
도파민은 해마 신경세포에서 단백질 합성을 증가시키며, 이를 통해 도파민 의존성 장기 강화(DA-LTP)를 가능하게 한다.


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The reward and novelty related neuromodulator dopamine plays an important role in hippocampal long-term memory, which is thought to involve protein synthesis-dependent synaptic plasticity. However, the direct effects of dopamine on protein synthesis, and the functional implications of newly synthesized proteins for synaptic plasticity, have not yet been investigated. We have previously reported that timing-dependent synaptic depression (t-LTD) can be converted into potentiation by dopamine application during synaptic stimulation (Brzsoko et al., 2015) or postsynaptic burst activation ([Fuchsberger et al., 2022][1]). Here we show that dopamine increases protein synthesis in mouse hippocampal CA1 neurons, enabling dopamine-dependent long-term potentiation (DA-LTP). We found that neuronal activity is required for the dopamine-induced increase in protein synthesis, which is mediated via the Ca2+-sensitive adenylate cyclase (AC) subtypes 1/8, cAMP, and cAMP-dependent protein kinase (PKA). Furthermore, dopamine induced a protein synthesis-dependent increase in the AMPA receptor subunit GluA1, but not GluA2. We found that DA-LTP is absent in GluA1 knock-out mice and that it requires calcium-permeable AMPA receptors. Taken together, our results suggest that dopamine together with neuronal activity controls synthesis of plasticity-related proteins, including GluA1, which enable DA-LTP via a signalling pathway distinct from that of conventional LTP.

### Competing Interest Statement

The authors have declared no competing interest.

 [1]: #ref-16

Dopamine increases protein synthesis in hippocampal neurons enabling dopamine-dependent LTP

도파민이-해마-신경세포에서-단백질-합성을-증가시켜-도파민-의존성-ltp를-가능하게-한다


도파민이 해마 신경세포에서 단백질 합성을 증가시켜 도파민 의존성 LTP를 가능하게 한다
