Fasciculus retroflexus

The placement of the FR makes it a vital pathway for contribution to proper functioning of sleep-wake cycles (Circadian rhythm). The FR has significant influence on REM sleep, specifically. When FR function is hindered, REM sleep was reduced by more than 50% in a study done on rats.

The habenula is largely identified as the reward center of the brain, and so a prime target for drug addiction.[3][6] By association, the fasciculus retroflexus plays a key role in transmitting the messages which cause dependence on certain controlled substances. Many trials have been done specifically linking these connections to nicotine addiction. The basis of drug addiction is tether to the fluctuating levels of dopamine found in our brains. A key inhibitor, which functions to keep these dopamine levels in check, is GABA. The Hbn-FR-IPN makes up the main pathway through which both GABA and dopamine flow. Once drugs are introduced, this area of the brain, the reward and pleasure center is heavily involved. The inhibitory GABAergic cells are location in the nuclei of the RMTg, with is the output of the fasciculus retroflexus's inner portion. The modulation, activation, and inhibition of dopamine is mediated by the habenula and by association the inner and outer fasciculus retroflexus for the duration of drug use; this idea exemplifying its participation in the formation of drug addiction.

Early brain development of the fasciculus retroflexus, like most tissues of the central nervous system, persists when embryotic non-specified neural tissues begin to grow and differentiate. Both the fasciculus retroflexus and the habenula have been observed to be dependent of the presence Wnt1,[7] as shown in a rat study.

When FR are lesioned artificially, a reduction in signal transduction is observed. This leads to an understanding that, at least for specific neurons,[8] the FR is vital to the signaling pathways related to the habenula; further solidifying the proposed structure and function of the FR, proving that its core channel is necessary for response output. The study of these lesions leads to an understanding of how defects in a mammal's Hbn-FR-IPN complex, or more specifically their fasciculus retroflexus, could potentially lead to decreased response time and signal transduction; insinuating that defects hold consequences in the central nervous system. Likewise, since the FR was found to be such a vital part of habenula function, loss of functionality in the FR would lead to co-malfunction in the habenula, which has been found to cause imbalances leading to anxiety, depression, and even schizophrenia.[3]