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17 results on '"Hamilos, Allison E."'

12. Slowly evolving dopaminergic activity modulates the moment-to-moment probability of reward-related self-timed movements.

Author

Hamilos, Allison E., Spedicato, Giulia, Ye Hong, Fangmiao Sun, Yulong Li, and Assad, John A.

Subjects
*REWARD (Psychology), *HUMAN mechanics, *TIME trials, *ANIMAL training, *PROBABILITY theory, *DOPAMINERGIC neurons
Abstract

Clues from human movement disorders have long suggested that the neurotransmitter dopamine plays a role in motor control, but how the endogenous dopaminergic system influences movement is unknown. Here, we examined the relationship between dopaminergic signaling and the timing of reward-related movements in mice. Animals were trained to initiate licking after a self-timed interval following a start-timing cue; reward was delivered in response to movements initiated after a criterion time. The movement time was variable from trial-to-trial, as expected from previous studies. Surprisingly, dopaminergic signals ramped-up over seconds between the start-timing cue and the self-timed movement, with variable dynamics that predicted the movement/reward time on single trials. Steeply rising signals preceded early lick-initiation, whereas slowly rising signals preceded later initiation. Higher baseline signals also predicted earlier self-timed movements. Optogenetic activation of dopamine neurons during self-timing did not trigger immediate movements, but rather caused systematic early-shifting of movement initiation, whereas inhibition caused late-shifting, as if modulating the probability of movement. Consistent with this view, the dynamics of the endogenous dopaminergic signals quantitatively predicted the moment-by-moment probability of movement initiation on single trials. We propose that ramping dopaminergic signals, likely encoding dynamic reward expectation, can modulate the decision of when to move. [ABSTRACT FROM AUTHOR]

Published
2022
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13. A therapeutic convection-enhanced macroencapsulation device for enhancing β cell viability and insulin secretion.

Author

Kisuk Yang, O'Cearbhaill, Eoin D., Liu, Sophie S., Zhou, Angela, Chitnis, Girish D., Hamilos, Allison E., Jun Xu, Verma, Mohan K. S., Giraldo, Jaime A., Yoshimasa Kudo, Lee, Eunjee A., Yuhan Lee, Pop, Ramona, Langer, Robert, Meltoni, Douglas A., Greiner, Dale L., and Karp, Jeffrey M.

Subjects
CELL survival, INSULIN, SECRETION, TYPE 1 diabetes, CINNAMON, IMMUNOCOMPETENT cells
Abstract

Islet transplantation for type 1 diabetes treatment has been limited by the need for lifelong immunosuppression regimens. This challenge has prompted the development of macroencapsulation devices (MEDs) to immunoprotect the transplanted islets. While promising, conventional MEDs are faced with insufficient transport of oxygen, glucose, and insulin because of the reliance on passive diffusion. Hence, these devices are constrained to two-dimensional, wafer-like geometries with limited loading capacity to maintain cells within a distance of passive diffusion. We hypothesized that convective nutrient transport could extend the loading capacity while also promoting cell viability, rapid glucose equilibration, and the physiological levels of insulin secretion. Here, we showed that convective transport improves nutrient delivery throughout the device and affords a threedimensional capsule geometry that encapsulates 9.7-fold-more cells than conventional MEDs. Transplantation of a convection-enhanced MED (ceMED) containing insulin-secreting β cells into immunocompetent, hyperglycemic rats demonstrated a rapid, vascular-independent, and glucose-stimulated insulin response, resulting in early amelioration of hyperglycemia, improved glucose tolerance, and reduced fibrosis. Finally, to address potential translational barriers, we outlined future steps necessary to optimize the ceMED design for long-term efficacy and clinical utility. [ABSTRACT FROM AUTHOR]

Published
2021
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14. Electroencephalogram signatures of ketamine anesthesia-induced unconsciousness

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Song, Andrew H., Hamilos, Allison E., Flores Plaza, Francisco Javier, Purdon, Patrick L., Akeju, Oluwaseun, Pavone, Kara J., Brown, Emery N., Purdon, Patrick Lee, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Song, Andrew H., Hamilos, Allison E., Flores Plaza, Francisco Javier, Purdon, Patrick L., Akeju, Oluwaseun, Pavone, Kara J., Brown, Emery N., and Purdon, Patrick Lee

