Decision-making is a complex behavior where one must weigh cost and benefit to maximize the likelihood of the best possible outcome. A common example of this is a decision between a small yet certain reward (e.g. $1 or 1 piece of candy), and a larger uncertain reward (e.g. $10 or 10 pieces of candy 50% of the time). It has been suggested that context and dopamine levels play a critical role in the willingness of decision makers to take risks. We tested this hypothesis by assessing behavioral and neural differences between groups of rats trained on an equivalent risk-based paradigm conducted in different contexts. Rats started training in an operant chamber or a decision maze, and then switched contexts (i.e. tasks). These tasks involved the rat making a decision between two levers or doors, one of which was associated with a certain small reward (1 sugar pellet), and the other which is associated with a large (4 sugar pellets) reward that appeared with decreasing probability (100%, 50%, 25%, 12.5%). To test the influence that dopamine has on risk taking behavior, we used a dopamine antagonist (flupenthixol) to inhibit dopamine in both the maze and operant chamber contexts. Our results suggest that when analyzed as a group, rats are less willing to take risks in the maze context. We hypothesize this is because risk taking on the maze is a more complex behavior, perhaps because of a longer delay between a choice and reward delivery. Our pharmacological findings of high numbers of trials in which levers were not pressed in the chamber, or trials not run on the maze, suggest that blocking dopamine interferes with the ability of rats to make risky decisions. Together, these results support the idea that risk-based decision-making is influenced by many factors, including context and dopamine.

 The vestibular system is composed of the semicircular canal system, which detects rotational movements, and the otolith organ system, which senses linear accelerations and tilt with respect to gravity. The two systems can interact in a complex way during movement. The vestibular-ocular reflex (VOR) stabilizes a retinal image during head movement by commanding the eyes to move in a direction opposite to that of the head movement. Under some conditions, both the otolith organs and the semicircular canals contribute to the VOR. Unilateral or bilateral loss of vestibular function often results in vertigo and oscillopsia, which are debilitating and could be life-threatening because they result in falls or injury. In principle, a vestibular prosthesis could treat a functional loss of inner ear vestibular function by sending electrical stimulation into the three semicircular canals via electrodes to help maintain balance and stable vision. However, if the otolith organs are still functional, the signals from the prosthesis might be interpreted incorrectly in different head orientations, limiting the efficacy of the treatment. The interaction between the output from the otolith organs and artificial electrical stimulations from the implant is not known. In this experiment, we oriented a head-fixed rhesus monkey in different static positions along either of the roll and pitch axes prior to electrically inducing a VOR using the implanted vestibular prosthesis. Results showed that stimulation in the posterior canal induced a higher eye velocity in backward-tilted position than in the upright position, while stimulation in the anterior canal induced a slower eye velocity in the forward position than in the upright position. This project demonstrates that the performance of the implant changes under different body orientations. The prosthesis provides a unique experimental tool allowing us to disambiguate canal and otolith inputs in the intact organism.

Previous studies have shown that neurologically healthy subjects learn to generate adaptive motor commands when either sensory feedback (e.g., visual or auditory information) or the movements themselves (e.g., arm movements for reaching or jaw movements for speech) are experimentally perturbed - a phenomenon known as sensorimotor adaptation. In parallel, a different line of research has shown that for both nonspeech and speech movements the central nervous system (CNS) differentiates between self-generated and externally-caused sensory input by comparing actual and predicted inputs - a detected mismatch causes the input to be attributed increasingly to external sources. Here, we investigate these two phenomena in combination by means of two experiments that examine whether sensorimotor adaptation in speech production is diminished, or even abolished, when an auditory feedback perturbation (shifted formant frequencies) is either delivered with increasing delays or made increasingly large. Based on our own pilot data and recent findings from other labs, we hypothesize that increasing either the delay or the extent of the formant perturbation will cause the CNS to increasingly interpret the perceived error as an external manipulation rather than a production error that requires adaptive corrections in future trials. For each experiment, acoustic analyses are used to determine adjustments in subjects’ produced formant frequencies from a baseline phase (unaltered feedback) to the perturbation phase (formant-shifted feedback) across conditions varying in delay and amount of shift in the auditory feedback signal.

