ABSTRACT
Recording and modulating neural activity in vivo enables investigations of the neurophysiology underlying behavior and disease. However, there is a dearth of translational tools for simultaneous recording and localized receptor-specific modulation. We address this limitation by translating multifunctional fiber neurotechnology previously only available for rodent studies to enable cortical and subcortical neural recording and modulation in macaques. We record single-neuron and broader oscillatory activity during intracranial GABA infusions in the premotor cortex and putamen. By applying state-space models to characterize changes in electrophysiology, we uncover that neural activity evoked by a working memory task is reshaped by even a modest local inhibition. The recordings provide detailed insight into the electrophysiological effect of neurotransmitter receptor modulation in both cortical and subcortical structures in an awake macaque. Our results demonstrate a first-time application of multifunctional fibers for causal studies of neuronal activity in behaving nonhuman primates and pave the way for clinical translation of fiber-based neurotechnology.
Subject(s)
Neurophysiology , Wakefulness , Animals , Neurophysiology/methods , Macaca mulatta , Brain/physiology , CognitionABSTRACT
The specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little or no spiking activity, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation 'awakened' anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.
Subject(s)
Anesthetics, Intravenous/pharmacology , Cerebral Cortex/drug effects , Hypnotics and Sedatives/pharmacology , Macaca mulatta/physiology , Propofol/pharmacology , Thalamus/drug effects , Unconsciousness/chemically induced , Animals , Cerebral Cortex/physiology , Female , Male , Recovery of Function/drug effects , Recovery of Function/physiology , Thalamus/physiologyABSTRACT
La encefalopatía hepática (EH) es una complicación grave y frecuente del daño hepático crónico (DHC), que se diagnostica clínicamente luego de descartar otras causas de disfunción cerebral. Su manejo consiste en identificar y corregir los factores desencadenantes, disminuir los niveles de amonio con disacáridos no reabsorbibles y eventualmente el uso de antibióticos de baja absorción intestinal, de preferencia rifaximina.
Hepatic encephalopathy is a serious and frequent complication of chronic liver disease and its clinical diagnosis is arrived at once other causes of cerebral dysfunction have been ruled out. It is managed by identifying and correcting triggering factors, lowering plasma ammonium levels by use of non-absorbable disaccharides and oral use of poorly absorbed antibiotics, preferably rifaximin.