Abstract

Objectives: Ketamine is an N-methyl-. d-aspartate (NMDA) receptor antagonist commonly administered as a general anesthetic. However, neural circuit mechanisms to explain ketamine anesthesia-induced unconsciousness in humans are yet to be clearly defined. Disruption of frontal-parietal network connectivity has been proposed as a mechanism to explain this brain state. However, this mechanism was recently demonstrated at subanesthetic doses of ketamine in awake-patients. Therefore, we investigated whether there is an electroencephalogram (EEG) signature specific for ketamine anesthesia-induced unconsciousness. Methods: We retrospectively studied the EEG in 12 patients who received ketamine for the induction of general anesthesia. We analyzed the EEG dynamics using power spectral and coherence methods. Results: Following the administration of a bolus dose of ketamine to induce unconsciousness, we observed a "gamma burst" EEG pattern that consisted of alternating slow-delta (0.1-4 Hz) and gamma (~27-40 Hz) oscillations. This pattern was also associated with increased theta oscillations (~4-8 Hz) and decreased alpha/beta oscillations (~10-24 Hz). Conclusions: Ketamine anesthesia-induced unconsciousness is associated with a gamma burst EEG pattern. Significance: The EEG signature of ketamine anesthesia-induced unconsciousness may offer new insights into NMDA circuit mechanisms for unconsciousness., National Institutes of Health (U.S.) (Grant DP2-OD006454)

Published
2017

15. GABAA circuit mechanisms are associated with ether anesthesia-induced unconsciousness

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Song, Andrew H., Purdon, Patrick L., Brown, Emery Neal, Akeju, Oluwaseun, Hamilos, Allison E., Pavone, Kara J., Purdon, Patrick Lee, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Song, Andrew H., Purdon, Patrick L., Brown, Emery Neal, Akeju, Oluwaseun, Hamilos, Allison E., Pavone, Kara J., and Purdon, Patrick Lee

Abstract

Objective: An emerging paradigm for understanding how anesthetics induce altered arousal is relating receptor targeting in specific neural circuits to electroencephalogram (EEG) activity. Enhanced gamma amino-butyric acid A (GABA[subscript A]) inhibitory post-synaptic currents (IPSCs) manifest with large-amplitude slow (0.1-1 Hz) and frontally coherent alpha (8-12 Hz) EEG oscillations during general anesthesia. Therefore, we investigated the EEG signatures of modern day derivatives of ether (MDDE) anesthesia to assess the extent to which we could obtain insights into MDDE anesthetic mechanisms. Methods: We retrospectively studied cases from our database in which patients received isoflurane anesthesia vs. isoflurane/ketamine anesthesia (n = 10 each) or desflurane anesthesia vs. desflurane/ketamine anesthesia (n = 9 each). We analyzed the EEG recordings with spectral power and coherence methods. Results: Similar to known GABA [subscript A] circuit level mechanisms, we found that MDDE anesthesia induced large amplitude slow and frontally coherent alpha oscillations. Additionally, MDDE anesthesia also induced frontally coherent theta (4-8 Hz) oscillations. Reduction of GABAergic IPSCs with ketamine resulted in beta/gamma (13-40 Hz) oscillations, and significantly reduced MDDE anesthesia-induced slow, theta and alpha oscillation power. Conclusions: Large amplitude slow oscillations and coherent alpha and theta oscillations are moderated by ketamine during MDDE anesthesia. Significance: These observations are consistent with the notion that GABA [subscript A] circuit-level mechanisms are associated with MDDE anesthesia-induced unconsciousness. Keywords: EEG Isoflurane Desflurane Ketamine Slow oscillations Alpha oscillations, National Institutes of Health (U.S.) (Grant DP2-OD006454), National Institutes of Health (U.S.) (Grant DP1-OD003646), National Institutes of Health (U.S.) (Grant TR01-GM104948)

Published
2017

16. Electroencephalogram Signatures of Ketamine-Induced Unconsciousness

Author

Akeju, Oluwaseun, Song, Andrew H., Hamilos, Allison E., Pavone, Kara J., Flores, Francisco J., Brown, Emery N., and Purdon, Patrick L.

