The adage practice makes perfect makes for sound advice when learning a novel motor skill. Be it typing a new password or hitting a forehand in tennis, proficiency increases with experience. Behavioral changes associated with motor skill acquisition can be broken down into three broad categories: (1) movements are executed faster and become more coordinated, (2) they come to rely on sensory information gained while executing the task, rather than just sensory information used during initial stages of learning the task, and (3) they seem to be executed with less conscious thought and attention. In addition, neural activity changes: many imaging and neural recording studies suggest that with experience, control is transferred from cortical planning areas to the basal ganglia. The two areas are thought to employ different learning and control schemes. In general, planning can quickly take new information into account to make reasonable decisions, but its control mechanisms have large computational requirements. The basal ganglia use a simpler and less computationally expensive control scheme, but they require much experience before they can produce reasonable behavior. In this thesis, I contribute to answering the question, "what goes on during practice?" More formally, I am interested in the mechanisms by which motor skills are acquired. I take a theoretical approach in that I hypothesize a multiple controller scheme, based on the learning and control mechanisms of cortical planning areas and the basal ganglia, and test it with simulations designed emulate generic motor skill tasks. Because skill proficiency increases with experience, I am particularly interested in the role of the experience-dependent mechanisms of the basal ganglia in motor skill acquisition. Thus, learning mechanisms attributed to cortical areas are artificially restricted so that any change in model behavior is attributed to the learning mechanisms of the basal ganglia. Model behaviors exhibit characteristics indicative of motor skills, supporting the plausibility of the multiple controller scheme as one used by our nervous system and suggesting that the learning mechanisms of the basal ganglia can contribute to developing most characteristics. In addition, I show how the strategies developed by the models are functionally advantageous, providing a reason why such a scheme may be used.

In female mammals reproduction is sensitive to the availability of metabolic fuels, and food deprivation has been shown to suppress pulsatile luteinizing hormone (LH) secretion, attenuate the preovulatory LH surge, and prevent ovulation. It has been suggested that food deprivation impairs fertility by reducing secretion of gonadotropin-releasing hormone (GnRH) by GnRH-producing neurons in the forebrain. A series of experiments using double-label immunocychemistry tested this hypothesis by examining the effects of estrous cycles and manipulations of metabolic fuel availability of expression of Fos-like proteins (Fos-IR) in GnRH-immunoreactive (GnRH-IR) neurons in the forebrain of Syrian hamsters. GnRH-IR neurons were detected in several areas, including the diagonal band of Broca (DBB), medial septum (MS), rostral medial preoptic area (mPOA), and caudal POA. In the more rostral regions (DBB and MS/mPOA) GnRH-IR neurons expressed Fos-IR almost exclusively ond day 4 of the cycle, just after the preovulatory LH surge. However, in the caudal POA, GnRH-IR neurons expressed Fos-IR across the entire cycle, including days 1-3 when LH secretion is pulsatile. Food deprivation on days 1 and 2 of the cycle, which attenuates the LH surge and blocks ovulation in hamsters, significantly reduced the proportion of GnRH-IR neurons which expressed Fos-IR on days 2 and 4 (caudal POA) or just on day 4 (DBB and MS/mPOA). Suppression of fuel availability with insulin or 2-deoxy-D-glucose on day 1 of the cycle mimicked the effects of food deprivation and reduced the proportion of caudal POA GnRH-IR neurons which expressed Fos-IR. The results of these experiments suggest that in Syrian hamsters there are separate populations of GnRH-IR neurons associated with pulsatile and surge modes of LH secretion. In addition, the fact that manipulations of metabolic fuel availability cause changes in expression of Fos-IR in both populations of GnRH-IR neurons provides strong support for the hypothesis that nutritional infertility is due in part to decreased GnRH secretion.

Reflexive and voluntary performance in four test batteries was examined in 12 able-bodied and 12 disabled (6 spinal cord injured, 6 with cerebral palsy) subjects. The batteries, administered pre and post to 4 weeks of training, consisted of tests for patellar tendon tap reflex, phasic vibratory response, knee extension isometric strength, reaction time, and speed of movement. Training involved 120 patellar tendon taps per session, 3 sessions per week. The training patellar taps were paired with an auditory tone; one half of the subjects were trained with a loud (100 db) auditory tone, the remaining were trained with a soft (50 db) auditory tone. No significant difference was observed for reflexive agonist and antagonist EMG amplitude and reflexive peak force during the training or posttraining sessions. The expected habituation of reflexive response was not observed, but the impact force to elicit a maximum reflexive response increased across sessions. These findings suggest that the muscle spindles became less responsive with repeated sessions, but this decreased responsiveness was masked by the increased impact force. Pre to posttraining increases were observed in: tendon tap reflex long motor time and long reflex time; phasic vibratory response; maximum isometric knee extension strength; and velocity of movement in both groups. Posttraining changes in reflexive and voluntary responses were likely due to increased Ia afferent presynaptic inhibition and a more efficient muscle contraction. Auditory effects on reflexive and voluntary responses were mainly limited to a shortening of reaction premotor time especially in the disabled group. The loud tone increased the agonist EMG during the strength test, without a concurrent increase in maximum strength. Between group differences, with regard to spinal and supraspinal influences during the reflex profile, indicated that the gain in reflexive response was greater for the disabled subjects under spinal conditions, and greater for the able-bodied subjects under supraspinal conditions. Another finding revealed greater absolute antagonist reflexive responses, and greater relative antagonist voluntary responses of the disabled group compared to the able-bodied group under all conditions. Adaptations across training sessions and descriptive differences between groups provide insight into future research and rehabilitation strategies.