Frontostriatal circuit

From a Striatofrontalen dysfunction (also: fronto - striatal dysfunction ) is called in neuroscience and brain research, if dysfunction of specific neuronal control circuits are available, the essential components are the striatum ( a part of the basal ganglia ) and the frontal lobe.

The control circuits in question a fundamental importance for the function of the frontal part of the cerebral cortex ( frontal lobe ) and thus for the so-called executive functions. They are instrumental in helping to realize the interaction of motivation, emotion, cognition and movement behavior of neuronal or control. Dysfunction ( dysfunction ) of feedback loops lead to an over or under supply of neurotransmitters (particularly dopamine and norepinephrine ) in specific brain regions and have errors of these psychological or behavioral functions result.

Striatofrontale dysfunctions occur among others in Parkinson's and Huntington 's disease, and (addiction ) are also discussed in tics, geriatric depression and addiction. Also in the Attention-Deficit/Hyperactivity striatofrontale dysfunctions were detected using imaging techniques.

The causes of such dysfunction are varied. Often genetic and developmental factors interact. The sequences comprise in most cases a failure of the executive functions.

Striatofrontale ( frontostriatale ) control loops

Striatofrontale or frontostriatale control loops ( loops; " loops" ) go from the cerebral cortex (cortex ) and extend over the basal ganglia and the thalamus back to the cerebral cortex, namely essentially the frontal lobe. Fast access from the entire cerebral cortex to the striatum information as input station of the basal ganglia ( cortico- striatal connections with excitatory glutamatergic neurotransmission ). About the output station of the basal ganglia, the substantia nigra pars reticulata (SNR) and the globus pallidus internus (GPI ) passes the processed by the basal ganglia end information ( inhibitory GABAergic neurotransmission ) to the thalamus and from there to a excitatory glutamatergic connection back to the cortex, and that primarily the frontal lobes.

So it is a "direct excitatory connection" from the striatum to the output structures (SNR and GPI) of a delineate " indirect inhibitory compound ". The striatum and the GPI are both GABAergic ( inhibitory ). Thus, a direct projection of the striatum to the GPI leads to an inhibition of the inhibition of the GPI, resulting in excitation of the thalamus / cortex.

In the indirect connection, it is a bit more complicated: The striatum inhibits externum the globus pallidus, which inhibits the subthalamic nucleus. Thus, it comes back to an inhibition of inhibition, with the result that the nucleus is excited subthalamic. This now acts excitation in the globus pallidus internum, which thus indirectly inhibits the thalamus and the cortex.

Through this interaction excitatory and inhibitory neurotransmission to the direct and indirect loops, the output modulation of Basalganglienaktivität is, so to speak at two oppositely directed reins.

Striatofrontale dysfunction in ADHD

Using functional magnetic resonance imaging decreased activation in the right-sided prefrontal system and increased frontal and decreased striatal activation ( in so-called Go-/No-go-Aufgaben ) was found in ADHD patients.

Positron emission tomography (PET ) a 8.1% decreased glucose turnover in the left frontal lobe and with single photon emission computed tomography ( SPECT) were detected low blood flow to the frontal lobe and the striatum and increased dopamine transporter concentration in the striatum.

In the dopaminergic system of ADHD patients many of dopamine transporter proteins are present in the presynaptic membrane, with the result that too much dopamine from the synaptic cleft (see also synapse ) is transported back into the presynaptic neuron. This ratio normalized by treatment with dopamine reuptake inhibitors such as methylphenidate, unless the person concerned is not a non-responder.

Striatofrontale dysfunction in Parkinson syndromes

Disorders of striatofrontalen compounds continue to be discussed in the context of Parkinson's disease and progressive supranuclear palsy.