scholarly journals Central neural mechanisms of the cerebral ischemic response. Characterization, effect of brainstem and cranial nerve transections, and simulation by electrical stimulation of restricted regions of medulla oblongata in rabbit.

1979 ◽  
Vol 45 (1) ◽  
pp. 48-62 ◽  
Author(s):  
R A Dampney ◽  
M Kumada ◽  
D J Reis
Keyword(s):  
Electrical Stimulation ◽  
Medulla Oblongata ◽  
Cranial Nerve ◽  
Neural Mechanisms ◽  
Cerebral Ischemic ◽  
Stimulation Of

Vasopressin secretion after stimulation of abdominal vagus in rabbit: role of A1 norepinephrine neurons

1994 ◽  
Vol 266 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Z. J. Gieroba ◽  
W. W. Blessing
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Medulla Oblongata ◽  
Vagal Stimulation ◽  
Vagal Afferents ◽  
Neuronal Function ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We determined whether electrical stimulation of the abdominal vagus nerve causes secretion of vasopressin in the rabbit and whether inhibition of neuronal function in the A1 region of the medulla oblongata impairs this secretion. In urethan-anesthetized rabbits, electrical stimulation of the abdominal vagus (5-min train of cathodal pulses, 0.5 ms duration, 20 Hz, 0.5-1 mA) increased plasma vasopressin from 37 +/- 8 to 133 +/- 19 pg/ml (P < 0.01, n = 11). Prior section of the cervical vagus completely prevented the increase seen with stimulation of the abdominal vagus. Injecting the inhibitory agent muscimol (1 nmol) 2 mm dorsal to the A1 area did not significantly reduce the vasopressin response to abdominal vagal stimulation. However, when muscimol was injected into the A1 area, the vagally mediated increase in plasma vasopressin was completely prevented. Our results show that stimulation of abdominal vagal afferents causes secretion of vasopressin in the rabbit via a central pathway that includes neurons in the A1 area.

scholarly journals Electrical Stimulation of the Ear, Head, Cranial Nerve, or Cortex for the Treatment of Tinnitus: A Scoping Review

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Derek J. Hoare ◽  
Peyman Adjamian ◽  
Magdalena Sereda
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Neural Activity ◽  
Cranial Nerve ◽  
Auditory Pathway ◽  
External Source ◽  
Acoustic Stimuli ◽  
Permanent Reduction ◽  
The Brain ◽  
Stimulation Of

Tinnitus is defined as the perception of sound in the absence of an external source. It is often associated with hearing loss and is thought to result from abnormal neural activity at some point or points in the auditory pathway, which is incorrectly interpreted by the brain as an actual sound. Neurostimulation therapies therefore, which interfere on some level with that abnormal activity, are a logical approach to treatment. For tinnitus, where the pathological neuronal activity might be associated with auditory and other areas of the brain, interventions using electromagnetic, electrical, or acoustic stimuli separately, or paired electrical and acoustic stimuli, have been proposed as treatments. Neurostimulation therapies should modulate neural activity to deliver a permanent reduction in tinnitus percept by driving the neuroplastic changes necessary to interrupt abnormal levels of oscillatory cortical activity and restore typical levels of activity. This change in activity should alter or interrupt the tinnitus percept (reduction or extinction) making it less bothersome. Here we review developments in therapies involving electrical stimulation of the ear, head, cranial nerve, or cortex in the treatment of tinnitus which demonstrably, or are hypothesised to, interrupt pathological neuronal activity in the cortex associated with tinnitus.

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