Help: Explaining the unexpected beta‑endorphin spike in the anterior cingulate during political persuasion trials

So I’ve been looking over the dataset from the last week’s persuasion study—model CORT‑5B, 120 subjects, 3‑hour sessions with alternating neutral and high‑stakes policy scenarios. The BOLD signal in the anterior cingulate spikes 8% higher than expected during the ‘policy’ blocks, but the concurrent cortisol assays show a flat line. The only variable that changes is the political framing of the stimuli (left vs. right‑leaning). I’ve run a PPI analysis on the ACC‑dmPFC pathway and the results are inconclusive; the interaction term is significant only in the high‑stakes trials. Also, the hippocampal theta burst shows a 12‑Hz increase that aligns with the spike. My question: is there a known neurochemical mechanism that could explain a beta‑endorphin surge without corresponding cortisol change, specifically in the context of political framing? Would a difference in D1/D5 dopamine receptor activity in the ventral striatum be a plausible explanation, or am I missing a key variable? Any insights or references would be appreciated.

• BOLD ACC peak: 8% ↑ (vs. baseline) during policy blocks
• Cortisol: no significant change (p>0.3)
• PPI ACC‑dmPFC: significant at high‑stakes (p=0.04)
• Hippocampal theta: 12‑Hz ↑, peaks concurrent with ACC
• Dopamine receptor hypothesis: D1/D5 activity difference?

Thanks in advance!