The basal ganglia receive inputs from the cerebral cortex and send outputs back to it.
These outputs influence motor function via two main pathways: the direct pathway (facilitating movement) and the indirect pathway (inhibiting movement).
Both pathways rely on excitatory glutamate signals from the cortex.
Dopamine from the substantia nigra pars compacta binds to D1 receptors to activate the direct pathway and to D2 receptors to suppress the indirect pathway, ultimately promoting movement.
Direct pathway
Excitation from cortex:Cortical areas (primary and premotor) release glutamate, stimulating substance P-containing GABA neurons in the striatum (especially the putamen).
Inhibiting the inhibitor: These GABA neurons inhibit the GABAergic neurons in the internal globus pallidus. Since the pallidal neurons are normally inhibitory, reducing their activity disinhibits the thalamic VA/VL nuclei.
Thalamic activation: Freed from inhibition, VA/VL nuclei send excitatory signals to the motor cortex, facilitating movement.
Nigrostriatal support:Dopaminergic neurons from the substantia nigra to the striatum, acting on D1 receptors, enhance the direct pathway’s excitatory effect.
Indirect pathway
Excitation from cortex: Glutamate from the cortex stimulates enkephalin-containing GABA neurons in the striatum.
Double inhibition and subthalamic activation: These striatal neurons inhibit GABA neurons in the external globus pallidus, which in turn leads to increased activity of the subthalamic nucleus (because the pallidum’s normal inhibition of the subthalamic nucleus is reduced).
Thalamic suppression: The subthalamic nucleus excites GABAergic neurons in the internal globus pallidus, increasing inhibition of VA/VL nuclei in the thalamus and decreasing motor cortex activity.
Neurotransmitters:Cholinergic neurons in the striatum further potentiate the indirect pathway, while nigrostriatal dopamine (D2 receptors) suppresses this pathway.
Reticular Activating System (RAS)
The RAS is a network of brainstem neurons projecting to the cortex through the thalamus and hypothalamus, governing arousal and wakefulness.
Its ascending fibers form the ascending reticular system, while the descending fibers (reticulospinal tract) modulate muscle tone, balance, and posture.
Lesions can cause disorders like narcolepsy or excessive sleepiness. PTSD may involve hyperactivity in the RAS.
Sleep physiology
Sleep alternates between non-rapid eye movement (NREM) and rapid eye movement (REM) stages every ~90 minutes.
With each cycle, NREM time decreases, and REM time increases.
Onset of NREM: Induced by GABA from the hypothalamic preoptic area and serotonin from raphe nuclei.
Stages I–IV: Progress from low-frequency theta waves (stage I) to sleep spindles and K complexes (stage II), then to slow, high-voltage delta waves (stages III–IV, with IV considered deep sleep).
Muscle tone is reduced but not absent; blood pressure and heart rate decrease.
REM sleep (paradoxical sleep)
EEG: Resembles awake patterns (desynchronized or “sawtooth” waves).
Induction: Driven by cholinergic neurons in the ascending arousal system.
Features:Rapid eye movements, muscle atonia, pupil constriction, and fluctuations in vital signs. NE and serotonin neurons terminate REM, transitioning to NREM.
Age-related changes:
Newborns spend ~50% of their sleep in REM; young adults ~25%; elderly significantly less.
Overall sleep time shortens with advanced age, with frequent awakenings and less stage IV/deep sleep.
These processes underscore the intricate neurophysiology behind motor regulation, arousal, and sleep, illustrating how various neural circuits and neurotransmitters work to fine-tune bodily functions.
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