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PubMedDate not supplied

Effect of phenytoin on cardiac slowing induced by cholinergic stimulation.

Phenytoin was tested for its ability to counteract cholinergic-induced slowing in sinus rate in chloralose-anesthetized cats subjected to bilateral cervical vagotomy and spinal cord transection. The cholinergic stimuli consisted of electrical stimulation of the cervical vagus nerves and injected acetylcholine. Phenytoin administered as a continuous infusion of 0.5 and 1.0 mg/kg/min was found to significantly reduce the cardiac slowing produced by both modes of cholinergic stimulation. Blockade of the acetylcholine response suggested that the inhibitory effect of phenytoin was on the postsynaptic membrane. Measurement of serum levels of phenytoin performed in selected experiments revealed that the anticholinergic effect corresponded to plasma levels in humans exposed to therapeutic doses of this agent.

Acetylcholine↗
PubMed2002

Neuronal tissue polarization induced by repetitive transcranial magnetic stimulation?

In a blinded cross-over design, 10 healthy controls received 900 monophasic and biphasic repetitive transcranial magnetic stimuli over the primary motor cortex. Stimulation frequency was 1 Hz, and stimulation intensity 90% of the individual resting motor threshold. Suprathreshold stimuli applied at 0.1 Hz before and after repetitive stimulation controlled for changes in corticospinal excitability. We found a lasting corticospinal inhibition that was significantly more pronounced after monophasic than after biphasic repetitive transcranial magnetic stimulation (motor evoked potential amplitude reduced by 35 +/- 20% vs 12 +/- 37%, mean+/- s.d.). We propose that the current flow in the coil plays a significant role in optimising after effects, and asymmetric current flow may be particularly efficient in building up tissue polarization.

Adult↗
PubMed1995

Afferent volley patterns and the spinal release of immunoreactive substance P in the dorsal horn of the anaesthetized spinal cat.

Microprobes bearing immobilized antibodies to the C-terminus of substance P were used to measure release of this neuropeptide in the spinal cord of the anaesthetized spinal cat in response to peripheral nerve stimulation. Release of substance P was just detectable in laminae I, II with 150 stimuli (0.5 Hz, 5 min) and was near maximal with 300 stimuli. Using two periods of stimulation of 10 min separated by 15 min, greater levels of substance P were detected during the second period. Fifteen to 25 min after two periods of peripheral nerve stimulation levels of substance P detected by microprobes were still elevated above those present prior to stimulation. Stimulation with bursts of three impulses when delivering a fixed number of stimuli resulted in detection of increased levels of substance P at sites adjacent to the areas of maximal release. The results suggest that maximal release of substance P from the central terminals of primary afferent fibres occurs with relatively few impulses and at low frequencies in agreement with what is known of release from the peripheral terminals of these fibres.

Afferent Pathways↗
PubMed1998

Arousal shifts in quiescent locusts

Locusts are usually quiescent at night, but this state can be interrupted by spontaneous periods of motor activity, or arousals, that can also be induced by exposure to light stimuli. To investigate whether repeated arousing stimulation has any lasting effect on behaviour, locusts were confronted at night with a series of 1 s light stimuli. Groups of three stimuli at intervals of 60 s were repeated 11 times at 10 min intervals during the first experimental night, and three stimuli at intervals of 90 s were repeated at 15 min intervals during the next night. Arousals and the effects of stimulation were monitored as changes in the spike activity of muscles in the basal part (the scapus) of the right antenna. In the early part of the night preceding the presentation of the light stimuli, neither 60 s nor 90 s periods were present as significant peaks in spontaneous changes in spike activity. The initial stimulus of a series evoked an arousal response that habituated on repetition of the stimulus. The end of the series of stimuli was followed by changes in spike activity that tended to have the same periodicity as the preceding stimuli. Furthermore, a single light stimulus at the end of the night evoked changes in spike activity that again tended to have the same periodicity as the preceding entraining stimuli. Repeated stimulation may therefore establish a memory trace for the period of stimulation that can be recalled either spontaneously or by the application of an appropriate external stimulus.

Journal Article↗
PubMed1988

Interaction of arachidonic acid metabolites and adrenergic nervous system.

