The spinocerebellar tract is a nerve tract originating in the spinal cord and terminating in the same side (ipsilateral) of the cerebellum. Origins of proprioceptive information
Proprioceptive information is obtained by Golgi tendon organs and muscle spindles. Golgi tendon organs consist of a fibrous capsule enclosing tendon fascicles and bare nerve endings that respond to tension in the tendon by causing action potentials in type Ib afferents. These fibers are relatively large, myelinated, and quickly conducting. Muscle spindles monitor the length within muscles and send information via faster Ia afferents. These axons are larger and faster than type Ib (from both nuclear bag fibers and nuclear chain fibers) and type II afferents (solely from nuclear chain fibers).All of these neurons are sensory (first order, or primary) and have their cell bodies in the dorsal root ganglia. They pass through Rexed laminae layers I-VI of the posterior grey column (dorsal horn) to form synapses with second order or secondary neurons in layer VII just beneath the dorsal horn. Subdivisions of the tract
The tract is divided into:

Dorsal spinocerebellar tract
The dorsal spinocerebellar tract (posterior spinocerebellar tract, Flechsigs fasciculus, Flechsigs tract) conveys proprioceptive information from proprioceptors in the skeletal muscles and joints to the cerebellum.It is part of the somatosensory system and runs in parallel with the ventral spinocerebellar tract. It carries proprioceptive information from muscle spindles and Golgi tendon organs of ipsilateral part of trunk and lower limb. Proprioceptive information is taken to the spinal cord via central processes of dorsal root ganglia (first order neurons).
GRMF  affects primarily the liver (rather than the kidneys) for some physiological processes.High-potassium media (which stimulates aldosterone secretion in vitro) also stimulate cortisol secretion from the fasciculata zone of canine adrenals — unlike corticosterone, upon which potassium has no effect.Potassium loading also increases ACTH and cortisol in humans. This is probably the reason why potassium deficiency causes cortisol to decline (as mentioned) and causes a decrease in conversion of 11-deoxycortisol to cortisol. This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA.Ascorbic acid presence, particularly in high doses has also been shown to mediate response to psychological stress and speed the decrease of the levels of circulating cortisol in the body post-stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol levels after treatment with ascorbic acid. Factors increasing cortisol levels
Viral infections increase cortisol levels through activation of the HPA axis by cytokines. Intense (high VO2 max) or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose; however, cortisol declines to normal levels after eating (i.e., restoring a neutral energy balance)
Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods. Low-carbohydrate diets cause a short-term increase in resting cortisol (~3 weeks), and increase the cortisol response to aerobic exercise in the short- and long-term. Biochemistry
Biosynthesis
Cortisol is synthesized from cholesterol. Synthesis takes place in the zona fasciculata of the adrenal cortex. (The name cortisol is derived from cortex.)