For instance, an afferent inhibitory signal may originate in the motor cortex; however, the release (or inhibition of release in this case) of the GABA neurotransmitter is controlled by the pars reticulate. How then does the afferent signal travel all the way from the very dorsal side of the motor cortex to the ventral side of the midbrain? The signal follows a pathway that connects the motor cortex to the caudate and putamen. The caudate and putamen are then connected to the globus pallidus which, in turn, sends a signal to the pars reticulata. For efferent motor signals, the same pathway is followed in reverse (Kuhn P, 2016). The motor signaling aspect of the system also plays a role in learning and higher-order behaviors. According to Kimura and Graybiel, the Basal Ganglia System may play some role in context-dependent behaviors such as those related to the rewards pathway. An example of a reward pathway behavior is teaching a dog to sit using a treat. If you hold a treat up and tell the dog to sit, rewarding the dog for sitting would activate the rewards pathway. The next time you tell the dog to sit and there is a treat present, the dog is much more likely to sit. Kimura and Graybiel found that, after creating lesions in the nigrostriatal dopamine system, the primates used in the study essentially forgot the learned, context-dependent behavior. This system consists of the connection between the substantia nigra and the caudate …show more content…
While many diseases are rooted within the Basal Ganglia System, two of the more well-known are Parkinson’s Disease and Huntington’s Disease. Parkinson’s Disease results from a lack of dopamine in the midbrain. The decrease in dopamine reduces the excitatory signals and, as indicated in the above paragraph, reduces learning and motivation behaviors. While excitatory signals decrease, the effects of inhibitory signals increase. This explains why the symptoms of Parkinson’s Disease include slower movement, rigid and unstable postural movement, and uncontrollable tremors. The body has essentially lost most of its ability to move and correct posture alignment (Schroll and Hamker, 2016). In contrast, Huntington’s Disease is marked by an increase in dopamine levels at the early stages of progression and a dramatic decrease in dopamine levels towards the very end of progression. This results in symptoms that, at first, display rapid and uncontrolled movement and an increasing inability to perform controlled movements. As such, Huntington’s Disease progresses from being the exact opposite of Parkinson’s Disease to closely mirroring it. There is also an evident decrease in behavior flexibility. That is, once a behavior is started, it is nearly impossible to end said behavior half-way through the motion (Chen, Wang, Cepeda, and Levine, 2013). Both disorders are marked by other psychological disorders like depression