Arachidonic acid, which is esterified mainly at the Sn-2 position of phospholipids, is deacylated in response to a wide variety of neurohormonal stimuli, including sympathetic nerve stimulation and catecholamines. In most cardiovascular tissues, arachidonic acid is metabolized via the cyclooxygenase pathway into prostaglandins. The kind and quantity of prostaglandins formed in response to adrenergic stimuli vary in different tissues. For example, PGE2 is the major product of arachidonic acid formed in the spleen and kidney and PGI2 in the heart in response to sympathetic nerve stimulation and norepinephrine. The sequence of events, including the type of adrenergic receptor involved in the action of catecholamines on PG synthesis, varies from tissue to tissue. For example, PG synthesis elicited by adrenergic stimulation in the heart is mediated via activation of beta-1 adrenergic receptors, whereas in the kidney it is linked to stimulation of alpha-1 adrenergic receptors. Moreover, prostaglandin synthesis elicited by alpha-1 adrenergic receptor activation in the kidney requires only partially extra- but mainly intracellular Ca++ and calmodulin. However, beta-1 adrenergic receptor stimulated PG synthesis in the heart is absolutely dependent upon extracellular Ca++ but not on calmodulin. Furthermore, alpha-1 but not beta-1 adrenergic receptor stimulated PG synthesis is inhibited by mepacrine, a phospholipase A2 and C inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed2000

Neural mechanisms of antinociceptive effects of hypnosis.

BACKGROUND: The neural mechanisms underlying the modulation of pain perception by hypnosis remain obscure. In this study, we used positron emission tomography in 11 healthy volunteers to identify the brain areas in which hypnosis modulates cerebral responses to a noxious stimulus. METHODS: The protocol used a factorial design with two factors: state (hypnotic state, resting state, mental imagery) and stimulation (warm non-noxious vs. hot noxious stimuli applied to right thenar eminence). Two cerebral blood flow scans were obtained with the 15O-water technique during each condition. After each scan, the subject was asked to rate pain sensation and unpleasantness. Statistical parametric mapping was used to determine the main effects of noxious stimulation and hypnotic state as well as state-by-stimulation interactions (i.e., brain areas that would be more or less activated in hypnosis than in control conditions, under noxious stimulation). RESULTS: Hypnosis decreased both pain sensation and the unpleasantness of noxious stimuli. Noxious stimulation caused an increase in regional cerebral blood flow in the thalamic nuclei and anterior cingulate and insular cortices. The hypnotic state induced a significant activation of a right-sided extrastriate area and the anterior cingulate cortex. The interaction analysis showed that the activity in the anterior (mid-)cingulate cortex was related to pain perception and unpleasantness differently in the hypnotic state than in control situations. CONCLUSIONS: Both intensity and unpleasantness of the noxious stimuli are reduced during the hypnotic state. In addition, hypnotic modulation of pain is mediated by the anterior cingulate cortex.

Adult↗
PubMed1995

Sympathetic skin responses evoked by magnetic stimulation of the neck.

We studied sympathetic skin responses (SSRs) following magnetic stimulation of the neck in 40 normal subjects and 54 patients with neurological diseases and active sweat gland densities (ASGDs) at the foot induced by pilocarpine in 39 patients. SSRs at the hand following magnetic stimulation showed the lowest coefficients of variability of the latencies and amplitudes in eight consecutive responses compared with SSRs following other types of stimuli (electrical and auditory stimulation, and deep inspiration) in 12 normal subjects. Fourteen of 38 patients with neuropathies (37%) showed the presence of SSRs after magnetic stimulation, but not after median nerve stimulation, although SSRs to magnetic stimulation corresponded with those to nerve stimulation in all patients with multiple sclerosis or multiple system atrophy. These results suggest that the absence of SSRs after nerve stimulation in patients with neuropathies may be due to abnormalities of the peripheral sensory afferent fibers. ASGDs significantly correlated with SSRs at the foot following magnetic stimulation, but not with those following nerve stimulation in patients with neuropathies. Magnetic stimulation of the neck is the highly reproducible method of evoking SSRs because this technique is able to produce strong sensory afferent inputs proximally. Furthermore, SSRs following magnetic stimulation, little influenced by sensory afferent fiber involvement, are very useful for evaluating the postganglionic sympathetic function in patients with neuropathies.

