medial prefrontal cortex

posterior cingulate cortex

Justification not yet generated — showing supporting facts

• Barrett and Griffiths (2017) identified parallels in the neural bases of psychedelic and meditative effects on the Default Mode Network (DMN), specifically hypothesizing that visionary experiences result from decreased activity and functional connectivity in the medial nodes of the DMN (PCC and MPFC), which mediate self-referential processing.
• The integrated cognitive and emotional functions of the dorsal and ventral anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), and posterior cingulate cortex (PCC) function as a 'life simulator' that uses past experiences to explore anticipated social events and future scenarios, according to Washington and VanMeter (2015).
• Classic psychedelics initiate a cascade of altered neural connectivity and blood-flow across brain regions including the default-mode network (medial prefrontal cortex, posterior cingulate cortex, inferior parietal lobule, lateral temporal cortex, hippocampus, and precuneus), the amygdala, the thalamus, and the claustrum.
• Epileptic seizures, including complex partial, generalized tonic-clonic, and absence seizures, impair primary nodes of the Default Mode Network (DMN), specifically the precuneus/PCC, medial frontal cortex, lateral parietal cortex, and the anterior cingulate cortex (ACC), resulting in long-lasting decreases in DMN activity.
• The reduction in oscillatory activity and power in the Default Mode Network caused by psilocybin results from decreased functional coupling between the frontal cortex and the medial temporal lobe components of the Default Mode Network, as well as between the medial prefrontal cortex and the posterior cingulate cortex.
• A 2017 study by Scheibnera et al. on mindful attention practices found significantly less neural activation in the medial prefrontal cortex (mPFC) and posterior cingulate cortex (PCC), as well as reduced activity in the left temporoparietal junction.
• Reductions of ΦR in the medial prefrontal cortex and posterior cingulate/precuneus are reliably observed across different analytic approaches, confirming the robustness of these specific findings.
• The default mode network (DMN) comprises the posterior cingulate, precuneus, medial prefrontal cortex, and inferior parietal cortices.
• In mindfulness meditation conditions, the posterior cingulate cortex (PCC) and medial prefrontal cortex (mPFC) show less activity in meditators compared to control groups.
• Palhano-Fontes et al. (2015) found that ayahuasca consumption causes a significant decrease in activity throughout most parts of the Default Mode Network, particularly in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, while also reducing functional connectivity within the posterior cingulate cortex/precuneus.
• Palhano-Fontes et al. (2015) reported that ayahuasca causes decreased posterior cingulate cortex (PCC) activity, increased medial prefrontal cortex (mPFC) activity, and decreased retrosplenial cortex (RSC) activity.
• The Default Mode Network primarily involves connections among the thalamus, posterior cingulate cortex (PCC), medial prefrontal cortex (mPFC), and areas of the limbic system (parahippocampal cortex and the hippocampus) that function as a network for information routing and integration, as described by Buckner et al. (2008).

default mode network

The medial prefrontal cortex is a core anatomical component of the default mode network, as explicitly defined in [1] and [2]. This relationship is further supported by evidence detailing how the medial prefrontal cortex functions as a key node within the network during various states of consciousness and neural activity, as described in [3], [4], [5], and [6]. — 11 supporting facts

psilocybin

Psilocybin reduces oscillatory activity in the Default Mode Network through decreased functional coupling between the medial prefrontal cortex and other components [1], and it alters functional connectivity of the medial prefrontal cortex in patients with treatment-resistant depression [2]. — 2 supporting facts