Activity-dependent beta-adrenergic modulation of low frequency stimulation induced LTP in the hippocampal CA1 region
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Thomas, MJ
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UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024
Thomas, MJ
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Moody, TD
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UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024
Moody, TD
[1
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Makhinson, M
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UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024
Makhinson, M
[1
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ODell, TJ
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UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024
ODell, TJ
[1
]
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[1] UNIV CALIF LOS ANGELES,SCH MED,INTERDEPT PHD PROGRAM NEUROSCI,LOS ANGELES,CA 90024
beta-Adrenergic receptor activation has a central role in the enhancement of memory formation that occurs during heightened states of emotional arousal. Although beta-adrenergic receptor activation may enhance memory formation by modulating long-term potentiation (LTP), a candidate synaptic mechanism involved in memory formation, the cellular basis of this modulation is not fully understood. Here, we report that, in the CA1 region of the hippocampus, beta-adrenergic receptor activation selectively enables the induction of LTP during long trains of 5 Hz synaptic stimulation. Protein phosphatase inhibitors mimic the effects of beta-adrenergic receptor activation on 5 Hz stimulation-induced LTP, suggesting that activation of noradrenergic systems during emotional arousal may enhance memory formation by inhibiting protein phosphatases that normally oppose the induction of LTP.