Characterizing Cortical and Subcortical Projections to the Posterior Parietal Cortex: an Anatomical and Functional Study

Abstract

Previous studies have shown that, in some domains, rats display significant cognitive similarity to both primates and humans, including the ability to hold information in working memory, and continuously update that information over the course of a task (Fassihi and Akrami, 2014). Rodents have also displayed systematic bias induced through stimulus statistics and trial history (Akrami et al, 2015). In fact, electrophysiological recordings from the posterior parietal cortex (PPC) show neurons carry significant amounts of information about the animal’s previous choice as well as recent sensory experience, thereby introducing the presence of a trial history signal (Akrami et al., 2015). However, the exact roles of other areas within the circuitry involved in the employment of a trial history signal are still unknown. This paper attempts to build upon these recent findings through the employment of anatomical and behavioral rodent paradigms. Anatomically, retrograde cholera toxin subunit B (CTB) was injected into the medial PPC (mPPC) to determine afferent projections. Histological analysis showed that the laterorostral part of the lateral posterior thalamus (LPLR) displayed the highest levels of fluorescent expression relative to other (non-sensory) areas. Therefore, it was selected as the upstream area with respect to the mPPC to study its role in working memory and trial history. A pilot study consisting of muscimol and saline infusions of the LPLR grossly deteriorated task performance, suggesting this area may be too sensitive to effectively inactivate using muscimol or liquid injection. The findings of this study may be useful in developing a better understanding of the circuitry underlying history signals as well as working memory as a whole. This knowledge may be applied to further the understanding of, and establishing diagnostic testing for learning disabilities (LD) and Alzheimer’s Disease (AD). However, further inactivation methods, with higher spatiotemporal resolution, are needed to help continue unraveling the circuitry underlying parametric working memory. Only then may its true clinical relevance be unveiled.