Effects of electrical stimulation of the central nucleus of the amygdala on the in vivo electrophysiological activity of rat nigral dopaminergic neurons

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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Do non-dopaminergic neurons in the ventral tegmental area play a role in the responses elicited in A10 dopaminergic neurons by electrical stimulation of the prefrontal cortex?

Experimental Brain Research ◽

10.1007/s002210050303 ◽

1998 ◽

Vol 118 (4) ◽

pp. 466-476 ◽

Cited By ~ 27

Author(s):

Z.-Y. Tong ◽

P. G. Overton ◽

C. Martinez-Cué ◽

D. Clark

Keyword(s):

Electrical Stimulation ◽

Prefrontal Cortex ◽

Ventral Tegmental Area ◽

Dopaminergic Neurons ◽

Ventral Tegmental ◽

Stimulation Of

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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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Pedunculopontine glutamatergic neurons control spike patterning in substantia nigra dopaminergic neurons

eLife ◽

10.7554/elife.30352 ◽

2017 ◽

Vol 6 ◽

Cited By ~ 13

Author(s):

Daniel J Galtieri ◽

Chad M Estep ◽

David L Wokosin ◽

Stephen Traynelis ◽

D James Surmeier

Keyword(s):

Substantia Nigra ◽

Dopaminergic Neurons ◽

Substantia Nigra Pars Compacta ◽

Glutamatergic Synapses ◽

Glutamatergic Neurons ◽

Oscillatory Mechanisms ◽

Goal Directed Behavior ◽

Stimulation Of

Burst spiking in substantia nigra pars compacta (SNc) dopaminergic neurons is a key signaling event in the circuitry controlling goal-directed behavior. It is widely believed that this spiking mode depends upon an interaction between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic oscillatory mechanisms. However, the role of specific neural networks in burst generation has not been defined. To begin filling this gap, SNc glutamatergic synapses arising from pedunculopotine nucleus (PPN) neurons were characterized using optical and electrophysiological approaches. These synapses were localized exclusively on the soma and proximal dendrites, placing them in a good location to influence spike generation. Indeed, optogenetic stimulation of PPN axons reliably evoked spiking in SNc dopaminergic neurons. Moreover, burst stimulation of PPN axons was faithfully followed, even in the presence of NMDAR antagonists. Thus, PPN-evoked burst spiking of SNc dopaminergic neurons in vivo may not only be extrinsically triggered, but extrinsically patterned as well.

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Characterization of Prejunctional Muscarinic Receptors: Effects on the Release of VIP and Functional Responses and Receptor Expression in the Ovine Submandibular Gland

Advances in Pharmacological Sciences ◽

10.1155/2009/787586 ◽

2009 ◽

Vol 2009 ◽

pp. 1-6

Author(s):

Anders T. Ryberg ◽

Ondrej Soukup ◽

Gunnar Tobin

Keyword(s):

Electrical Stimulation ◽

Submandibular Gland ◽

Muscarinic Receptor ◽

Muscarinic Receptors ◽

Receptor Expression ◽

Receptor Subtypes ◽

Chorda Tympani Nerve ◽

Functional Responses ◽

Stimulation Of

In the in vivo experiments on anaesthetized sheep, it was presently examined whether muscarinic receptor antagonists with diverse selectivity affect the release of VIP in response to electrical stimulation of the parasympathetic chorda tympanic nerve differently, and if the changes in the release could be associated to altered secretory and vasodilator responses. The location of the muscarinic receptor subtypes was examined also. In the experiments, blood was collected out of the submandibular venous drainage before and during electrical stimulation of chorda tympani nerve in the absence and presence either of pirenzepine or methoctramine. While metchoctramine increased the output of protein, pirenzepine inhibited flow of saliva and increased protein output, vasodilatation, and VIP output. In morphological examinations, the inhibitory muscarinic M4 receptor occurred interacinarily in the gland. It is concluded that prejunctional muscarinic receptors, most likely of the M4 subtype, exert inhibitory modulation of the parasympathetic release of VIP in the ovine submandibular gland.

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Salivary gland K+ transport: in vivo studies with K+-specific microelectrodes.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1978.234.1.e79 ◽

1978 ◽

Vol 234 (1) ◽

pp. E79 ◽

Cited By ~ 3

Author(s):

J H Poulsen ◽

S W Bledsoe

Keyword(s):

Electrical Stimulation ◽

Salivary Gland ◽

Lingual Nerve ◽

In Vivo Studies ◽

Submandibular Salivary Gland ◽

K Concentration ◽

K Transport ◽

K Release ◽

Stimulation Of

Stimulation-induced transport of K+ in the submandibular salivary gland of cats and dogs anesthetized with pentobarbital was studied with an extracellular K+-specific microelectrode. Electrical stimulation of the para-sympathetic chorda-lingual nerve caused a rapid transient increase in extracellular K+ concentration from 2.2 to 18.7 meq/liter in the cat and from 2.3 to 15.2 meq/liter in the dog. Eventually the K+ concentration fell below the prestimulatory level, indicating uptake of K+ by the gland cells. In case of prolonged stimulation (2-10 min), the uptake began during stimulation. However, a further reduction in extracellular K+ concentration occurred upon cessation of stimulation, a result that demonstrated that the cells did not fully recover their K+ ,content during stimulation. The latency of the release of K+, defined as the time from the beginning of stimulation to the point at which, the K+-specific microelectrode signal had increased by 2 mV, was 0.6 s in the cat and 0.8 s in the dog. Because these are overestimates of the "true" latencies, we conclude that the K+ release begins simultaneously with the hyperpolarization of the acinar cell membrane.

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