Biomedical subjects

Victor Pikov

Publications and source records attributed to Victor Pikov.

5 recordsLinked to original sources

PubMed2006

Functional reinnervation of the rat lower urinary tract after cauda equina injury and repair.

Conus medullaris and/or cauda equina forms of spinal cord injury commonly result in a permanent loss of bladder function. Here, we developed a cauda equina injury and repair rodent model to investigate whether surgical implantation of avulsed lumbosacral ventral roots into the spinal cord can promote functional recovery of the lower urinary tract. Adult female rats underwent sham surgery (n = 6), bilateral L5-S2 ventral root avulsion (VRA) injury (n = 5), or bilateral L5-S2 VRA followed by an acute implantation of the avulsed L6 and S1 ventral roots into the conus medullaris (n = 6). At 12 weeks after operation, the avulsed group demonstrated urinary retention, absence of bladder contractions and external urethral sphincter (EUS) electromyographic (EMG) activation during urodynamic recordings, increased bladder size, and retrograde death of autonomic and motoneurons in the spinal cord. In contrast, the implanted group showed reduced urinary retention, return of reflexive bladder voiding contractions coincident with EUS EMG activation, anatomical reinnervation of the EUS demonstrated by retrograde neuronal labeling, normalization of bladder size, and a significant neuroprotection of both autonomic and motoneurons. In addition, a positive correlation between motoneuronal survival and voiding efficiency was observed in the implanted group. Our results show that implantation of avulsed lumbosacral ventral roots into the spinal cord promotes reinnervation of the urinary tract and return of functional micturition reflexes, suggesting that this surgical repair strategy may also be of clinical interest after conus medullaris and cauda equina injuries.

Amidines↗

PubMed2006

Microelectrode array for chronic deep-brain microstimulation and recording.

We have developed an array of microelectrodes that is suitable for long-term implantation into the subthalamic nucleus (STN) or the globus pallidus and is able to record from single neurons, as well as deliver localized microstimulation. This device can be used to investigate the mechanisms by which deep brain stimulation can ameliorate the symptoms of Parkinson's disease and other movement disorders, and also may be the basis for a new clinical tool for the treatment of Parkinson's disease, by capitalizing on the high spatial specificity of intranuclear microstimulation. The array includes 16 activated iridium microelectrodes, 5-6 mm in length, within a cluster approximately 1.8 mm in diameter. We have fabricated the array using materials carrying the USP Category VI classification, and we have developed an apparatus and a procedure for implanting the microelectrode arrays into the deep brain. Ten arrays have been implanted into the STN of domestic cats, and one into the internal segment of the globus pallidus, for 140-415 days. During that time, we were able to record action potentials from individual neurons, on 4 to 8 of the 16 channels. The microelectrode' active surface areas ranged from 500 to 2000 microm2. Controlled-current pulses, 26.5 microA in amplitude and 150 micros/phase in duration (4 nC/phase) were used to excite neurons in the cat's STN. In addition to direct activation, the stimulus modulated the neuronal activity over a distance of at least 1.2 mm from the site of stimulation. These parameters did not induce histologically detectable changes around the tip sites after 35 hours of stimulation at 100 Hz (7 hours of stimulation per day, on 5 successive days), if the electrode' active surface area was 1000 microm2 or greater.

Action Potentials↗

PubMed2004

Mapping of spinal cord circuits controlling the bladder and external urethral sphincter functions in the rabbit.

AIMS: A primary purpose of this study was to evaluate the rabbit as a model for studying the spinal circuitry controlling the bladder emptying. We aimed to map the locations of the neuronal circuitry controlling the external urethral sphincter (EUS) and the detrusor by stimulating at different spinal cord locations with a microelectrode, while recording the responses from these muscles. METHODS: Spinal cord microstimulation was performed in the intermediate zone of the gray matter at the L7-S4 spinal cord levels in eight rabbits with empty and full bladders. Bladder activity was measured as intravesical pressure (IVP) changes and EUS activity was measured via electromyographic (EMG) electrodes positioned within the urethra. RESULTS: Under both bladder conditions, EUS activation was produced from similar locations in the spinal cord comprising a continuous area in the intermediate zone of the S2-S3 spinal cord. This region extended 25 mm in the rostrocaudal dimension, at least 1 mm lateral to the midline, and 0.5-1 mm in the dorsoventral dimension at a depth of 2-3 mm beneath the dorsal surface. No locations in the intermediate zone produced EUS inhibition. The S2-S3 spinal region, stimulation of which produced the strongest EUS activation, also produced modest bladder contractions. CONCLUSIONS: Overall, the results indicate that spinal cord networks controlling bladder and EUS activation in the rabbit are overlapping and clustered into columns extending rostrocaudally. The lack of spinal locations producing EUS inhibition and large bladder contractions make the rabbit an unattractive model for studies of neuroprosthetic spinal control of micturition.

Animals↗

PubMed2004

Arrays for chronic functional microstimulation of the lumbosacral spinal cord.

Our objective is to develop neural prostheses based on an array of microelectrodes implanted into the sacral spinal cord, that will allow persons with spinal cord injuries to regain control of their bladder and bowels. For our chronic cat model, we have developed two microelectrode arrays, one type containing nine discrete activated iridium microelectrodes and the second utilizing silicon substrate probes with multiple electrode sites on each probe. Both types can elicit an increase in the pressure within the urinary bladder of more than 40-mm Hg and/or relaxation of the urethral sphincter. A stimulus of 100 microA and 400 micros/ph at 20 Hz (charge-balanced pulses) was required to induce a large increase in bladder pressure or relaxation of the urethral sphincter. We found that 24 h of continuous stimulation with these parameters induced tissue injury (disrupted neuropil, infiltration of inflammatory cells, and loss of neurons close to the tip sites). However, a neural prosthesis that is intended to restore bladder control after spinal cord injury would not operate continuously. Thus, when this stimulus was applied for 24 h, at a 10% duty cycle (1 min of stimulation, then 9 min without stimulation) only minimal histologic changes were observed.

Animals↗

PubMed2002

Altered glutamate receptor function during recovery of bladder detrusor-external urethral sphincter coordination in a rat model of spinal cord injury.

Coordination of the bladder detrusor and the external urethral sphincter is a supraspinally controlled reflex that is essential for efficient micturition. This coordination is permanently lost after spinal cord transection but can recover chronically after incomplete spinal cord injury (SCI). As glutamatergic transmission plays a key role in all levels of detrusor-external urethral sphincter coordination, we examined the role of potential alterations in glutamatergic control in its recovery after SCI. Rats were subjected to standardized incomplete contusion injury. Detrusor-external urethral sphincter coordination was evaluated urodynamically at 5 days (subacute) and 8 weeks (chronic) after SCI. Sensitivity of coordinated activation of the external urethral sphincter in response to bladder distension to the alpha -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid/kainate antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo(f)quinoxaline-7-sulfonamide disodium (NBQX) and to the N-methyl-D-aspartate (NMDA) antagonist R(--3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP) was determined by intrathecal application at the L6 spinal cord level during urodynamic recordings. We found that while detrusor contractions recovered at 5 days after SCI, coordinated activation of the external urethral sphincter was significantly impaired at 5 days and recovered only by 8 weeks. There was no difference in sensitivity of detrusor-external urethral sphincter coordination to NBQX at the subacute or chronic time points. However, external urethral sphincter response to bladder distension was sensitive to a 50% lower dose of CPP at 5 days compared with uninjured rats or chronic recovered SCI rats. Thus, alterations in NMDA receptor function appeared to be involved in recovery of detrusor-external urethral sphincter coordination after incomplete SCI.

Animals↗