The basal ganglia are not part of the HPA axis. However, together with the thalamus, they are the central filter and control circuit that regulates the HPA axis and the cortex.
The basal ganglia are a group of different brain structures that perform a filtering function in the communication between the thalamus and the cortex. The striatum is the input filter of the basal ganglia and consists of different nuclei: the caudate nucleus, the lentiform nucleus and the nucleus accumbens.
The striatum receives information from the cerebral cortex and other areas of the brain and, after filtering, sends it to the substantia nigra and the inner pallidum, which filter it again and pass it on to the thalamus. The thalamus sends the filtered information to the cortex.
In ADHD, it is assumed that the filter function of the basal ganglia is disturbed, which leads to increased inappropriate behavior and a faulty inhibition of new behavioral plans.
1. Elements of the basal ganglia¶
1.1. Anatomical parts of the basal ganglia (basal ganglia, basal nuclei, nuclei basales):¶
1.1.1. Striatum¶
The striatum is the input filter of the basal ganglia.
The striatum consists of:
-
Caudate nucleus (curved nucleus)
- Nucleus lentiformis (lenticular nucleus)
-
Putamen (shell body)
- Pallidum (globus pallidus, pale globe)
- Internal pallidum (pallidum internum/mediale or globus pallidus internus/medialis, GPI)
- External pallidum (pallidum externum/laterale or globus pallidus externus/lateralis, GPE)
-
Nucleus accumbens
- Connects caudate nucleus and ventral putamen directly (ventral striatum)
- Reinforcement center, regulates behavior (motivation):
- Narrow bridges of gray matter (pontes grisei caudatolenticulares)
- Also connect the caudate nucleus and putamen
- Namesake for the striatum (the striated)
The striatum receives efferent (incoming) projections from, among other things:
-
Cortex (cerebral cortex)
-
Substantia nigra
- Raphe cores
- Formatio reticularis
Neurons of the striatum:
Over 95 % of these are medium spiny neurons (MSN; i.e. medium-sized neurons (diameter 12-15 µm in rodents) with large and extensive dendrite trees).
There are two types of MSN in the dorsal striatum, both of which communicate GABAergically.
- MSN of the direct route:
- send direct (monosynaptic) projections into the
- Substantia nigra
- Globus pallidus internus
- express
- Dopamine D1 receptors
- the peptide dynorphin, together with substance P
-
MSN of the indirect route
- communicate with substantia nigra and globus pallidus internus (indirectly) via
- Globus pallidus externus
- Subthalamic nucleus
- express
-
Dopamine D2 receptors
- the peptide enkephalin
1.1.1.1. Caudate nucleus¶
One study found that with ADHD
- Lower volume of gray matter (GM) in the right putamen
- Lower volume of white matter (WM) in left parieto-insular
- Reduced volume
- Of the right anterior hippocampus
- Of the white matter on the right parieto-insular
- Of the connections between the caudate nucleus and the cortices
-
Frontal
-
Parietal
-
Occipital
-
Temporal
- Insular
- A reduced value of fractional anisotropy of the left caudate-parietal tract correlated with hyperactive/impulsive symptoms
1.2. Functional parts of the basal ganglia¶
Individual areas of the brain outside the striatum perform the filtering functions of the basal ganglia together with the striatum.
-
Substantia nigra (black substance, SN)
- SN Pars compacta (SNc)
- SN Pars reticularis (SNr)
- SN lateralis
- Nucleus subthalamicus (STN, Corpus Luysi).
2. Tasks of the basal ganglia: support of the thalamus through filtering¶
The main task of the basal ganglia is to filter communication between the thalamus and the cortex.
The neurons of layer V of all cortex areas (except the primary visual and auditory cortex) transmit information to the striatum (glutamaterg = excitatory).
The information filtered by the basal ganglia passes from the substantia nigra and the globus pallidus internus to the thalamus (GABAerg = inhibitory). The thalamus passes the information on to the (frontal) cortex (glutamaterg = excitatory).
The striatum (input of the basal ganglia) has a direct and an indirect connection to the output of the basal ganglia (substantia nigra and internal pallidum).
The direct connection between the striatum and the internal pallidum is GABAergic (= inhibitory) and inhibits the internal pallidum. As this in itself has an inhibitory effect on the thalamus, the striatum inhibits the inhibition of the thalamus by the internal pallidum (disinhibition), which in turn activates the thalamus, which activates the cortex.
The indirect connection involves inhibition of the external pallidum (which inhibits the subthalamic nucleus). This leads to the disinhibition of the subthalamic nucleus, which now has an excitatory effect on the internal pallidum, resulting in its inhibition of the thalamus, which in turn inhibits the cortex.
Since the external pallidum also directly inhibits the internal pallidum, inhibition of the external pallidum causes additional disinhibition of the internal pallidum, which further increases its inhibitory effect on the thalamus.
As a result, the basal ganglia cause an inhibition or amplification of the thalamus, which strengthens and modulates its filter function, which information reaches the cortex.
3. Basal ganglia and ADHD¶
In ADHD, it is assumed that the filter function of the basal ganglia is broadband disturbed, which is why redundant or inappropriate behavior (hyperactivity) is reinforced, while new behavioral plans are incorrectly inhibited (attention deficit).
The deviations of the basal ganglia found in ADHD are also found in chronic stress and are quite functional there. In ADHD, however, they are dysfunctional, as the deviation exists permanently without an adequate stressor.
This could also be an elementary difference to severe depression. We suspect that in severe depression, the dopaminergic activity of the nucleus accumbens is not only reduced in reward anticipation (as in ADHD, which causes anhedonia and reward discounting), but also in reward retention (which could explain the complete lack of pleasure that is not present in ADHD).
