ArticleMethods in molecular biology (Clifton, N.J.)2026
Analysis of Prefrontal-Amygdala Synaptic Functions Using Optogenetics and Patch-Clamp Recording.
Article in Methods in molecular biology (Clifton, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular disease characterized by progressive muscle wasting caused by a mutation in the DMD gene encoding the dystrophin protein. Dystrophin is highly expressed in the central nervous system (CNS), and DMD patients are often diagnosed with abnormalities in emotional and social functions. However, the pathophysiology of the CNS in DMD patients is not fully understood. The DMD mouse models show abnormalities in anxiety, fear and social behavior, and synaptic dysfunction in the amygdala, which is involved in emotional and social processing. The direct input from the prefrontal cortex (PFC) to the amygdala (PFC-amygdala pathway) plays a crucial role in emotional and social processing. Hence, examination of the PFC-amygdala synaptic function is important for not only investigating the pathophysiology of related psychiatric symptoms but also for assessing the efficacy of novel treatments. Here, we present a protocol of an electrophysiological method combined with optogenetics to examine the PFC-amygdala synaptic functions in mice.
Indexed as
Identifiers
41028687What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.