A Method of Flexible Micro-Wire Electrode Insertion in Rodent for Chronic Neural Recording and a Device for Electrode Insertion

Arafat, Muhammad Abdullah; Rubin, Logan N.; Jefferys, John G. R.; Irazoqui, Pedro P.

doi:10.1109/tnsre.2019.2932032

Cited by 17 publications

(22 citation statements)

References 39 publications

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“…This offers a potential explanation for the “secondary mechanism” we hypothesized in our previous work, 38 wherein we speculated that, if laryngospasm alone was not the cause of death, it may be one symptom of an underlying neural circuit. Further elucidation of the brainstem pathophysiology, and any potential relationship with changes in brainstem activity observed during spontaneous death in KA studies, 39 requires additional direct current (DC)‐coupled and single‐unit recording 49 in the cardiorespiratory control centers. Further physiological studies are also needed to explore the role of central and peripheral chemoreceptors, typically primary initiators of respiratory drive, in OCR regulation and the effects of seizure activity on the brainstem's processing of their input.…”

Section: Discussionmentioning

confidence: 99%

Ictal activation of oxygen‐conserving reflexes as a mechanism for sudden death in epilepsy

et al. 2021

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Objective To test the hypothesis that death with physiological parallels to human cases of sudden unexpected death in epilepsy (SUDEP) can be induced in seizing rats by ictal activation of oxygen‐conserving reflexes (OCRs). Methods Urethane‐anesthetized female Long‐Evans rats were implanted with electrodes for electrocardiography (ECG), electrocorticography (ECoG), and respiratory thermocouple; venous and arterial cannulas; and a laryngoscope guide and cannula or nasal cannula for activation of the laryngeal chemoreflex (LCR) or mammalian diving reflex (MDR), respectively. Kainic acid injection, either systemic or into the ventral hippocampus, induced prolonged acute seizures. Results Reflex challenges during seizures caused sudden death in 18 of 20 rats—all MDR rats (10) and all but two LCR rats (8) failed to recover from ictal activation of OCRs and died within minutes of the reflexes. By comparison, 4 of 4 control (ie, nonseizing) rats recovered from 64 induced diving reflexes (16 per rat), and 4 of 4 controls recovered from 64 induced chemoreflexes (16 per rat). Multiple measures were consistent with reports of human SUDEP. Terminal central apnea preceded terminal asystole in all cases. Heart and respiratory rate fluctuations that paralleled those seen in human SUDEP occurred during OCR‐induced sudden death, and mean arterial pressure (MAP) was predictive of death, showing a 17 or 15 mm Hg drop (MDR and LCR, respectively) in the 20 s window centered on the time of brain death. OCR activation was never fatal in nonseizing rats. Significance These results present a method of inducing sudden death in two seizure models that show pathophysiology consistent with that observed in human cases of SUDEP. This proposed mechanism directly informs previous findings by our group and others in the field; provides a repeatable, inducible animal model for the study of sudden death; and offers a potential explanation for observations made in cases of human SUDEP.

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Section: Discussionmentioning

confidence: 99%

Ictal activation of oxygen‐conserving reflexes as a mechanism for sudden death in epilepsy

et al. 2021

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“…When the bionic guide is placed on the implantation site, the critical flexion force of the probe is increased by 3.8 times, which increases the success rate of probe implantation from 37.5% to 100%. In order to increase the critical flexion force during implantation, Muhammad A et al [150] can be achieved by inserting a rotation and guiding device, as shown in Figure 13. For the implantation of cylindrical electrodes, CBF (critical buckling force) is calculated by Euler's column formula, as follows:…”

Section: Guiding Devicementioning

confidence: 99%

“…In order to increase the critical flexion force during implantation, Muhammad A et al [150] can be achieved by inserting a rotation and guiding device, as shown in Figure 13.…”

Section: Guiding Devicementioning

confidence: 99%

Research Progress on the Flexibility of an Implantable Neural Microelectrode

et al. 2022

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Neural microelectrode is the important bridge of information exchange between the human body and machines. By recording and transmitting nerve signals with electrodes, people can control the external machines. At the same time, using electrodes to electrically stimulate nerve tissue, people with long-term brain diseases will be safely and reliably treated. Young’s modulus of the traditional rigid electrode probe is not matched well with that of biological tissue, and tissue immune rejection is easy to generate, resulting in the electrode not being able to achieve long-term safety and reliable working. In recent years, the choice of flexible materials and design of electrode structures can achieve modulus matching between electrode and biological tissue, and tissue damage is decreased. This review discusses nerve microelectrodes based on flexible electrode materials and substrate materials. Simultaneously, different structural designs of neural microelectrodes are reviewed. However, flexible electrode probes are difficult to implant into the brain. Only with the aid of certain auxiliary devices, can the implant be safe and reliable. The implantation method of the nerve microelectrode is also reviewed.

