Min Zhuo

In 1992, Zhuo joined Eric Kandel's laboratory at Columbia University where he showed CO-cGMP as key messengers for presynaptic LTP.

[15][16] Together with Dr. Yinhe Hu, he further discovered that soluble guanylyl clcyaes (sGC) and cGMP-dependent protein kinase (PKG) act downstream from these diffusible messengers.

[18][19][20] In 1995, after being offered an independent faculty job at Washington University in St. Louis, Zhuo joined Richard Tsien’s laboratory in Stanford for one year.

While at Stanford, Zhuo mastered whole-cell patch-clamp techniques and was the first one to show that direct patching of dendrites in isolated hippocampal neuronal preparations.

Together with Ege Kavalali and Haruhiko Bito, they published together a key study on voltage-gated calcium channels in neuronal dendrites (or called dendrosomes).

He decided to combine his knowledge of pain and synaptic plasticity of hippocampal memory, and explored possible changes in spinal cord dorsal horn.

[27] These genetic and behavioral studies provide the first direct evidence that forebrain NMDA receptors play important roles in persistent pain.

[28] In Toronto, Zhuo decided to focus on synaptic plasticity in the anterior cingulate cortex, a key cortical region for pain, and has mapped the signalling pathways for LTP and LTD in the ACC.

Upregulation of AMPARs and/or the increase of presynaptic release are known to contribute to synaptic potentiation and behavioural learning, while postsynaptic NMDA receptors are not significantly affected.

[33] Between the time in St Louis and Toronto, Zhuo identified calcium stimulated adenylyl cyclase subtype 1 as being a key enzyme for triggering injury-related LTP in the ACC.

Considering AC1 is highly expressed in neurons including the ACC, Zhuo proposed that AC1 acts as a key drug target for inhibiting chronic pain related plasticity in the brains.