Action Potentials↗
PubMed1993

Neurobiological effects of extensive transcranial electromagnetic stimulation in an animal model.

The effects of transcranial electromagnetic stimulation (TEMS) on the cellular morphology of the cortex, cerebellum, and brain-stem were systematically investigated in rabbits exposed to 1000 pulsed stimuli at 100% maximum stimulation level (2.0 Tesla at the skull) over a 12 month period with a 5 cm circular magnetic coil positioned over the cranium. Also, the acute effects of TEMS on heart rate and respiration were examined. (1) T1 and T2 weighted magnetic resonance images (MRI) of 1-3 mm sections in both sagittal and axial planes revealed no evidence of gross morphological changes or subtler tissue damage to the cerebrum, cerebellum, or brain-stem. (2) Light microscopic examination of 60 microns hematoxylin-eosin/Cresyl Violet Luxol Fast Blue stained sections of the brain-stem, cerebellum, and cerebral cortex showed no TEMS-related changes in cellular organization or histological damage. (3) Autonomic activity as reflected by heart rate was also unaffected by high intensity TEMS. Normal heart rate was maintained during repeated TEMS at 100% of maximum. (4) Respiration rate was briefly altered at the time of the stimulus, but returned to normal immediately after the stimulus. These findings in experimental animals revealed no biohazardous effects on the brain following extensive exposure to high intensity, low frequency time-varying magnetic field stimulation from the coil of a clinical instrument.

Animals↗
PubMed1997

Effects of cholinergic denervation on seizure development and neurotrophin messenger RNA regulation in rapid hippocampal kindling.

Intraventricular 192 IgG-saporin was used to induce a selective lesion of basal forebrain cholinergic neurons in rats. When subjected to 40 rapid hippocampal kindling stimulations with 5-min intervals, these animals exhibited increased number of generalized seizures and a higher mean seizure grade in response to the first five stimulations, and required fewer stimuli to develop focal behavioural seizures, as compared to non-lesioned rats. In contrast, both groups showed similarly enhanced responsiveness when test stimulated four weeks later. Using in situ hybridization, cholinergic denervation was found to cause a significant decrease of basal brain-derived neurotrophic factor messenger RNA levels in the hippocampal formation and piriform cortex, whereas gene expression for nerve growth factor, neurotrophin-3, and TrkB and TrkC was unchanged. Four weeks after rapid kindling stimulations, basal levels of brain-derived neurotrophic factor messenger RNA in the dentate granule cells were restored to normal in the lesioned rats, whereas neurotrophin-3 messenger RNA levels were decreased. No differences in the seizure-evoked levels of neurotrophin and Trk messenger RNAs were detected, except in the dentate granule cell layer, which had significantly higher brain-derived neurotrophic factor messenger RNA expression in the lesioned animals at 2 h. In conclusion, the basal forebrain cholinergic system (i) dampens the severity of recurring seizures induced by rapid hippocampal kindling stimulations, but has no effect on the subsequent delayed phase of epileptogenesis; and (ii) exerts a tonic stimulation of basal brain-derived neurotrophic factor messenger RNA levels in the hippocampal formation and piriform cortex. The findings also indicate that the cholinergic lesion does not affect neurotrophin and Trk gene expression after recurring seizures, and that the kindling process leads to long-term changes in basal brain-derived neurotrophic factor and neurotrophin-3 messenger RNA levels in the denervated animals.

Acetylcholinesterase↗
PubMed1992

Respiratory burst metabolic status of macrophages in experimental leprosy.

Peritoneal macrophages from uninfected controls and Mycobacterium leprae infected Swiss albino mice were studied for their respiratory burst (RB) activity at different time intervals. The RB metabolic activity of macrophages declined significantly after 3 month infection using latex (p less than 0.001) and M. leprae (p less than 0.01) as stimuli. However, significant rise (p less than 0.001) in the oxidative metabolic activity was seen at 6 and 9 months postinfection period on stimulation with both the stimuli. The sharp rise in the oxidative metabolic status at peak period of infection in the experimental animals suggests that the macrophages are functionally normal though M. leprae is unable to trigger the respiratory burst sufficiently.

Animals↗
PubMed2004

[Neural organization of different types of fear: implications for the understanding of anxiety].