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“…25 The initial target in the right brainstem pre-Bötzinger complex was 12.8 mm caudal and 0.6 mm left of bregma, for a 10-degree angle in the coronal plane to reach the target 1.9 mm right of bregma. A Hamilton microsyringe containing KA (10 mg/mL) was positioned with its tip in the right ventral hippocampus (5.4 mm caudal, 4.5 mm lateral to bregma, 6.8 mm below cortical surface); the target was CA3 stratum radiatum.…”

Section: Key Pointsmentioning

confidence: 99%

“…Respiratory unit activity was recorded with 25-µm diameter parylene-insulated Pt/Ir wire, inserted using a system that rotates the electrode to allow it to penetrate the brain without bending. 25 The initial target in the right brainstem pre-Bötzinger complex was 12.8 mm caudal and 0.6 mm left of bregma, for a 10-degree angle in the coronal plane to reach the target 1.9 mm right of bregma. If no respiratory-related neurons were found in the first track, the angle of subsequent tracks was varied up to 14 degrees.…”

Section: Key Pointsmentioning

confidence: 99%

Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats

et al. 2019

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Objective: To investigate how prolonged seizure activity affects cardiorespiratory function and activity of pre-Bötzinger complex, leading to sudden death. Methods: Urethane-anesthetized female Long-Evans rats were implanted with nasal thermocouple; venous and arterial cannulae; and electrodes for electrocardiography (ECG) and hippocampal, cortical, and brainstem recording. Kainic acid injection into the ventral hippocampus induced status epilepticus. Results: Seizures caused hypertension, tachycardia, and tachypnea punctuated by recurrent transient apneas. Salivation increased considerably: in 11 of 12 rats, liquid with alkaline pH consistent with saliva was expelled from the mouth. Most transient apneas were obstructive: nasal airflow ceased, while, in 83%, efforts to breathe persisted as continued rhythmic activity of respiratory pre-Bötzinger neurons, inspiratory electromyography (EMG), and excursions of the chest wall and abdomen. Blood pressure oscillated in time with respiratory efforts. This pattern also occurred in a minority of cases (16%) of incomplete apnea, but not in rare cases (1%) of transient central apneas. During transient obstructive apneas, the frequency of all inspiratory efforts decreased abruptly by ~30%, suggesting a resetting of the central respiratory rhythm generator. Twenty-two of thirty-one rats died, due either to obstructive apnea (12) or central apnea following progressive slowing of respiration (10). Most rats dying of central apnea had experienced several transient obstructive apneas.Negative DC field potential shifts of the brainstem followed the final breath, consistent with previous reports on spreading depolarization in mouse models. Timing suggests that the DC shift is a consequence rather than cause of respiratory collapse.Cardiac activity continued for tens of seconds. Significance: Seizure activity in forebrain induces pronounced autonomic activation and disrupts activity in medullary respiratory centers, resulting in death from either obstructive or central apnea. These results directly inform mechanisms of death in status epilepticus, and indirectly provide clues to mechanisms of sudden unexpected death in epilepsy (SUDEP). K E Y W O R D SHeart rate, obstructive apnea, status epilepticus, SUDEP | 2347 JEFFERYS Et al.

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A Method of Flexible Micro-Wire Electrode Insertion in Rodent for Chronic Neural Recording and a Device for Electrode Insertion

Cited by 17 publications

References 39 publications

Ictal activation of oxygen‐conserving reflexes as a mechanism for sudden death in epilepsy

Ictal activation of oxygen‐conserving reflexes as a mechanism for sudden death in epilepsy

Research Progress on the Flexibility of an Implantable Neural Microelectrode

Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats

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