The D1 neurons in the striatum are inhibitory (GABA-erga), equipped with type 1 dopamine receptors and make direct contact with GPi-SNr. Unless the D1 neuron is excited from the cerebral cortex, the D1 neuron discharges itself with the eigenfrequency 0.1-1 Hz; something with almost negligible braking power on the GPi-SNr. If the excitation from the cerebral cortex increases, then the D1 neuron increases its discharge frequency, its brake, on the GPi-SNr (marked with a star around the GPi-SNr in the figures). As a result, the GPi-SNr's brake on the thalamus will decrease.
Thalamus is disinhibited!! The signal flow from the thalamus to the cerebral cortex increases!
Note that activation of the D1 receptors (dopamine) increases the slowing ability of the D1 neuron.