The basal ganglia are not part of the HPA axis. However, together with the thalamus, they are the central filter and regulatory circuit that controls the HPA axis.
The basal ganglia have an important filtering function in the communication between thalamus and cortex. The thalamus (the “gateway to consciousness”) controls what information is passed on to the cortex. The basal ganglia are thought to regulate the selection, activation, and inhibition (inhibition / suppression) of motor and non-motor patterns of action and activation.
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:
- Nucleus caudatus (curved nucleus)
- Nucleus lentiformis (lenticular nucleus)
-
Putamen (shell body)
- Pallidum (globus pallidus, pale sphere)
- Internal pallidum (pallidum internum/mediale or globus pallidus internus/medialis, GPI)
- External pallidum (pallidum externum/lateral or globus pallidus externus/lateralis, GPE)
-
Nucleus accumbens
- Connects caudate nucleus and putamen ventrally directly (ventral striatum)
- Reinforcement center, regulates behavior up (motivation):
- Narrow bridges of gray matter (pontes grisei caudatolenticulares)
- Also connect nucleus caudatus and putamen
- Eponymous for the striatum (the striped)
The striatum receives efferent (incoming) projections from, among others:
-
Cortex (cerebral cortex)
-
Substantia nigra
- Raphe cores
- Formatio reticularis
Neurons of the striatum:
- over 95% of them 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 GABAergic.
-
MSN of the direct path:
- send direct (monosynaptic) projections in
-
Substantia nigra
- Globus pallidus internus
- express
-
Dopamine D1 receptors
- the peptide dynorphin, together with substance P
-
MSN of the indirect path
- communicate with substantia nigra and globus pallidus internus (indirectly) via
- Globus pallidus externus
- Nucleus subthalamicus
- express
-
Dopamine D2 receptors
- the peptide enkephalin
1.1.1.1. Caudate nucleus¶
One study found in ADHD
- Lower gray matter (GM) volume in the right putamen
- Lower white matter (WM) volume in left parieto-insular
- Reduced volume
- Of the right anterior hippocampus
- Of the white matter right parieto-insular
- Of the connections between caudate nucleus and cortices
-
Frontal
-
Parietal
-
Occipital
-
Temporal
- Insular
- A decreased value of fractional anisotropy of the left caudate-parietal tract correlated with hyperactive/impulsive symptoms
1.2. Functional parts of the basal ganglia¶
Individual brain areas outside the striatum exert 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 by filtering¶
The main task of the basal ganglia is to filter the communication between the thalamus and the cortex.
From layer V neurons of all cortex areas (except from primary visual and auditory cortex) information is given 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 (GABAergic = inhibitory). The thalamus passes the information to the (frontal) cortex (glutamaterg = excitatory).
The striatum (entrance of the basal ganglia) has a direct and an indirect connection to the exit of the basal ganglia (substantia nigra and internal pallidum).
The direct connection between striatum and internal pallidum is GABAergic (= inhibitory) and inhibits the internal pallidum. Since 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 result activates the thalamus, which activates the cortex.
The indirect connection involves inhibition of the external pallidum (which inhibits the nucleus subthalamicus). This leads to the disinhibition of the nucleus subthalamicus, which now has an excitatory effect on the internal pallidum, so that its inhibition of the thalamus occurs, which thus inhibits the cortex.
Moreover, because the external pallidum directly inhibits the internal pallidum, inhibition of the external pallidum causes additional disinhibition of the internal pallidum, further enhancing its inhibitory effect on the thalamus.
As a result, the basal ganglia cause inhibition or amplification of the thalamus, which reinforces and modulates its filtering function of what information goes to the cortex.
3. Basal ganglia and ADHD¶
In ADHD, the filtering function of the basal ganglia is thought to be broadly impaired, which is why redundant or inappropriate behavior (hyperactivity) is reinforced, while new behavioral plans are defectively inhibited (attention deficit).
However, we are of the opinion that there is no disturbance of the basal ganglia in ADHD. The deviations of the basal ganglia found in ADHD are also found in chronic stress and are quite functional. What is dysfunctional in ADHD is that the deviation exists permanently without an adequate stressor.
Certainly, the basal ganglia moderate excessive reinforcement or inhibition of various behaviors in ADHD. However, these control contributions of the basal ganglia are likely to be quite identical in healthy individuals in the case of a chronic stress reaction (depending on the stressor) (in particular dopamine deficiency in the nucleus accumbens in the case of reward anticipation and increased dopaminergic activity in the case of reward maintenance) and there also trigger precisely these behavioral pattern changes as then meaningful and survival-promoting symptoms (functional stress symptoms).
Here we might also find an elementary difference from major depression. We suspect that in major depression the dopaminergic activity of the nucleus accumbens is reduced not only in reward anticipation (as in ADHD, causing anhedonia and reward discounting), but also in reward maintenance (which could explain the complete joylessness that is not present in ADHD).
