Dopamine, the Basal Ganglia, and Learning

A significant proportion of dopamine (DA) is produced in the substantia nigra pars compacta (SNpc) and is carried to the striatum via the nigrostriatal pathway. While this pathway has been traditionally linked with motor functioning, recent research has implicated striatal DA involvement in language (Crosson, 2003) and learning (Seger, 2006). One disease in which there is considerable DA disruption is Huntington’s Disease (HD). In HD the head of the caudate is typically the first brain structure affected by neuronal cell loss. This cell loss not only affects connections with the SNpc but also affects the connections between the striatum and the prefrontal cortex. In HD the disruption of these dopaminergic pathways leads to disruptions in motor and cognitive functioning.

How DA disruptions affect cognition has been explained by theories that are modifications of Mink’s model (1996) of center and surround (i.e., direct and indirect) basal ganglia regulation. Within the caudate there are two main families of DA receptors – D1 and D2. These receptors have been shown to have different functioning within the basal ganglia (Seger, 2006) – the D1 receptor is involved with the direct pathway and the D2 receptor is involved in the indirect pathway. The D1, or direct pathway, can be viewed as increasing the strength of the signal of the desired response while the D2, or indirect pathway, serves to reduce the noise of the competing undesired responses. Dopaminergic systemic disruption in HD should thus decrease the signal-to-noise ratio, which results in the person having a greater difficulty selecting the desired response (see model below).

Center-surround model of basal ganglia-based learning and memory

*Model based on Mink (1996) and Frank, Seeberger, and O’Reilly (2004)

There is evidence that in early stages of Huntington’s disease, D2 receptors are the first to be affected, with less binding occurring at D2 receptors presumably due to receptor loss. As the disease progresses, the D1 receptors also start to become depleted, with the end result of widespread DA dysfunction (Glass, Dragunow, & Faull, 2000). This DA dysfunction possibly affects verbal learning and recall by impacting the indirect pathway in the early stages of HD and indiscriminately the whole direct and indirect system in later stages of the disease process.


Crosson (2003). Left and right basal ganglia and frontal activity during language generation: Contributions to lexical, semantic, and phonological processes. Journal of the International Neuropsychological Society, 9, 1061-1077.

Frank, M. J., Seeberger, L. C., & O’Reilly, R. C. (2004). By carrot or by stick: Cognitive reinforcement learning in Parkinsonism. Science, 306, 1940-1943.

Glass, M., Dragunow, M., & Faull, R. L. M. (2000). The pattern of neurodegeneration in Huntington’s disease: A comparative study of cannabinoid, dopamine, adenosine and GABAA receptor alterations in the human basal ganglia in Huntington’s disease. Neuroscience, 97(3), 505-19.

Seger, C. A. (2006). The basal ganglia in human learning. Neuroscientist, 12(4), 285-290.

The basal ganglia and cognition

The basal ganglia are a collection of subcortical structures that were traditionally viewed as only being involved in movement. The basal ganglia include the caudate, globus pallidus, putamen, and nucleus accumbens (the subthalamic nucleus and the substantia nigra are also often included as part of the basal ganglia). Scientists have known about the basal ganglia’s role in movement for a number of years but have only recently really started studying their role in cognition, executive function, and memory.

Dissections of the brain have shown that there are a number of white matter “loops” exiting and entering the basal ganglia. We know that the striatum, which consists of the putamen and the caudate and is so named because there are connections between the two structures that look like stripes (striations), receives excitatory input from all over the cortex (Seger & Cincotta, 2002). The prefrontal cortex (roughly the very front of the brain) connects to the anterior putamen and the head of the caudate but the tail of the caudate and the posterior parts of the putamen receive inputs from parts of the temporal and parietal lobes. The frontal lobes are involved in tasks such as planning, remembering, organizing, and many other of the “higher-order” cognitive abilities. The parietal lobes are involved in visuo-spatial tasks and the temporal lobes are involved in memory and object recognition (these are gross simplifications of lobular function – all lobes have more functions than I wrote about). So if parts of the basal ganglia receive inputs from the frontal lobes, what are the basal ganglia doing if not just moderating movement?

Seger and Cincotta (2002) demonstrated that the striatum is involved in a type of learning. Lamar, Price, Libon, Penney, Kaplan, Grossman, and Heilman (2007) demonstrated that dementia patients with higher levels of white matter disruption (which likely interferes with basal ganglia connectivity) have poorer working memory performance. One example of what working memory is is performing a multiplication task in your head without using any paper – having to remember the digits and manipulate them is a process of working memory. Benke, Delazer, Bartha, and Auer (2003) reported on two clinical cases of patients with hematoma disrupting the left basal ganglia. Both patients had “executive function” disruption, short- and long-term memory impairment, and attentional difficulties. Many other researchers have demonstrated the role the basal ganglia has in cognition but we are still in the early stages of this area of research.