His Ph.D. thesis was based conceptually on prior work that had determined that bilateral legions in the hippocampus of humans resulted in short-term memory loss.
Despite failing to yield positive results, Moore cited his thesis work as having played an integral role in the development of his passion for research.
During his senior year, Moore worked as a graduate assistant in the neuroanatomy course, giving several lectures and unearthing a love for teaching.
Moore’s combined passions of research, teaching, and clinical medicine, would continue to influence his career through various awards and faculty positions.
Using a Halasz knife and his microsurgery experience gained in prior laboratory work, Moore lesioned the SCN of the mice in the test group.
The resulting arrhythmicity in corticosterone levels in these mice compared to the control group’s maintained rhythmicity, revealed the SCN’s function as the master circadian clock.
This was determined by a comparative anatomy of the SCN in a mouse, guinea pig, cat, and opossum with immunohistochemistry studies that identified segregation of afferents and distinct neuropeptides between the core and shell.
[4] The core is a division lying above the optic chiasm composed of vasoactive intestinal polypeptide (VIP)-producing neurons that receive RHT and secondary visual inputs.
The shell surrounds the core and is composed of vasopressin-producing neurons and receives input from the hypothalamus, brainstem, and basal forebrain.
These subdivisions function as individual pacemakers, and their neurochemical organization reflects intercellular communication that posit potential coupling mechanisms.
In 1988, Moore, along with Ralph F. Johnson and Lawrence P. Morin, established the role of the RHT as a light entrainment pathway of the SCN and thus a critical element of the circadian clock.