Evoked Neuronal Activity Accompanied by Transmitter Release Increases Oxygen Concentration in Rat Striatum in vivo but Not in vitro

Dopamine and oxygen (O2) were measured in the caudate nucleus of anesthetized rats and in striatal slices during electrical stimulation. Simultaneous electrochemical detection of dopamine and O2 was accomplished with fast-scan cyclic voltammetry at a Nafion-coated carbon-fiber microelectrode. Stimulation of the medial forebrain bundle resulted in synaptic overflow of dopamine in the caudate nucleus. At the same time, O2 concentration increased in the extracellular fluid with two separate phases. The amplitude of the initial increase directly correlated with the frequency of the stimulus, with the time of maximum concentration reproducible across a range of frequencies. The second increase occurred at later times with a more random amplitude and with a broad, variable shape. Agents which blocked vasodilation affected both phases: Atropine attenuated the initial increase, while the second feature was nearly absent after theophylline. Yohimbine and α-methyl- p-tyrosine did not affect the O2 responses. Local electrical stimulation of the slice preparation also resulted in dopamine overflow, but a prolonged decrease in O2 concentration accompanied this event. Striatal field stimulation in vivo produced changes in O2 concentration dependent on the relative position of the stimulating and working electrodes, but none of the responses resembled that seen in the caudate slice. Thus, while measurements in brain slices show O2 consumption as a result of stimulated neuronal activity, an apparent elevation of local cerebral blood flow during and after stimulation dominate the in vivo response.

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Evidence for Neuronal Origin and Metabotropic Receptor-Mediated Regulation of Extracellular Glutamate and Aspartate in Rat Striatum In Vivo Following Electrical Stimulation of the Prefrontal Cortex

Journal of Neurochemistry ◽

10.1046/j.1471-4159.1998.70020617.x ◽

2002 ◽

Vol 70 (2) ◽

pp. 617-625 ◽

Cited By ~ 84

Author(s):

Mark W. Lada ◽

Thomas W. Vickroy ◽

Robert T. Kennedy

Keyword(s):

Electrical Stimulation ◽

Prefrontal Cortex ◽

Rat Striatum ◽

Extracellular Glutamate ◽

Metabotropic Receptor ◽

Stimulation Of

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Electrical stimulation of the auditory nerve: direct current measurement in vivo

IEEE Transactions on Biomedical Engineering ◽

10.1109/10.752943 ◽

1999 ◽

Vol 46 (4) ◽

pp. 461-469 ◽

Cited By ~ 89

Author(s):

C.Q. Huang ◽

R.K. Shepherd ◽

P.M. Center ◽

P.M. Seligman ◽

B. Tabor

Keyword(s):

Electrical Stimulation ◽

Direct Current ◽

Auditory Nerve ◽

Current Measurement ◽

Direct Current Measurement ◽

Stimulation Of

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THE RELEASE IN VIVO OF [3H]ACETYLCHOLINE FROM CAT CAUDATE NUCLEUS AND CEREBRAL CORTEX BY ATROPINE, PENTYLENETETRAZOL, K+-DEPOLARIZATION AND ELECTRICAL STIMULATION

Journal of Neurochemistry ◽

10.1111/j.1471-4159.1975.tb12238.x ◽

1975 ◽

Vol 25 (2) ◽

pp. 123-130 ◽

Cited By ~ 10

Author(s):

T. L. Yaksh ◽

H. I. Yamamura

Keyword(s):

Cerebral Cortex ◽

Electrical Stimulation ◽

Caudate Nucleus

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458. Extracellular levels of GABA and glutamate increase in response to direct electrical stimulation of the hippocampus in humans: an in vivo microdialysis study

Biological Psychiatry ◽

10.1016/s0006-3223(00)00728-9 ◽

2000 ◽

Vol 47 (8) ◽

pp. S140

Author(s):

W.M. Abi-Saab ◽

D.D. Spencer ◽

V. Srihari ◽

J.L. Thompson ◽

R.H. Roth ◽

...

Keyword(s):

Electrical Stimulation ◽

In Vivo Microdialysis ◽

Direct Electrical Stimulation ◽

Microdialysis Study ◽

Stimulation Of

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Short-Term Plasticity at Inhibitory Synapses in Rat Striatum and Its Effects on Striatal Output

Journal of Neurophysiology ◽

10.1152/jn.2001.85.5.2088 ◽

2001 ◽

Vol 85 (5) ◽

pp. 2088-2099 ◽

Cited By ~ 25

Author(s):

John S. Fitzpatrick ◽

Garnik Akopian ◽

John P. Walsh

Keyword(s):

