Skip to content

Journal article

Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain

Neurobiology of Pain, 2021

DOI 10.1016/j.ynpai.2021.100078 · PubMed 34877437 · PMC8628014

Licence: CC-BY-4.0

2 claims from this source

clm-13a6rtv5w7presentelectrical stimulationproposed

BLA (Basolateral amygdalar nucleus) MBA:295 functionally connects to CEA (Central amygdalar nucleus) MBA:536 · Mouse

Electrical stimulation with an electrode placed in the ventral BLA close to the CeA border evoked short, stable-latency excitatory postsynaptic currents in CeC/L neurons held at -70 mV in brain slices from naive, saline- and formalin-treated mice. Pregabalin reduced these BLA-evoked EPSCs and raised the paired-pulse ratio only in formalin-treated animals, indicating a presynaptic site of action at BLA terminals; EPSC amplitude at fixed 100 µA stimulation did not differ between saline and formalin groups.

Figs. 1A, 2, 3, 5; Results

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5-5) agrees.

clm-a38wage5x6presentelectrical stimulationproposed

PB (Parabrachial nucleus) MBA:867 functionally connects to CEA (Central amygdalar nucleus) MBA:536 · Mouse

Stimulating the fiber bundle of LPB origin running dorsomedial to the CeA evoked short-latency excitatory postsynaptic currents in CeC/L neurons recorded at -70 mV; these responses were larger in formalin-treated than saline-treated mice and, unlike BLA-evoked responses, were unaffected by pregabalin. Both LPB- and BLA-evoked EPSCs could be recorded in the same CeC/L neurons, showing convergence of the two inputs.

Figs. 1B, 4, 5; Results

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5-5) agrees.