BASAL GANGLIA 2. NORMAL
STRUCTURE AND FUNCTION
Schematic – Penney and Young
The basal ganglia per se: Caudate-putamen
(“striatum”) and globus pallidus
(“pallidum”) (all basal forebrain /
• Basal ganglia, strictly defined, is caudate, putamen, and GP. All in the basal
• The caudate putamen is a single structure in lower animals. In higher animals, the
internal capsule (white matter tract) goes down and splits it into caudate AND
putamen. When you’re looking at it as one structure will be called striatum.
• Corpus striatum: old name for basal ganglia
• Neostriatum: may also be applied to caudate-putamen. In justaposition to ventral
striatum, which is nucleus accumbens and parts of olfactory tubercule.
• Globus pallidus is also called the pallidum. Related structures: Substantia nigra
(mesencephalon) and subthalamic nucleus
• There are related structures, one in floor of midbrain (substantia nigra) and one in
the diaencephalon (subthalamic nucleus)
• SN: group of dopaminergic cell bodies lie here. Cell bodies here mostly go to
caudate-putamen. Its right next to the VTA which projects to the nucleus
accumbens and PFC.
• Substantia nigra pars compacta to striatum, and this connection is called the
nigrostriatal pathwayaffected in parkinson’s disease.
• Subthalamic nucleus: floor of diencephalon. This is also going to be part of basal
ganglia. Some books include both these structures as part of the BG, others
consider it as related structures (like the prof)
Figure: Carlson 8:24 • Globus pallidus has two divisions. External and internal division.
• Basal ganglia next to the thalamus.
Note: there is a connection to the motor
centers of the brain stem that give rise to the
• There is a connection from the GP down to the brain stem. What we’re dealing
here is old motor structure. Later as neocortex developed, it was rewired so that it
heavily interacts with frontal neocortex specifically with the motor areas of
frontal neocortex, but it still has old connections down to brainstem, which are
probably important in some aspects.
• These old connections of BG down to brainstem innervate parts of brainstem that
give rise to ventromedial pathway, which would be from reticular core of
brainstem, reticulospinal being most important onehas to do with posture and
2. PHYSIOLOGY / FUNCTION
• The motor cortex is up here. It’s connected to the thalamus, and two thalamic
nuclei important are va and vl. Ventro anterior and ventro lateral.
• This connection is essentially an excitatory feedback loop.
• Thalamus excites cortex, cortex reexcites thalamus.
• Up in motor cortex, you’re going to have movement programs. When you want to
move voluntarily, it will be generated here with support from the thalamus, and
this support is crucial because it can’t function without it.
• Here we have corticothalamic loop which creates voluntary behaviour.
• Next to it, you have GP internal, which tonically inhibits VA/VL. If it weren’t
doing that, you would move constantly. In other words, thalamocortical is
excitatory, if functioned unchecked, would move all the time, like in huntington’s
• But when does GP release its inhibition? Have two pathways, the direct pathway
and indirect pathway. • So thalamus wants to move, GP is holding it down, and when movement isamus).
appropriate, caudate-putamen will inhibit proper part of GP which allows
movement to occur in corticothalamic pathway. (inhibition of inhibition)
• The direct pathway is the GO pathway, will cause voluntary movement to occur.
i) Direct path - Structure: Whole cortex to
striatum (excitatory); striatum to
internal globus pallidus
(inhibitory); internal globus
pallidus to VA/VL thalamus
(inhibitory), VA/VA thalamus to cortex
and frontal cortical areas
(two inhibitory neurons makes the
whole pathway excitatory – when
they’re all active)
- This is the “go “ pathway. It promotes
Function: Internal globus pallidus tonically
inhibits thalamocortical circuits.
Striatum phasically disinhibits
thalamocortical circuits by
inhibiting internal globus pallidus.
Cortex tells the striatum when to
act. • The indirect pathway is the stop pathway and its longer.
• Instead of reducing inhibition of thalamocortical circuits, it increases it.
• It starts off in caudate-putamen, which projects to GP EXTERIOR, so goes to
GPe and inhibits it. GPe goes to subthalamic nucleus and inhibits that. And the
subthalamic nucleus excites GPI.
• Essentially GPi is the stop structure, direct pathway removes activity of the stop
structure, and indirect pathway reinforces it.
• it removes inhibition to subthalamic nucleus which then excites GPi.bits GPe,
ii) Indirect path - Structure: Whole cortex
to striatum (excitatory); striatum to
external globus pallidus
(inhibitory); external globus
pallidus to subthalamic nucleus
nucleus to internal globus pallidus
(excitatory); internal globus pallidus to
VA/VL thalamus (inhibitory), VA/VA
thalamus to cortex and frontal
cortical areas (excitatory).
(three inhibitory neurons makes the
whole pathway inhibitory – when
they’re all active)
- This is the “stop” pathway. It
Function Internal globus pallidus tonically
inhibits thalamocortical circuits. Subthalamic nucleus
phasically reinforces the
inhibition of the
thalamocortical circuits. External
globus pallidus tonically (?) inhibits the
subthalamic nucleus. Striatum
phasically inhibits the external
globus pallidus (releasing the
subthalamus, and therefore inhibiting
the thalamocortical circuits). Cortex
tells the striatum when to act.
• What governs caudate-putamen? The whole neocortex, although most heavily
innervated from pre or post central gyrus.