Subjects
Adult, Male, Anesthetics, General, Brain, Gamma Rhythm, Humans, Female, Ketamine, Middle Aged, Article
Abstract

Ketamine is an N-methyl-d-aspartate (NMDA) receptor antagonist commonly administered as a general anesthetic. However, neural circuit mechanisms to explain ketamine anesthesia-induced unconsciousness in humans are yet to be clearly defined. Disruption of frontal-parietal network connectivity has been proposed as a mechanism to explain this brain state. However, this mechanism was recently demonstrated at subanesthetic doses of ketamine in awake-patients. Therefore, we investigated whether there is an electroencephalogram (EEG) signature specific for ketamine anesthesia-induced unconsciousness.We retrospectively studied the EEG in 12 patients who received ketamine for the induction of general anesthesia. We analyzed the EEG dynamics using power spectral and coherence methods.Following the administration of a bolus dose of ketamine to induce unconsciousness, we observed a "gamma burst" EEG pattern that consisted of alternating slow-delta (0.1-4Hz) and gamma (∼27-40Hz) oscillations. This pattern was also associated with increased theta oscillations (∼4-8Hz) and decreased alpha/beta oscillations (∼10-24Hz).Ketamine anesthesia-induced unconsciousness is associated with a gamma burst EEG pattern.The EEG signature of ketamine anesthesia-induced unconsciousness may offer new insights into NMDA circuit mechanisms for unconsciousness.

Published
2016

17. Electroencephalogram signatures of ketamine anesthesia-induced unconsciousness

Author

Andy Song, Emery N. Brown, Francisco J. Flores, Kara J. Pavone, Oluwaseun Akeju, Patrick L. Purdon, Allison E. Hamilos, Institute for Medical Engineering and Science, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Song, Andrew H., Hamilos, Allison E., Flores Plaza, Francisco Javier, and Purdon, Patrick L.

Subjects
medicine.diagnostic_test, Unconsciousness, Alpha (ethology), Electroencephalography, Sensory Systems, 03 medical and health sciences, 0302 clinical medicine, Brain state, Neurology, 030202 anesthesiology, Physiology (medical), Anesthesia, Gamma Rhythm, Anesthetic, medicine, NMDA receptor, Ketamine, Neurology (clinical), medicine.symptom, Psychology, Neuroscience, 030217 neurology & neurosurgery, medicine.drug
Abstract

Objectives: Ketamine is an N-methyl-. d-aspartate (NMDA) receptor antagonist commonly administered as a general anesthetic. However, neural circuit mechanisms to explain ketamine anesthesia-induced unconsciousness in humans are yet to be clearly defined. Disruption of frontal-parietal network connectivity has been proposed as a mechanism to explain this brain state. However, this mechanism was recently demonstrated at subanesthetic doses of ketamine in awake-patients. Therefore, we investigated whether there is an electroencephalogram (EEG) signature specific for ketamine anesthesia-induced unconsciousness. Methods: We retrospectively studied the EEG in 12 patients who received ketamine for the induction of general anesthesia. We analyzed the EEG dynamics using power spectral and coherence methods. Results: Following the administration of a bolus dose of ketamine to induce unconsciousness, we observed a "gamma burst" EEG pattern that consisted of alternating slow-delta (0.1-4 Hz) and gamma (~27-40 Hz) oscillations. This pattern was also associated with increased theta oscillations (~4-8 Hz) and decreased alpha/beta oscillations (~10-24 Hz). Conclusions: Ketamine anesthesia-induced unconsciousness is associated with a gamma burst EEG pattern. Significance: The EEG signature of ketamine anesthesia-induced unconsciousness may offer new insights into NMDA circuit mechanisms for unconsciousness., National Institutes of Health (U.S.) (Grant DP2-OD006454)

Published
2016

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