Editing Basal ganglia (section)

== Function ==

===Eye movements=== <!-- Please preserve this link. It is used elsewhere -->
One intensively studied function of the basal ganglia is its role in controlling [[eye movement]]s.<ref name=Hikosaka2000>{{cite journal | vauthors = Hikosaka O, Takikawa Y, Kawagoe R | title = Role of the basal ganglia in the control of purposive saccadic eye movements | journal = Physiological Reviews | volume = 80 | issue = 3 | pages = 953–978 | date = July 2000 | pmid = 10893428 | doi = 10.1152/physrev.2000.80.3.953 | s2cid = 7502211 }}</ref> Eye movement is influenced by an extensive network of brain regions that converges on a [[diencephalon|midbrain]] area called the [[superior colliculus]] (SC).  The SC is a layered structure whose layers form two-dimensional [[retinotopic]] maps of visual space.  A "bump" of neural activity in the deep layers of the SC drives an eye movement directed toward the corresponding point in space.

The SC receives a strong inhibitory projection from the basal ganglia, originating in the [[substantia nigra]] [[pars reticulata]] (SNr).<ref name=Hikosaka2000 /> Neurons in the SNr usually fire continuously at high rates, but at the onset of an eye movement they "pause", thereby releasing the SC from inhibition. Eye movements of all types are associated with "pausing" in the SNr; however, individual SNr neurons may be more strongly associated with some types of movements than others.  Neurons in some parts of the caudate nucleus also show activity related to eye movements.  Since the great majority of caudate cells fire at very low rates, this activity almost always shows up as an increase in firing rate.  Thus, eye movements begin with activation in the caudate nucleus, which inhibits the SNr via the direct GABAergic projections, which in turn disinhibits the SC.

===Role in motivation===

Extracellular dopamine in the basal ganglia has been linked to motivational states in rodents, with high levels being linked to satiated state, medium levels with seeking, and low with aversion.  The limbic basal ganglia circuits are influenced heavily by extracellular [[dopamine]].  Increased dopamine results in inhibition of the [[Ventral pallidum]], entopeduncular nucleus, and [[substantia nigra pars reticulata]], resulting in disinhibition of the thalamus.  This model of direct D1, and indirect D2 pathways explain why selective agonists of each receptor are not rewarding, as activity at both pathways is required for disinhibition.  The disinhibition of the thalamus leads to activation of the [[prefrontal cortex]] and [[ventral striatum]], selective for increased D1 activity leading to reward.<ref name="DABG"/> There is also evidence from non-human primate and human electrophysiology studies that other basal ganglia structures including the globus pallidus internus and subthalamic nucleus are involved in reward processing.<ref>{{cite journal | vauthors = Eisinger RS, Urdaneta ME, Foote KD, Okun MS, Gunduz A | title = Non-motor Characterization of the Basal Ganglia: Evidence From Human and Non-human Primate Electrophysiology | journal = Frontiers in Neuroscience | volume = 12 | pages = 385 | date = 2018 | pmid = 30026679 | pmc = 6041403 | doi = 10.3389/fnins.2018.00385 | doi-access = free }}</ref>

===Decision making===

Two models have been proposed for the basal ganglia, one being that actions are generated by a "critic" in the ventral striatum and estimates value, and the actions are carried out by an "actor" in the dorsal striatum.  Another model proposes the basal ganglia acts as a selection mechanism, where actions are generated in the cortex and are selected based on context by the basal ganglia.<ref>{{cite journal | vauthors = Redgrave P, Prescott TJ, Gurney K | title = The basal ganglia: a vertebrate solution to the selection problem? | journal = Neuroscience | volume = 89 | issue = 4 | pages = 1009–1023 | date = April 1999 | pmid = 10362291 | doi = 10.1016/S0306-4522(98)00319-4 | url = http://eprints.whiterose.ac.uk/107033/1/Redgrave%20Neuroscience%201999%20preprint.pdf | access-date = 23 September 2019 | url-status = live | s2cid = 3187928 | archive-url = https://web.archive.org/web/20180725132701/http://eprints.whiterose.ac.uk/107033/1/Redgrave%20Neuroscience%201999%20preprint.pdf | archive-date = 25 July 2018 }}</ref> The [[Cortico-basal ganglia-thalamo-cortical loop|CBGTC]] loop is also involved in reward discounting, with firing increasing with an unexpected or greater than expected reward.<ref>{{cite journal | vauthors = Maia TV, Frank MJ | title = From reinforcement learning models to psychiatric and neurological disorders | journal = Nature Neuroscience | volume = 14 | issue = 2 | pages = 154–162 | date = February 2011 | pmid = 21270784 | pmc = 4408000 | doi = 10.1038/nn.2723 }}</ref> One review supported the idea that the cortex was involved in learning actions regardless of their outcome, while the basal ganglia was involved in selecting appropriate actions based on associative reward based trial and error learning.<ref>{{cite journal | vauthors = Hélie S, Ell SW, Ashby FG | title = Learning robust cortico-cortical associations with the basal ganglia: an integrative review | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 64 | pages = 123–135 | date = March 2015 | pmid = 25461713 | doi = 10.1016/j.cortex.2014.10.011 | s2cid = 17994331 }}</ref>

===Working memory===

The basal ganglia has been proposed to gate what enters and what doesn't enter [[working memory]].  One hypothesis proposes that the direct pathway (Go, or excitatory) allows information into the [[Prefrontal cortex|PFC]], where it stays independent of the pathway, however another theory proposes that in order for information to stay in the PFC the direct pathway needs to continue reverberating.  The short indirect pathway has been proposed to, in a direct push pull antagonism with the direct pathway, close the gate to the PFC.  Together these mechanisms regulate working memory focus.<ref name="BG models"/>