Why does gamma‑motor‑neuron activity decrease after a transection between the medulla and spinal cord, causing an initial loss of tone and only partial recovery (greater in flexors than extensors) in the animal?

Gamma Motor Neuron Activity Decreases After Spinal Transection Due to Loss of Supraspinal Excitatory Drive

Gamma motor neuron activity decreases after transection between the medulla and spinal cord because these neurons lose their primary source of tonic excitatory input from supraspinal descending pathways, particularly from brainstem reticular formation and vestibular nuclei, which normally maintain their baseline firing rate and responsiveness to reflex inputs.

Mechanism of Decreased Gamma Motor Neuron Activity

Loss of Descending Facilitation

• The spinal cord below the transection becomes disconnected from supraspinal control centers that normally provide continuous excitatory drive to both alpha and gamma motor neurons 1
• Gamma motor neurons are particularly dependent on descending inputs to maintain their tonic activity, as they have lower intrinsic excitability compared to alpha motor neurons 2
• The loss of descending pathways results in reduced state of excitability in spinal motor circuits, inhibiting execution of normal motor programs 1

Spinal Shock Physiology

• During the initial spinal shock period, there is profound loss of all reflex activity and muscle tone due to sudden withdrawal of facilitatory supraspinal influences 1
• The spinal cord circuits below the lesion enter a state of reduced excitability affecting both alpha and gamma motor neuron pools 1
• This hyperpolarized state particularly affects gamma motor neurons, which require higher levels of synaptic drive to reach firing threshold 2

Partial Recovery Pattern Explained

Differential Recovery in Flexors vs Extensors

• After spinal shock resolves, local spinal reflex circuits gradually recover some function through reorganization of remaining intraspinal connections 3, 1
• Flexor reflex pathways recover more robustly than extensor pathways because flexor withdrawal reflexes are organized primarily at the spinal level and less dependent on supraspinal control 3
• Extensor tone, which normally relies heavily on vestibulospinal and reticulospinal facilitation for antigravity function, remains more severely depressed 1

Intraspinal Circuit Reorganization

• Glutamatergic and GABAergic synapses on motor neurons below the transection remain intact (46% glutamatergic, 39% GABAergic inputs preserved), providing anatomical substrate for residual reflex activity 3
• However, the balance shifts toward relatively greater inhibitory tone due to loss of descending excitatory modulation, contributing to persistent hypotonia 3
• Local proprioceptive reflexes can still modulate gamma motor neuron activity through preserved spinal pathways, but at reduced overall levels 4, 5

Why Gamma Activity Remains Depressed

Lack of Tonic Supraspinal Drive

• Gamma motor neurons normally receive continuous facilitation from brainstem centers that is completely eliminated by the transection 1
• Unlike alpha motor neurons, which can be activated by strong peripheral sensory inputs alone, gamma motor neurons require both peripheral and central drive to maintain adequate firing rates 2, 4
• The absence of descending input leaves gamma motor neurons operating at subthreshold membrane potentials, responsive only to very strong local reflex inputs 4, 5

Alpha-Gamma Linkage Disruption

• Normal motor control involves coordinated activation of alpha and gamma motor neurons (alpha-gamma coactivation) mediated by shared descending commands 4, 5
• After spinal transection, this linkage is disrupted, and gamma motor neurons lose the parallel activation that normally accompanies alpha motor neuron recruitment 4
• Residual spinal reflexes can activate alpha motor neurons through strong sensory inputs, but the parallel gamma activation is diminished or absent 5

Clinical Implications

Muscle Spindle Dysfunction

• Reduced gamma motor neuron activity results in decreased muscle spindle sensitivity to stretch, impairing proprioceptive feedback 2, 4
• This contributes to the abnormal quality of muscle tone recovery, with muscles remaining hypotonic despite some return of reflex activity 4
• The fusimotor system cannot properly adjust spindle sensitivity to match changing muscle lengths during movement 4, 5

Incomplete Tone Recovery

• Even when alpha motor neuron activity partially recovers through spinal reflex reorganization, the lack of adequate gamma motor neuron activity prevents normal muscle tone restoration 2, 1
• Flexors show better recovery because flexor withdrawal reflexes can generate adequate alpha motor neuron activation through local circuits, but gamma coactivation remains impaired in both flexors and extensors 3, 1