A Neural Circuit from Thalamic Paraventricular Nucleus to Cen

RV virus was used for anterograde transsynaptic tracing. Optogenetic viruses were used to observe the effects on the mechanical nociceptive threshold. Chemogenetic viruses were used to inhibit excitatory neuronal activity in the pPVT. (all viruses were packaged by BrainVTA)

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

RV	R01002 RV-ENVA-ΔG-DsRed
Tracing Helper	PT-0021 AAV2/9-Ef1a-DIO- EGFP-TVA PT-0023 AAV2/9-Ef1a-DIO-RVG
Optogenetic	PT-0005 AAV2/9-CaMKIIa-ChR2(E123T/T159C)-mCherry
Chemogenetic	PT-0017 AAV2/9-CaMKIIa-hM4Di-mCherry
Control	PT-0108 AAV2/9-CaMKIIa-mCherry PT-0012 AAV2/9-Ef1a-DIO-EYFP

Pub Date: 2020-10-07, DOI: 10.1523/JNEUROSCI.2487-19.2020 Email:[email protected]
Shao-Hua Liang, Wen-Jun Zhao, Jun-Bin Yin, Ying-Biao Chen, Jia-Ni Li, Ban Feng, Ya-Cheng Lu, Jian Wang, Yu-Lin Dong and Yun-Qing Li
As one of the thalamic midline nuclei, the thalamic paraventricular nucleus (PVT) is considered to be an important signal integration site for many descending and ascending pathways that modulate a variety of behaviors, including feeding, emotions, and drug-seeking. A recent study has demonstrated that the PVT is implicated in the acute visceral pain response, but it is unclear whether the PVT plays a critical role in the central processing of chronic pain. Here, we report that the neurons in the posterior portion of the PVT (pPVT) and their downstream pathway are involved in descending nociceptive facilitation regarding the development of neuropathic pain conditions in male rats. Lesions or inhibition of pPVT neurons alleviated mechanical allodynia induced by spared nerve injury (SNI). The excitability of pPVT-central amygdala (CeA) projection neurons was significantly increased in SNI rats. Importantly, selective optogenetic activation of the pPVT-CeA pathway induced obvious mechanical hypersensitivity in naive rats. In addition, we used rabies virus (RV)-based and cell-type-specific retrograde trans-synaptic tracing techniques to define a novel neuronal circuit in which glutamatergic neurons in the vlPAG were the target of the pPVT-CeA descending facilitation pathway. Our data suggest that this pPVT^Glu+-CeA-vlPAG^Glu+ circuit mediates central mechanisms of descending pain facilitation underlying persistent pain conditions.

Fig.1 Fluorescent photomicrographs observation of the pPVT-CeA-vlPAG pathway.

Using virus tracing (From BrainVTA), chemogenetic manipulations, electrophysiological recording and rabies virus retrograde trans-synaptic labeling, the researchers confirmed that activation of the VGLUT2⁺ neurons in the PVT with chronic pain increases the excitability of pPVT-CeA projection neurons, establishing a pPVT^Glu+-CeA-vlPAG^Glu+ descending nociceptive pathway, which showed that CeA neurons received glutamatergic pPVT projections and sent projections to the glutamatergic neurons in the vlPAG to contribute to neuropathic pain signaling.

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