Action Potentials ◽

Brain Slices ◽

Current Injection ◽

Inhibitory Synapses ◽

Rat Striatum ◽

Short Term ◽

Short Term Plasticity ◽

Adult Rat ◽

Glutamate Receptor Antagonists

Two forms of short-term plasticity at inhibitory synapses were investigated in adult rat striatal brain slices using intracellular recordings. Intrastriatal stimulation in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (20 μM) andd,l-2-amino-5-phosphonovaleric acid (50 μM) produced an inhibitory postsynaptic potential (IPSP) that reversed polarity at −76 ± 1 (SE) mV and was sensitive to bicuculline (30 μM). The IPSP rectified at hyperpolarized membrane potentials due in part to activation of K+ channels. The IPSP exhibited two forms of short-term plasticity, paired-pulse depression (PPD) and synaptic augmentation. PPD lasted for several seconds and was greatest at interstimulus intervals (ISIs) of several hundred milliseconds, reducing the IPSP to 80 ± 2% of its control amplitude at an ISI of 200 ms. Augmentation of the IPSP, elicited by a conditioning train of 15 stimuli applied at 20 Hz, was 119 ± 1% of control when sampled 2 s after the conditioning train. Augmentation decayed with a time constant of 10 s. We tested if PPD and augmentation modify the ability of the IPSP to prevent the generation of action potentials. A train of action potentials triggered by a depolarizing current injection of constant amplitude could be interrupted by stimulation of an IPSP. If this IPSP was the second in a pair of IPSPs, it was less effective in blocking spikes due to PPD. By contrast, augmented IPSPs were more effective in blocking spikes. The same results were achieved when action potentials were triggered by a depolarizing current injection of varying amplitude, a manipulation that produces nearly identical spike times from trial to trial and approximates the in vivo behavior of these neurons. These results demonstrate that short-term plasticity of inhibition can modify the output of the striatum and thus may be an important component of information processing during behaviors that involve the striatum.

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Hyperinsulinemia of preobese and obese fa/fa rats is partly vagus nerve mediated

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1983.244.4.e317 ◽

1983 ◽

Vol 244 (4) ◽

pp. E317-E322 ◽

Cited By ~ 7

Author(s):

F. Rohner-Jeanrenaud ◽

A. C. Hochstrasser ◽

B. Jeanrenaud

Keyword(s):

Electrical Stimulation ◽

Insulin Secretion ◽

B Cells ◽

Vagus Nerve ◽

Zucker Rats ◽

Glucose Load ◽

Parasympathetic System ◽

Enhanced Sensitivity ◽

Stimulation Of

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.

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Suppression of Superficial Microglial Activation by Spinal Cord Stimulation Attenuates Neuropathic Pain Following Sciatic Nerve Injury in Rats

International Journal of Molecular Sciences ◽

10.3390/ijms21072390 ◽

2020 ◽

Vol 21 (7) ◽

pp. 2390

Author(s):

Masamichi Shinoda ◽

Satoshi Fujita ◽

Shiori Sugawara ◽

Sayaka Asano ◽

Ryo Koyama ◽

...

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Electrical Stimulation ◽

Dorsal Horn ◽

Nerve Injury ◽

Spinal Cord Stimulation ◽

Microglial Activation ◽

In Vivo Optical Imaging ◽

Stimulation Of

We evaluated the mechanisms underlying the spinal cord stimulation (SCS)-induced analgesic effect on neuropathic pain following spared nerve injury (SNI). On day 3 after SNI, SCS was performed for 6 h by using electrodes paraspinally placed on the L4-S1 spinal cord. The effects of SCS and intraperitoneal minocycline administration on plantar mechanical sensitivity, microglial activation, and neuronal excitability in the L4 dorsal horn were assessed on day 3 after SNI. The somatosensory cortical responses to electrical stimulation of the hind paw on day 3 following SNI were examined by using in vivo optical imaging with a voltage-sensitive dye. On day 3 after SNI, plantar mechanical hypersensitivity and enhanced microglial activation were suppressed by minocycline or SCS, and L4 dorsal horn nociceptive neuronal hyperexcitability was suppressed by SCS. In vivo optical imaging also revealed that electrical stimulation of the hind paw-activated areas in the somatosensory cortex was decreased by SCS. The present findings suggest that SCS could suppress plantar SNI-induced neuropathic pain via inhibition of microglial activation in the L4 dorsal horn, which is involved in spinal neuronal hyperexcitability. SCS is likely to be a potential alternative and complementary medicine therapy to alleviate neuropathic pain following nerve injury.

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A Tissue Engineering Chamber for Continuous Pulsatile Electrical Stimulation of Vascularized Cardiac Tissues In Vivo

Bioelectricity ◽

10.1089/bioe.2020.0035 ◽

2020 ◽

Vol 2 (4) ◽

pp. 391-398

Author(s):

Damián Hernández ◽

Rodney Millard ◽

Anne M. Kong ◽

Owen Burns ◽

Priyadharshini Sivakumaran ◽

...

Keyword(s):

Tissue Engineering ◽

Electrical Stimulation ◽

Cardiac Tissues ◽

Stimulation Of

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Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

Journal of Neurophysiology ◽

10.1152/jn.1991.66.6.2084 ◽

1991 ◽

Vol 66 (6) ◽

pp. 2084-2094 ◽

Cited By ~ 24

Author(s):

R. W. Blair ◽

A. R. Evans

Keyword(s):

Electrical Stimulation ◽

Neuronal Activity ◽

Vagal Stimulation ◽

Discharge Rate ◽

Stellate Ganglion ◽

Cell Activity ◽

Conditioning Stimulus ◽

Vagal Afferents ◽

Early Peak ◽

Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

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