AI Article Synopsis

  • Pain relief typically relies on chemical methods, which can have side effects and may not always be effective, leading to issues like anesthesia awareness and chronic pain.
  • A new approach using magnetically induced deep brain modulation aims to provide a non-invasive, side-effect-free treatment by modifying neuronal firing in the anterior cingulate cortex (ACC), where pain is processed.
  • This method involves using a specially developed pulse magnetic field projector to reduce high-frequency nociceptive neuronal firing associated with pain, which has been successfully simulated, showing promise for improved pain relief.

Article Abstract

Pain, either acute pain or chronic pain, is usually treated/relieved by chemical means, in which nociceptive signals are blocked from transmitting into the pain registration sites in the brain. However, besides their side effects, chemical means of pain relief are not always effective, causing some serious clinical incidents like anesthesia awareness and chronic pains that are not treatable. A physical means of pain relief that physically modifies pain perception at the brain sites responsible for pain registration could be more effective, for both acute pain and chronic pain. In this paper a novel approach of magnetically induced deep brain modulation of neuronal firing is proposed for pain treatment/relief, in which pain treatment/relief is bioelectronics based and is non-invasive and free of side effects. A novel pulse magnetic field projector has been developed for pain relief through modulation of neuronal firing at the anterior cingulate cortex (ACC). It is based on the neuroscience findings that pain registration in the brain is closely related to the excitation of nociceptive neurons at the ACC, in which the nociceptive neuronal firing rate increases as pain gets more intense. The mechanism of pain relief in the proposed approach is to modify the nociceptive neuronal firing rate at the ACC by magnetically inducing a pulse electric field applying on the neurons in the ACC, hyperpolarizing the neurons that are firing at high frequency during pain perception, resulting in a low level firing rate associated to no pain. A parametric study has been carried out to determine the physical and technical parameters of the proposed approach. The feasibility of the approach has been verified by simulation with the modulation implemented on a reconstructed ACC LV pyramidal cell using Hodgkin-Huxley style model. Action potentials recorded in the soma indicated that the firing frequency can be modulated by the applied pulse electric field.

Download full-text PDF

Source
http://dx.doi.org/10.1109/EMBC.2012.6346035DOI Listing

Publication Analysis

Top Keywords

neuronal firing
20
pain relief
20
pain
19
pain registration
12
firing rate
12
magnetically induced
8
induced deep
8
deep brain
8
firing
8
acute pain
8

Similar Publications

The inferior colliculus (IC) has traditionally been regarded as an important relay in the auditory pathway, primarily involved in relaying auditory information from the brainstem to the thalamus. However, this study uncovers the multifaceted role of the IC in bridging auditory processing, sensory prediction, and reward prediction. Through extracellular recordings in monkeys engaged in a sound duration-based deviation detection task, we observed a 'climbing effect' in neuronal firing rates, indicative of an enhanced response over sound sequences linked to sensory prediction rather than reward anticipation.

View Article and Find Full Text PDF

Spiking Flip-Flop Memory in Resonant Tunneling Diode Neurons.

Phys Rev Lett

December 2024

University of Strathclyde, Institute of Photonics, SUPA Dept of Physics, Glasgow, United Kingdom.

We report a spiking flip-flop memory mechanism that allows controllably switching between neural-like excitable spike-firing and quiescent dynamics in a resonant tunneling diode (RTD) neuron under low-amplitude (<150  mV pulses) and high-speed (ns rate) inputs pulses. We also show that the timing of the set-reset input pulses is critical to elicit switching responses between spiking and quiescent regimes in the system. The demonstrated flip-flop spiking memory, in which spiking regimes can be controllably excited, stored, and inhibited in RTD neurons via specific low-amplitude, high-speed signals (delivered at proper time instants) offers high promise for RTD-based spiking neural networks, with the potential to be extended further to optoelectronic implementations where RTD neurons and RTD memory elements are deployed alongside for fast and efficient photonic-electronic neuromorphic computing and artificial intelligence hardware.

View Article and Find Full Text PDF

Transcription and epigenetic factor dynamics in neuronal activity-dependent gene regulation.

Trends Genet

January 2025

Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan; Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, Guangdong 518132, China. Electronic address:

Neuronal activity, including sensory-evoked and spontaneous firing, regulates the expression of a subset of genes known as activity-dependent genes. A key issue in this process is the activation and accumulation of transcription factors (TFs), which bind to cis-elements at specific enhancers and promoters, ultimately driving RNA synthesis through transcription machinery. Epigenetic factors such as histone modifiers also play a crucial role in facilitating the specific binding of TFs.

View Article and Find Full Text PDF

The hippocampus has a known role in learning and memory, with the ventral subregion supporting many learning tasks involving affective responding, including fear conditioning. Altered neuronal intrinsic excitability reflects experience-dependent plasticity that supports learning-related behavioral changes. Such changes have previously been observed in the dorsal hippocampus following fear conditioning, but little work has examined the effect of fear conditioning on ventral hippocampal intrinsic plasticity.

View Article and Find Full Text PDF

Activation of the brain-penetrant beta3-adrenergic receptor (Adrb3) is implicated in the treatment of depressive disorders. Enhancing GABAergic inputs from interneurons onto pyramidal cells of prefrontal cortex (PFC) represents a strategy for antidepressant therapies. Here, we probed the effects of the activation of Adrb3 on GABAergic transmission onto pyramidal neurons in the PFC using in vitro electrophysiology.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!