Changes in cortical and tegmental evoked responses to sensory stimuli reinforced by electrical stimulation of the area of recording

1970 ◽  
Vol 19 (2) ◽  
pp. 249-261
Author(s):  
E. Caviedes ◽  
J. Buresˇ
Keyword(s):  
Electrical Stimulation ◽  
Evoked Responses ◽  
Sensory Stimuli ◽  
Stimulation Of

Effect of Various Sensory Stimuli on Reflex Laryngeal Adduction

1977 ◽  
Vol 86 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Masafumi Suzuki ◽  
Clarence T. Sasaki
Keyword(s):  
Splanchnic Nerve ◽  
Laryngeal Nerve ◽  
Organ System ◽  
Sensory Nerves ◽  
The Other ◽  
Evoked Responses ◽  
Sensory Stimuli ◽  
Adult Cats ◽  
Repetitive Electrical Stimulation ◽  
Stimulation Of

Various types of sensory stimuli may influence reflex laryngeal adduction. The recurrent laryngeal nerve responses evoked by single shock and repetitive electrical stimulation of a number of sensory nerves have been neurophysiologically observed in twenty-five adult cats. Stimulation of major cranial afferents produces strong adductor responses. The magnitude of these evoked responses is approached only by stimulation of the splanchnic nerve in the abdomen. On the other hand, comparable stimulation of special sensory and spinal somatic sensory nerves produces rapidly attenuated evoked adductor responses. We postulate that while these latter adductor responses may be insufficient to produce strong glottic closure, they may effectively modify phonatory function of the larynx. We have, therefore, attempted to demonstrate the effects of various sensory elicitations upon reflex laryngeal adduction as they may compositely influence both protective and phonatory control of this organ system.

scholarly journals Propofol Suppresses Synaptic Responsiveness of Somatosensory Relay Neurons to Excitatory Input by Potentiating GABAA Receptor Chloride Channels

2005 ◽  
Vol 1 ◽  
pp. 1744-8069-1-2 ◽  
Author(s):  
Shui-Wang Ying ◽  
Peter A Goldstein
Keyword(s):  
Electrical Stimulation ◽  
Chloride Channel ◽  
Temporal Summation ◽  
Brain Slices ◽  
Excitatory Input ◽  
Dependent Manner ◽  
Sensory Stimuli ◽  
Shunting Inhibition ◽  
Stimulation Of ◽  
Relay Neurons

Propofol is a widely used intravenous general anesthetic. Propofol-induced unconsciousness in humans is associated with inhibition of thalamic activity evoked by somatosensory stimuli. However, the cellular mechanisms underlying the effects of propofol in thalamic circuits are largely unknown. We investigated the influence of propofol on synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex (VB) to excitatory input in mouse brain slices, using both current- and voltage-clamp recording techniques. Excitatory responses including EPSP temporal summation and action potential firing were evoked in VB neurons by electrical stimulation of corticothalamic fibers or pharmacological activation of glutamate receptors. Propofol (0.6 – 3 μM) suppressed temporal summation and spike firing in a concentration-dependent manner. The thalamocortical suppression was accompanied by a marked decrease in both EPSP amplitude and input resistance, indicating that a shunting mechanism was involved. The propofol-mediated thalamocortical suppression could be blocked by a GABAA receptor antagonist or chloride channel blocker, suggesting that postsynaptic GABAA receptors in VB neurons were involved in the shunting inhibition. GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked in VB neurons by electrical stimulation of the reticular thalamic nucleus. Propofol markedly increased amplitude, decay time, and charge transfer of GABAA IPSCs. The results demonstrated that shunting inhibition of thalamic somatosensory relay neurons by propofol at clinically relevant concentrations is primarily mediated through the potentiation of the GABAA receptor chloride channel-mediated conductance, and such inhibition may contribute to the impaired thalamic responses to sensory stimuli seen during propofol-induced anesthesia.

Effects of norepinephrine on the activity of visual neurons in the superior colliculus of the hamster

1999 ◽  
Vol 16 (3) ◽  
pp. 541-555 ◽  
Author(s):  
YI ZHANG ◽  
RICHARD D. MOONEY ◽  
ROBERT W. RHOADES
Keyword(s):  
Electrical Stimulation ◽  
Visual Cortex ◽  
Superior Colliculus ◽  
Visual Stimulation ◽  
Optic Chiasm ◽  
Evoked Responses ◽  
Visual Responses ◽  
Signal To Noise ◽  
Direct Stimulation ◽  
Stimulation Of

