Dorsal striatum

Striatum dorsale

Neostriatum, MSN, TAN, Striosome, Matrix substance, Matrixoma, D1 neuron, striatum, D2 neuron, striatum

The dorsal striatum (neostriatum) is counted among the basal ganglia and includes, on hay. and on the left. side, caudate nucleus (nucleus caudatus) + shell nucleus (putamen).

The dorsal striatum, with a volume of about 10 cm3, constitutes the largest nuclear complex of the human brain.

Vävnadally, the two parts of the dorsal striatum, the caudal nucleus and the shell nucleus, are identical and together contain about 100 million neurons. A clear majority of these, with a cell body diameter of about 15 μm, are GABA-ergic inhibitory so-called medium-sized spinous projection neurons (MSNs). The rest, about 25%, consists of several different neuron types including the Tonic Active Acetylcholine-ergic Neuron (TAN) and thorn-poor neuron, both varieties with, as it seems, only local distribution within the dorsal striatum. These local networks are complex and difficult to investigate. The TAN group is thought to receive excitatory signals from the thalamus (CM-PF complex) and in turn modulate the activity of the MSN group.

The group MSN (medium-sized spiny projection neurons), whose dendrites are really strewn with thorns, comprises two different inhibitory neuron types (1/ and 2/ below), both of which spontaneously discharge themselves at the low natural frequency of 0.1-1 Hz and receive propulsive/excitatory/glutamate-ergic signals from the cerebral cortex/cortex and from several thalamus nuclei (note the CM-PF complex):

1/ D1 neurons, which in addition to GABA also contain substance P + dynorphine, are equipped with dopaminereceptors of type 1 (D1 receptors). If the D1 receptors (of dopamine) are activated, the D1 neuron's braking ability increases. The D1 neuron makes direct contact with the GPi-SNr, thus forming the "Direct Pathway" through the basal ganglia towards the thalamus. Since the D1 neurons are inhibitory, their activity in turn slows down the GPi-SNr neuron's brake on the thalamus, which is thus disinhibited and can increase its signal flow to the cortex.

2/ D2 neurons, which in addition to GABA also contain enkephalin, are equipped with dopamine receptors of type 2 (D2 receptors). If the D2 receptors are activated (by dopamine), the D2 neuron's braking ability decreases. The D2 neuron has no direct contact with GPi-SNr and corresponds to the first part of the "Indirect pathway" through the basal ganglia towards the thalamus.

The cerebral cortex thus makes contact with the D1 and D2 neurons via propulsive/excitatory signaling. Ifthe contacting bark area is "at rest",the contacted D1 and D2 neurons emit their braking signals with low frequency (0.1-1Hz) and weak braking power. If the contacting bark area is activated, then the contacted D1 and D2 neurons increase their signal frequency and their braking effects make themselves felt.

Notice that an activity increase in the D1 neuron's braking effect results in an increased signaling from the thalamus back to the bark and that an activity's increase in the D2 neuron's braking effect results in a decreased signaling from the thalamus back to the bark! Should there be an imbalance in the effects of the increased activity of the D1 and D2 neurons, the compact part of the black nucleus (SNc) intervenes and increases its dopamine signaling to the dorsal striatum.

If you stain a thin incision through the brain to detect the enzyme acetylcholinesterase you can, both in the dorsal striatum and in the nucleus accumbens, already with the naked eye, see half-millimeter-sized uncolored/enzyme-negative spots against a gray-black/enzyme-positive background. The light spots are called strugosomes and the dark background is called matrix substance. Especially dark spots in the matrix substance are called matrixomes.
The triosomes receive signals from the limbic system, especially from the limbic cortex and amygdala.
The matrixomes consist of packed D1 and D2 neuronal bodies.