ERK plays a regulatory role in induction of LTP by theta frequency stimulation and its modulation by beta-adrenergic receptors.

Winder DG, Martin KC, Muzzio IA, Rohrer D, Chruscinski A, Kobilka B, Kandel ER
Neuron. 1999 24 (3): 715-26

PMID: 10595521 · DOI:10.1016/s0896-6273(00)81124-1

MAP kinase (ERK) translates cell surface signals into alterations in transcription. We have found that ERK also regulates hippocampal neuronal excitability during 5 Hz stimulation and thereby regulates forms of long-term potentiation (LTP) that do not require macromolecular synthesis. Moreover, ERK-mediated changes in excitability are selectively required for some forms of LTP but not others. ERK is required for the early phase of LTP elicited by brief 5 Hz stimulation, as well as for LTP elicited by more prolonged 5 Hz stimulation when paired with beta1-adrenergic receptor activation. By contrast, ERK plays no role in LTP elicited by a single 1 s 100 Hz train. Consistent with these results, we find that ERK is activated by beta-adrenergic receptors in CA1 pyramidal cell somas and dendrites.

MeSH Terms (21)

Action Potentials Adrenergic beta-Agonists Animals Cyclic AMP-Dependent Protein Kinases Dendrites Electric Stimulation Female In Vitro Techniques Isoproterenol Long-Term Potentiation Macromolecular Substances Male Mice Mice, Inbred C57BL Mitogen-Activated Protein Kinase Kinases Mitogen-Activated Protein Kinases Phosphorylation Pyramidal Cells Receptors, Adrenergic, beta Synapses Theta Rhythm

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