ESTD : 1897 | TYPE : Government | AFFILIATION : WHO | RECOGNITION : MCI
A world-class university (with three essential qualities – comprehensive, research-intensive, and innovative) that will transform lives and improve China and the world
To nurture future leaders and useful citizens with a global vision and social responsibility;
To conduct interdisciplinary and innovative research that addresses pressing challenges facing the world today;
To translate knowledge and creativity to benefit the local and global communities.
Seeking Truth, Pursuing Innovation
The University logo consists of two components: the round emblem and the wordmark.
The round emblem features a flying eagle in the center, a ZJU mascot known as the “qiushi eagle”. The eagle symbolizes the University’s tradition of seeking truth and pursuing innovation, which has been inherited and further developed by the ZJU community.
Normally, the wordmark must always appear in conjunction with the emblem. If desired, the emblem may be used alone (for instance, when space is limited).
|#||Course||Seats||1st Yr Fee||From Next Yr||Total Fee||Cash Back||Lodging Fee||Fooding Fee||Course Duration|
|1||MBBS||60||RMB -51,800 =INR- 5, 18,000||RMB- 48,800= INR- 3,43,800||RMB-2,47,000=INR-2,470,000||INR-10000||lodging included first year package||RMB-100=INR-6,500||5 YEARS|
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Discovering Ketamine’s antagonist
In the first article, HU’s team found that ketamine blocks bursting activity in the lateral habenula (LHb), an anti-reward center in the brain, to rapidly relieve depression. They discovered that in various animal models of depression, the intrinsic burst firing activity of LHb neurons is significantly increased. Burst firing, a particular spike pattern with clusters of high-frequency spikes, provides a robust form of information coding and a stronger output from LHb to inhibit the reward-related dopaminergic and serotonergic centers.
A model for mechanisms of depression and ketamine treatment in LHb: Upregulation of Kir4.1 on astrocytic processes surrounding neuronal soma leads to enhanced K+ buffering at the tight neuron-glia junction, decreased Kout and hyperpolarized neuronal RMP. Consequently, de-inactivation of T-VSCCs initiates NMDAR-dependent bursts, causing a stronger output of LHb to trigger depression. Ketamine blockade of NMDARs stops bursts and relieves depression.
The team discovered that LHb burst firing strongly depends on NMDAR, a major subtype of excitatory glutamate receptors within the brain. Ketamine, as a NMDAR antagonist, completely eliminates LHb bursting in vitro and reduces bursting of depressive-like animals to the level of naïve control animals in vivo.
Collectively, these data suggest a simple and novel mechanism whereby ketamine quickly elevates mood by instantaneously blocking NMDAR-dependent bursting activity of LHb to disinhibit downstream dopaminergic and serotonergic neurons.
Going deeper: molecular determinant of depression
In the second research article, the team further identified the molecular mechanism by which neuron-glia interaction at the LHb regulates burst firing in depression. Through an unbiased, mass spectrometry-based, quantitative proteomic screening, they identified an inward-rectifying potassium channel, Kir4.1, which is upregulated in depression. Kir4.1 is exclusively expressed in the astrocytes, one type of glia cells, in the LHb.
The results point to the important role of a glia-specific ion channel in the regulation of neuronal firing pattern, and provide compelling evidence for Kir4.1 being a powerful molecular determinant of depression.
The two articles, with one addressing how LHb neurons increase burst firing in depression and the other revealingthis burst firing to be a prominent target of rapid antidepressant ketamine, make a strong case that the firing mode of LHb neurons is critical in depression.
The newly discovered structure-function mechanism at the glial-neural interface in burst regulation may enrich our understanding of the basic cell biology of how glia regulates neural activity in physiological and pathological states.
Together, they provide a new framework for understanding the molecular, cellular and circuit mechanism of depression and shed important light on developing new rapid-acting antidepressants.