Single-unit recording and micropressure ejection techniques were used to test the effects of norepinephrine (NE) on the responses of neurons in the superficial layers (the stratum griseum superficiale and stratum opticum) of the hamster's superior colliculus (SC). Application of NE suppressed visually evoked responses by ≥30% in 75% of 40 neurons tested and produced ≥30% augmentation of responses in only 5%. The decrement in response strength was mimicked by application of the α2 adrenoceptor agonist, p-aminoclonidine, the nonspecific β agonist, isoproterenol, and the β1 agonist, dobutamine. These agents had similar effects on responses evoked by electrical stimulation of the optic chiasm and visual cortex. The α1 agonist, methoxamine, augmented the light-evoked responses of 53% of 49 SC cells by ≥30%, but had little effect on responses evoked by electrical stimulation of optic chiasm or visual cortex. The effects of adrenergic agonists upon the glutamate-evoked responses of SC cells that were synaptically “isolated” by concurrent application of Mg2+ were similar to those obtained during visual stimulation. Analysis of effects of NE on visually evoked and background activity indicated that application of this amine did not significantly enhance signal-to-noise ratios for most superficial layer SC neurons, and signal-to-noise ratios were in some cases reduced. These results indicate that NE acts primarily through α2 and β1 receptors to suppress the visual responses of SC neurons. Activation of either of these receptors reduces the responses of SC neurons to either of their two major visual inputs as well as to direct stimulation by glutamate, and it would thus appear that these effects are primarily postsynaptic.

scholarly journals Characterizing and predicting cortical evoked responses to direct electrical stimulation of the human brain

2020 ◽  
Vol 13 (5) ◽  
pp. 1218-1225
Author(s):  
Cynthia R. Steinhardt ◽  
Pierre Sacré ◽  
Timothy C. Sheehan ◽  
John H. Wittig ◽  
Sara K. Inati ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Human Brain ◽  
Direct Electrical Stimulation ◽  
Evoked Responses ◽  
Stimulation Of

Neurobiological Background for Performing Surgical Intervention in the Inferior Thalamic Peduncle for Treatment of Major Depression Disorders

Neurosurgery ◽  
2005 ◽  
Vol 57 (3) ◽  
pp. 439-448 ◽  
Author(s):  
Francisco Velasco ◽  
Marcos Velasco ◽  
Fiacro Jiménez ◽  
Ana Luisa Velasco ◽  
Rafael Salin-Pascual
Keyword(s):  
Electrical Stimulation ◽  
Major Depression ◽  
Orbitofrontal Cortex ◽  
Frontal Lobes ◽  
Sleep Stages ◽  
Orbital Frontal Cortex ◽  
Sensory Stimuli ◽  
Surgical Interventions ◽  
Depression Disorders ◽  
Stimulation Of

ABSTRACT OBJECTIVE: To present a review of evidence for an inhibitory thalamo-orbitofrontal system related to physiopathology of major depression disorders (MDDs) and to postulate that interfering with hyperactivity of the thalamo-orbitofrontal system by means of chronic high-frequency electrical stimulation of its main fiber connection, the inferior thalamic peduncle (ITP), may result in an improvement in patients with MDD. METHODS: Experimentally, the thalamo-orbitofrontal system has been proposed as part of the nonspecific thalamic system. Under normal conditions, the nonspecific thalamic system induces characteristic electrocortical synchronization in the form of recruiting responses that mimic some sleep stages. It also inhibits input of irrelevant sensory stimuli, thus facilitating the process of selective attention. Permanent disruption of the system, via lesioning or temporary inactivation through cooling of the ITP with cryoprobes, results in a state of hyperkinesia, increased attention, and cortical desynchronization. RESULTS: Surgical lesioning of the medial part of orbitofrontal cortex and white matter overlying area 13, which includes the ITP, may result in significant improvement in MDD. Imaging studies (functional magnetic resonance imaging and positron emission tomography) consistently demonstrate hyperactivity in the orbitofrontal cortex and midline thalamic regions during episodes of MDD. This hyperactivity decreases with efficient control of MDD by medical treatment, indicating that orbitofrontal cortex and midline thalamic overactivity are related to the depressive condition. Conversely, noradrenergic and serotoninergic systems in the frontal lobes have been implicated in the pathophysiology of MDD. Although noradrenergic receptor density in the frontal lobe is consistently increased in depressed patients who commit suicide, 5-hydroxytryptamine reuptake blockers, which are potent antidepressive drugs, decrease hypermetabolism in the orbital frontal cortex in MDD. Therefore, the serotonin hypothesis for depression postulates that norepinephrine and serotonin in the frontal lobes are required to maintain antidepressive responsiveness. Dysregulation of the secretion of both neurotransmitters initiates overactivity of orbitofrontal cortex, resulting in depression. It is possible that surgical interventions in this region, including electrical stimulation of ITP, disrupt adrenergic and serotoninergic dysregulation in patients with MDD. CONCLUSION: Circumscribed lesions or electrical stimulation of the ITP, a discrete target easily identified by electrophysiological studies, may improve MDD. Electrical stimulation may have the advantage of being less invasive and more adjustable to patient needs.

