Elevated Level of PKMz Underlies the Excessive Anxiety in an

AAV- PKMζ was used to overexpress PKMz in the BLA. (From BrainVTA)

The viruses used in this article from BrainVTA are in the table below

Control	PT-0241 rAAV-hSyn-GFP-pA
Custom-Made AAV	rAAV-hSyn- PKMζ-pA

Xiaoli Gao, Rui Zheng, Xiaoyan Ma, Zhiting Gong1, Dan Xia and Qiang Zhou
Pub Date: 2019-11-28, DOI: 10.3389/fnmol.2019.00291， Email: [email protected]
Anxiety affects the life quality of a signiﬁcant percentage of autism patients. To understand the possible biological basis of this high anxiety level, we used a valproic acid (VPA) model of autism. Anxiety level is signiﬁcantly higher in VPA-injected mice, at both P35 and P70. In addition, protein kinase Mz (PKMz) level in the basolateral amygdala (BLA) is signiﬁcantly higher in VPA mice at both ages. Consistent with this ﬁnding, infusion of a PKMz-blocking peptide z-pseudosubstrate inhibitory peptide (ZIP) into BLA signiﬁcantly reduced anxiety levels in VPA mice. Furthermore, viral overexpression of PKMz in the BLA led to elevated anxiety level in Wild Type (WT) mice, with concomitant higher intrinsic excitability of BLA excitatory neurons. Altogether, our results indicate a key contribution of BLA PKMz level to anxiety, especially in autism; and this ﬁnding may provide a further understanding of the pathogenesis as well as treatment of anxiety symptoms in autism patients.

Fig 1. Overexpression of PKMz resulted in higher intrinsic excitability in the excitatory neurons in BLA.

To further identify potential mediators of the hyperactivity in the amygdala, the authors decided to focus on protein kinase Mζ(PKMζ). By using AAV viral transfection to overexpress PKMζ (From BrainVTA), the results show that PKMζ level in BLA is highly relevant to the anxiety level, and may contribute to the pathological anxiety in autism patients.

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