Peripheral nerve injury reduces the excitation-inhibition balance of basolateral amygdala inputs to prelimbic pyramidal neurons projecting to the periaqueductal gray
| Autor: | Patrick L. Sheets, John Cheriyan |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male SNi Prefrontal Cortex Optogenetics Inhibitory postsynaptic potential Periaqueductal gray lcsh:RC346-429 Micro Report 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Slice preparation Peripheral Nerve Injuries Cortex (anatomy) medicine Animals Periaqueductal Gray Prefrontal cortex Molecular Biology lcsh:Neurology. Diseases of the nervous system Chemistry Basolateral Nuclear Complex Pyramidal Cells Neural Inhibition Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure nervous system Female Neuroscience 030217 neurology & neurosurgery Basolateral amygdala |
| Zdroj: | Molecular Brain Molecular Brain, Vol 13, Iss 1, Pp 1-4 (2020) |
| ISSN: | 1756-6606 |
| Popis: | Cellular and synaptic mechanisms underlying how chronic pain induces maladaptive alterations to local circuits in the medial prefrontal cortex (mPFC), while emerging, remain unresolved. Consistent evidence shows that chronic pain attenuates activity in the prelimbic (PL) cortex, a mPFC subregion. This reduced activity is thought to be driven by increased inhibitory tone within PL circuits. Enhanced input from the basolateral amygdala (BLA) to inhibitory neurons in PL cortex is one well-received mechanism for this circuit change. In mice, we used retrograde labeling, brain slice recordings, and optogenetics to selectively stimulate and record ascending BLA inputs onto PL neurons that send projections to the periaqueductal gray (PAG), which is a midbrain structure that plays a significant role in endogenous analgesia. Activating BLA projections evoked both excitatory and inhibitory currents in cortico-PAG (CP) neurons, as we have shown previously. We measured changes to the ratio of BLA-evoked excitatory to inhibitory currents in the spared nerve injury (SNI) model of neuropathic pain. Our analysis reveals a reduced excitation-inhibition (E/I) ratio of BLA inputs to PL-CP neurons 7 days after SNI. The E/I ratio of BLA inputs to CP neurons in neighboring infralimbic (IL) cortex was unchanged in SNI animals. Collectively, this study reveals that the overall E/I balance of BLA inputs to PL neurons projecting to the PAG is reduced in a robust neuropathic pain model. Overall, our findings provide new mechanistic insight into how nerve injury produces dysfunction in PL circuits connected to structures involved in pain modulation. |
| Databáze: | OpenAIRE |
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