The dangerous stimuli may be potentially dangerous, distal or proximal and the recognition by the animals of each one of these conditions is determinant for the nature of the fear responses. In the present article a parallel with this particular process is drawn taking into account that different fear responses are generated by light, tones and contexts used as conditioned stimuli and by unconditioned stimulation of the dorsal periaqueductal gray (dPAG). In this review we summarize the efforts that have been made to characterize the neural circuits recruited in the organization of defensive reactions to the conditioned and unconditioned aversive stimulations, particularly evidence linking the brain's defense response systems to the concept of fear-stress-anxiety. The dPAG constitute the main neural substrates for the integration of aversive states in response to proximal aversive stimuli. In fact, panic-like behaviors often result when this structure is electrically or chemically stimulated. On the other hand, successful preparatory processes of danger-orientation and preparedness to flee seem to be linked to anxiety. The pre-frontal and cingulate cortex, median raphe nucleus, septum and hippocampus seem to be implicated in the elaboration and organization of these responses. As a working hypothesis, it is advanced that increasing the intensity and proximity of the danger may lead to an emotional shift. When the animals are submitted to this gradual increase in aversiveness there is a switch from the neural circuits responsible for the production of the orientated and organized motor patterns of appropriate defensive response to a conditioned stimulus towards the incomplete and uncoordinated defense responses related to panic attacks. The circuits in the amygdala and the medial hypothalamus responsible for the organization of the defense reaction may well subserve to this switch process.

Amygdala↗
PubMed2001

Hyperalgesic responses in methadone maintenance patients.

Opioid substitution treatment for dependence may alter sensitivity to pain. Previous studies on pain sensitivity in methadone maintenance patients have yielded contradictory results. This study compared nociceptive responses between 16 patients on stable, once daily, doses of methadone and 16 matched control subjects. Two types of nociceptive stimuli were used: (1) electrical stimulation; and (2) a cold pressor test. Two parameters were measured: detection for onset of pain, and pain tolerance. Methadone patients were tested over an inter-dosing period: at the time of trough plasma methadone concentration (0 h), and 3 h after their daily dose. Control subjects were tested twice 3 h apart. Blood samples were collected to determine plasma methadone concentration. In methadone patients, trough to peak increases in mean R-(-)- and S-(+)-methadone concentrations (118 and 138 ng/ml to 185 and 259 ng/ml, respectively) resulted in significant increases in pain detection and tolerance values for both nociceptive stimuli. Using electrical stimulation, methadone patients' pain tolerance values were lower than controls at 0 h, but higher than controls at 3 h; no significant differences in pain detection values were found. For the cold pressor test, methadone patients detected pain significantly earlier than controls at 0 h, and were also substantially less pain tolerant than controls at both 0 and 3 h. There were no significant differences in pain detection values between the two groups at 3 h. Pain tolerance to pain detection ratios for methadone patients were significantly lower than controls for the cold pressor test at 0 and 3 h, and for electrical stimulation at 0 h only. In summary, the relative pain sensitivity of methadone maintenance patients is determined by the nature of the nociceptive stimulus (e.g. cold pressor test versus electrical stimulation), the plasma methadone concentration (trough versus peak plasma concentration), and whether thresholds are determined for detection of pain or pain tolerance. Although responding to changes in plasma methadone concentration, maintenance patients are markedly hyperalgesic to pain induced by the cold pressor test.

Adult↗
PubMed1980

Initiation and termination of ventricular tachycardia by supraventricular stimuli. Incidence and electrophysiologic determinants as observed during programmed stimulation of the heart.

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longst ventricular premature stimulus interval resulting in tachycardia and th duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Adult↗
PubMed2006

An illusion of proximal radiation of pain due to distally directed inhibition.