Despite major advancements in our understanding of the neural systems involved in persistent developmental stuttering (PDS), the causal mechanisms underlying acquired neurogenic stuttering (ANS) remain poorly understood. ANS typically occurs after stroke, and its primary symptoms resemble those of PDS (i.e., within-word dysfluencies). However, individuals with ANS often show no adaptation effect and no fluency-enhancement with altered auditory feedback. To date, little is known about differences and similarities between ANS and PDS in terms of the loci of stuttering—that is, the locations of stuttering moments within spoken utterances. Brown’s research on PDS has shown that stuttering is more likely to occur on (1) longer words, (2) words that occur early in the sentence, (3) content words, and (4) words that start with a consonant. In this study, we therefore compared ANS and PDS with regard to the distribution of stuttering moments as quantified by Brown’s word weights (for each stuttered or fluent word, 0-4 points are assigned based on the aforementioned four factors). As expected, adults with PDS showed greater word weights for stuttered versus fluent words. Individuals with ANS showed a highly similar pattern with greater word weights for stuttered versus fluent words. Calculating word weights for each factor separately (word length, sentence position, grammatical class, initial consonant) revealed that the ANS group also did not differ from the PDS group in the relative influence of each individual factor. Thus, although there are several known differences between acquired neurogenic and developmental stuttering, the loci of stuttering appear to be influenced by similar factors in both disorders. Of those factors, word length and grammatical class had the strongest influence on the occurrence of dysfluencies in both groups. These findings can be used to generate new hypotheses regarding the neural basis of fluent and dysfluent speech production.

Despite a surge in research efforts over the past two decades, scientific understanding of the mechanisms underlying motor learning remains limited. Although many procedures have been designed to assess an individual’s ability to update motor commands in an altered environment, few attempts have been made to design procedures that assess, and possibly improve, an individual’s ability to learn a completely novel mapping of motor commands and sensory consequences. This is unfortunate because the latter approach has potential clinical applications: various brain disorders cause sensorimotor deficits, and learning alternative movement strategies may aid recovery. Whereas the above studies focused on hand or arm movements, our own research focus is on the speech motor system. The present project aims to design protocols to test and quantify the ability of the speech motor system to learn neural representations of a novel link between motor commands and sensory results. We make use of 3D electromagnetic motion capture technology that tracks 3 position coordinates and 2 angles for up to 9 sensors on the tongue, lips, and jaw; thus for a maximum of 45 dimensions. These 45 dimensions are mapped onto 2 dimensions of movement for a cursor displayed on a computer monitor. As subjects are instructed to move the cursor, their performance (i.e., learning of the novel mapping) is quantified. We will also test individuals from a clinical population (such as those with motor speech disorders or stuttering) and analyze their performance over time to design the most optimal techniques and procedures for quantifying the speech sensorimotor system’s ability to learn the complex relationship between a high-dimensional movement space and a 2D visual space.

Fear conditioning is a form of classical conditioning where an initially neutral conditioned stimulus (CS) is paired with an inherently aversive unconditioned stimulus (US). After multiple CS-US pairings, CS alone produces conditioned fear responses. The amygdala has long been considered the key brain structure where fear learning-related plasticity primarily occurs. However, it has not been well studied how the US directs CS-US association in the amygdala. We recently found that stimulation of the dorsal periaqueductal gray (dPAG) could serve as a US in tone fear conditioning, indicating the dPAG may be a key structure in relaying US information to the amygdala during fear conditioning. In this study, we investigated the role of the amygdala in auditory fear conditioning where dPAG stimulation acted as the US. Male Sprague-Dawley rats were bilaterally implanted with stimulating electrodes in their dPAG and with guide cannulae in their amygdala. Prior to training, muscimol (0.3 µg/0.3 µL per side) was infused into the amygdala using infusion cannula and a microsyringe pump. For training, a tone (2.9 kHz, 85 dB, 20 sec) was used as a CS, and electrical stimulation (0.1-ms width, 100 Hz, 2 sec) of the dPAG as a US which co-terminated with the CS. Next day, an 8-min tone was presented continuously in a novel chamber as a tone testing, and the following day, 8-min exposure to the training chamber was given to the rats as a context testing. While the muscimol-injected animals displayed comparable level of freezing to the control animals during training, their freezing to the tone and context was disrupted during the testing, indicating fear conditioning was blocked by the amygdalar inactivation. These results suggest that the amygdala is critical for dPAG stimulation fear conditioning and may be the center of dPAG-directed US and tone CS convergence and plasticity.