Pyriform Responses to Electrical Stimulation of Olfactory Fila, Bulb and Tract

1957 ◽  
Vol 189 (2) ◽  
pp. 395-400 ◽  
Author(s):  
Paul D. MacLean ◽  
Burton S. Rosner ◽  
Franklin Robinson
Keyword(s):  
Electrical Stimulation ◽  
Olfactory Bulb ◽  
Low Frequency ◽  
Posttetanic Potentiation ◽  
Evoked Responses ◽  
Pyriform Cortex ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Repetitive Electrical Stimulation ◽  
Stimulation Of

Single shock stimulation of the olfactory fila in anesthetized animals evokes slow potentials from the olfactory bulb and pyriform cortex. Conduction velocity in the fila is estimated at 0.4 m/sec. Repetitive electrical stimulation of fila, bulb or tract, produces four phenomena in the pyriform cortex: a) gradual recruitment with low frequency stimulation (3–30/sec.); b) alternation in size of evoked responses at frequencies of 6/sec. and above; c) decline in amplitude of responses with frequencies above 20/sec. (‘decrementation’); and d) posttetanic potentiation after stimulation of the olfactory bulb or tract. Potentiation may persist for several minutes following tetanization of the tract. Recruitment and decrementation are observed in the bulb also upon stimulation of the fila.

Variable Responsiveness of a Visual Interneurone in the Free-Moving Locust, and its Relation to Behaviour and Arousal

1971 ◽  
Vol 55 (3) ◽  
pp. 727-747
Author(s):  
C. H. FRASER ROWELL
Keyword(s):  
Electrical Stimulation ◽  
Motor Activity ◽  
Motor System ◽  
Complete Recovery ◽  
Wide Field ◽  
Movement Detector ◽  
Response Level ◽  
Sensory Stimuli ◽  
Site Specific ◽  
Stimulation Of

1. Recorded from a dissected immobilized animal, or from an unrestrained animal which is quiescent, the descending contralateral movement detector (DCMD) neurone shows an exponential decremental response to a repetitive stimulus (habituation), reaching a plateau level characteristic of the stimulus conditions. The process is site-specific on the retina, and movement to a new area of retina gives a complete recovery. In the absence of stimulation responsiveness returns over minutes or hours. 2. Immediate recovery without a rest (dishabituation) can be obtained by a variety of strong sensory stimuli of several different modalities (‘extra-stimuli’) or by non specific electrical stimulation of parts of the CNS. The dishabituating efficacy of all these wanes with repetition. When the habituating stimulus is moved to a new retinal site the previous site is not dishabituated. 3. Dishabituation is not site-specific but affects the whole retina simultaneously. It appears to reverse the original decremental process (‘re-set’) rather than to produce an independent enhancement elsewhere in the pathway, as it does not increase the response from a submaximally stimulated, but unhabituated, retinal site. 4. In unrestrained animals dishabituating extra-stimuli also cause behavioural arousal or other motor activity. When motor activity starts, the DCMD is dishabituated and shows no regular decremental trend thereafter until movement ceases. DCMD background activity is also increased. These effects are not due to the visual stimulus of the moving appendages. 5. The association between motor activity and dishabituation suggests that the latter derives either from motor system collaterals or from mechanoreceptive reafference. Stimulation of the antennal nerve of a totally de-efferented brain cause some dishabituation; this eliminates the lower motor system (below command-fibre level) as the source of dishabituation and suggests it is purely sensory. 6. The activity of a thoracic cord unit (of possibly a wide-field mechanoreceptor interneurone) precedes by 5-20 sec, and closely correlates with, changes in responsiveness of the DCMD. It is either an important input to, or an output from, the dishabituating system. 7. Progressive reduction of sensory input to the brain affects DCMD responsiveness as follows: (i) spontaneous dishabituation is less frequent, (ii) dishabituation is less easily induced and smaller, (iii) rate of habituation is increased, (iv) plateau response level after habituation is lower. 8. Electrical stimulation of the circumoesophageal connective can depress DCMD responsiveness for many minutes. 9. The probable anatomical and physiological bases for modulation of DCMD responsiveness are discussed.

Sign in / Sign up

Export Citation Format

Share Document