UNLABELLED: The perceived site of pain can frequently radiate from the site of tissue injury. However, the mechanisms supporting spatial aspects of cutaneous pain radiation remain poorly understood. Such mismatches between the actual location and the perceived location of stimuli are also found across other somatosensory modalities. During simultaneous innocuous stimulation at multiple sites, proximal stimuli are perceived as more intense than distal stimuli. To determine if pain radiates in a predominantly proximal direction, 20 subjects rated pain intensity from simultaneously applied pairs of noxious (49 degrees C) thermal stimuli. Proximal and distal stimuli were each rated separately. As the distance between probes was decreased, pain from the proximal site increased relative to that arising from the distal site. Comparisons between paired stimuli and single control (49 degrees C) stimuli revealed that pain arising from the distal stimulus site was inhibited. This distally directed inhibition produced an illusion that pain radiates in a proximal direction. The proximal radiation/distal inhibition of pain observed in the present investigation may represent a perceptual "copy" of neural information used to modulate withdrawal responses. Thus, supraspinally mediated responses to pain can be coordinated with spinally mediated withdrawal reflexes. PERSPECTIVE: Radiation of pain is a perplexing clinical problem. The present findings indicate that the perceived location of pain may be shaped by inhibitory as well as facilitatory processes.

Adult↗
PubMed1976

Rocking waterbeds and auditory stimuli to enhance growth of preterm infants. Preliminary report.

In this study certain features of intrauterine environment were stimulated. Preterm infants were placed on waterbeds, gently rocked, and exposed to auditory stimuli. The stimulated group exhibited significantly better growth for weight, head circumference, and biparietal diameter of the head than did the control infants. Healthy preterm infants placed on rocking waterbeds and exposed to auditory stimuli had growth characteristics comparable to fetuses during the thirty-second to the thirty-sixth week of gestation.

Acoustic Stimulation↗
PubMedDate not supplied

Does nerve impulse activity modulate fast axonal transport?

The possibility that the amount of newly synthesized material made available for fast axonal transport is regulated by nerve impulse activity was examined in an in vitro preparation of bullfrog dorsal root ganglia (DRG) and sciatic nerve. Under conditions that precluded effects of impulse activity on either uptake or incorporation of precursor, patterned stimulation of the sciatic nerve (1 out of every 2 s) produced a frequency- and time-dependent decrease in the amount of radiolabeled protein accumulating at a nerve ligature. The response to patterned stimulation was significantly greater than that to continuous stimulation when the same number of stimuli were delivered. In unligated nerve preparations, patterned stimulation decreased the amplitude of the transport profile with no concomitant change in the wave front distance. Nerve stimulation produced no observable ultrastructural alterations within neuronal cell bodies of the DRG. We propose that the physiological significance of these results is not that nerve impulse activity decreases fast axonal transport, but that the amount of transport increases during periods of electrical quiescence. According to this hypothesis, activity-dependent macromolecules of the axolemma and nerve terminals are replenished during periods when the neuron is firing less frequently. These findings are discussed in light of reports that chronic in vivo stimulation increases the amount of fast-transported, radiolabeled protein (Chan et al., 1989) and that TTX-blockade of neuronal activity has no effect on protein transport (Edwards and Grafstein, 1984; Riccio and Matthews, 1985).

Animals↗
PubMed2006

Rhythmic cortical EEG synchronization with low frequency stimulation of the anterior and medial thalamus for epilepsy.

OBJECTIVE: To investigate the neurophysiological characteristics and prognostic impact of EEG synchronization with low frequency thalamic stimulation in patients with intractable epilepsy. METHODS: Electrical stimuli were delivered through deep brain stimulating (DBS) electrodes at 2, 5 or 10Hz to the anterior nucleus (AN) and the dorsomedial nucleus (DM) of six patients using the implanted programmable stimulation device. EEGs were recorded from 27 scalp electrodes. "Modeled" responses for 5 and 10Hz stimulation were computed based on the cerebral responses (CRs) evoked by "single pulse" (2Hz) stimulation and compared with the recorded EEG results. RESULTS: Rhythmic cortical 5Hz EEG synchronization occurred in 4/6 patients, with stimulation at 6/11 AN and 5/11 DM sites. Three of four patients with synchronization, but neither of the two patients without, had a significant reduction in seizure frequency. The magnitude of 5 and 10Hz EEG synchronization was positively related to the amplitudes of "single pulse" CRs. Simple temporal superposition of "single pulse" CRs resulted in "modeled" responses with strikingly similar morphology and scalp voltage distribution. CONCLUSIONS: Rhythmic EEG synchronization with low frequency stimulation primarily reflects spatiotemporal summation (interference) of "single pulse" CRs. SIGNIFICANCE: Rhythmic EEG synchronization might not serve as a physiologic verification of optimal localization of DBS electrodes. Its usefulness for the prediction of clinical efficacy is questionable.

Adult↗