutamate induced calcium influx most likely work through the ϐ receptor pathway. It is further postulated that ocular dominance plasticity may be at least partially implemented via a calcium dependent cascade.

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