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

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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Effect of ethanol tolerance on release of acetylcholine and norepinephrine by rat cerebral cortex slices

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y77-103 ◽

1977 ◽

Vol 55 (4) ◽

pp. 758-768 ◽

Cited By ~ 46

Author(s):

J. W. Clark ◽

H. Kalant ◽

F. J. Carmichael

Keyword(s):

Cerebral Cortex ◽

Electrical Stimulation ◽

Inhibitory Effect ◽

Rat Cerebral Cortex ◽

Gas Liquid Chromatography ◽

Ach Release ◽

Direct Inhibitory Effect ◽

Release Of Acetylcholine ◽

Cortex Slices

The release of acetylcholine (ACh) by rat cerebral cortex slices, with and without electrical stimulation, and the effect of ethanol (EtOH) on this release were examined during the acquisition and loss of EtOH tolerance in vivo. ACh was measured by pyrolytic monodemethylation and gas–liquid chromatography. Electrical stimulation of control slices in medium containing diisopropyl phosphofluoridate (1.26 μM) and atropine (0.3 μM) increased ACh release by 88 ± 12%. Addition of 0.11 M EtOH to the medium had negligible effect on ACh release from unstimulated slices, but reduced the effect of stimulation to 51 ± 10%. After chronic treatment with EtOH by gavage or in a liquid diet, rats became tolerant to EtOH in vivo as shown by reduced impairment on the moving belt test. Slices from tolerant rats showed increased release of ACh in response to electrical stimulation and less inhibition of this response by added EtOH. The changes had disappeared by 2 weeks after cessation of EtOH treatment.Similar findings were obtained by measurement of release of [14C]ACh from slices preloaded with [14C]choline, except that electrical stimulation in the absence of EtOH appeared to cause a smaller increase in slices from chronic EtOH animals than from controls. This may reflect differences in isotope dilution. Release of [3H]norepinephrine was less affected by EtOH than that of ACh. The findings suggest that tolerance to EtOH is accompanied by increased ACh release by cortical neurones, as well as decreased direct inhibitory effect of EtOH on this, but do not permit any conclusion about the relative importance of such changes in various parts of the brain.

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In Vivo Measurements of Cranial Electrical Stimulation Using Stereotactic-EEG: A Pilot Study

2021 10th International IEEE/EMBS Conference on Neural Engineering (NER) ◽

10.1109/ner49283.2021.9441106 ◽

2021 ◽

Author(s):

Minmin Wang ◽

Shenghua Zhu ◽

Haonan Guan ◽

Hongjie Jiang ◽

Jianmin Zhang ◽

...

Keyword(s):

Electrical Stimulation ◽

Pilot Study ◽

In Vivo Measurements

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High-resolution in vivo imaging of rhesus cerebral cortex with ultrafast portable photoacoustic microscopy

NeuroImage ◽

10.1016/j.neuroimage.2021.118260 ◽

2021 ◽

pp. 118260

Author(s):

Wei Qin ◽

Qi Gan ◽

Lei Yang ◽

Yongchao Wang ◽

Weizhi Qi ◽

...

Keyword(s):

Cerebral Cortex ◽

High Resolution ◽

In Vivo Imaging ◽

Photoacoustic Microscopy

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Brain-Specific SNAP-25 Deletion Leads to Elevated Extracellular Glutamate Level and Schizophrenia-Like Behavior in Mice

Neural Plasticity ◽

10.1155/2017/4526417 ◽

2017 ◽

Vol 2017 ◽

pp. 1-11 ◽

Cited By ~ 12

Author(s):

Hua Yang ◽

Mengjie Zhang ◽

Jiahao Shi ◽

Yunhe Zhou ◽

Zhipeng Wan ◽

...

Keyword(s):

Cerebral Cortex ◽

Mouse Model ◽

Glutamate Release ◽

Critical Role ◽

Conditional Knockout ◽

Snare Complex ◽

Extracellular Glutamate ◽

Glutamate Level

Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. It is suggested that a SNAP-25 cKO mouse, a valuable model for schizophrenia, could address questions regarding presynaptic alterations that contribute to the etiopathophysiology of SZ and help to consummate the pre- and postsynaptic glutamatergic pathogenesis of the illness.

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Somatostatin modulates cholinergic neurotransmission in canine antral muscle

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.254.2.g201 ◽

1988 ◽

Vol 254 (2) ◽

pp. G201-G209 ◽

Cited By ~ 1

Author(s):

C. B. Koelbel ◽

G. van Deventer ◽

S. Khawaja ◽

M. Mogard ◽

J. H. Walsh ◽

...

Keyword(s):

Electrical Stimulation ◽

Substance P ◽

Prostaglandin E2 ◽

Positive Inotropic Effect ◽

Mechanical Response ◽

Inhibitory Effect ◽

Inotropic Effect ◽

Inotropic Response ◽

Cholinergic Neurotransmission

Somatostatin has been shown to inhibit antral motility in vivo. To examine the effect of somatostatin on cholinergic neurotransmission in the canine antrum, we studied the mechanical response of and the release of [3H]acetylcholine from canine longitudinal antral muscle in response to substance P, gastrin 17, and electrical stimulation. In unstimulated tissues, somatostatin had a positive inotropic effect on spontaneous phasic contractions. In tissues stimulated with substance P and gastrin 17, but not with electrical stimulation, somatostatin inhibited the phasic inotropic response dose dependently. This inhibitory effect was abolished by indomethacin. Somatostatin stimulated the release of prostaglandin E2 radioimmunoreactivity, and prostaglandin E2 inhibited the release of [3H]acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of [3H]acetylcholine from unstimulated tissues by a tetrodotoxin-sensitive mechanism but inhibited the release induced by substance P and electrical stimulation. These results suggest that somatostatin has a dual modulatory effect on cholinergic neurotransmission in canine longitudinal antral muscle. This effect is excitatory in unstimulated tissues and inhibitory in stimulated tissues. The inhibitory effect is partially mediated by prostaglandins.

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Subthreshold electrical stimulation as a low power electrical treatment for stroke rehabilitation

Scientific Reports ◽

10.1038/s41598-021-93354-x ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Kyungsoo Kim ◽

Seung-Jun Yoo ◽

So Yeon Kim ◽

Taeju Lee ◽

Sung-Ho Lim ◽

...

Keyword(s):

Electrical Stimulation ◽

Energy Consumption ◽

Functional Recovery ◽

Stroke Rehabilitation ◽

Brain Regions ◽

Implantable Devices ◽

Rehabilitation Process ◽

Neural Excitability ◽

Spike Firing

AbstractAs a promising future treatment for stroke rehabilitation, researchers have developed direct brain stimulation to manipulate the neural excitability. However, there has been less interest in energy consumption and unexpected side effect caused by electrical stimulation to bring functional recovery for stroke rehabilitation. In this study, we propose an engineering approach with subthreshold electrical stimulation (STES) to bring functional recovery. Here, we show a low level of electrical stimulation boosted causal excitation in connected neurons and strengthened the synaptic weight in a simulation study. We found that STES with motor training enhanced functional recovery after stroke in vivo. STES was shown to induce neural reconstruction, indicated by higher neurite expression in the stimulated regions and correlated changes in behavioral performance and neural spike firing pattern during the rehabilitation process. This will reduce the energy consumption of implantable devices and the side effects caused by stimulating unwanted brain regions.

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