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PubMed1983

Suppression of bulboreticular unit responses to noxious stimuli by analgesic mesencephalic stimulation.

The responses of 302 neurons in the medial medullary reticular formation (MRF) to a variety of noxious and innocuous somatic stimuli were studied in anesthetized and awake rats. In addition, the effects of analgesic electrical stimulation in the mesencephalon (MES) on unit responses were examined. Tail shock was the most effective stimulus, exciting more than 80% of all units recorded. This stimulus was considered separately during data analysis, since it could not be classified as noxious or innocuous. Noxious somatic stimuli (including pinch, firm pressure, pin prick, and radiant heating of the tail above 45 degrees C were especially effective in eliciting discharge in a significant fraction of all cells in both awake (123/205) and anesthetized (45/97) animals. Nociceptive neurons could be classified as nociceptive specific (NS) or wide dynamic range (WDR) depending on their responses to all somatic stimuli tested. Nociceptive neurons showed no preferential anatomical distribution. Most neurons, including those responsive to noxious inputs, exhibited large, often bilateral receptive fields which frequently covered the tail, one or more limbs, and extensive areas of the body or head. Electrical stimulation within or adjacent to the mesencephalic periaqueductal gray matter depressed the spontaneous and evoked discharge of MRF neurons in both acute and chronic preparations. This inhibition showed a significant preference (p less than 0.001, chi-square statistic) for units that were excited by somatic and especially noxious stimuli. No units were facilitated by MES stimulation. In the awake rat, unit suppression closely followed the time course and level of MES-induced analgesia. Excitability data from the acute experiments suggest that this response inhibition may be the result of a direct action on MRF neurons. Anesthesia severely depressed the spontaneous discharge of MRF neurons as well as the activity evoked by innocuous somatic stimulation. Our data suggest that analgesia produced by MES stimulation is at least in part due to the depression of MRF unit activity, and support the hypothesis that MRF neurons play a critical role in the mediation of behavioral responses to noxious stimuli.

Analgesia↗

PubMed1980

Immunoglobulin C-gene expression. I. The commitment to IgG subclass of secretory cells is determined by the quality of the nonspecific stimuli.

Polyclonal stimulation of normal splenic B lymphocytes with either lipopolysaccharide (LPS) or helper T lymphocytes specific for B cell surface antigens results in the selective expression of IgG subclasses by the secretory cells: in addition to IgM-secreting plaque-forming cells (PFC), thymus-independent stimulation leads to the development of IgG2 and IgG3 PFC, while helper cell-dependent activation leads to IgG1 and IgG2 PFC. This cannot be solely explained by selective stimulation of distinct B cell subpopulations, because purified LPS-reactive blasts if restimulated by helper cells switch to IgG1 while if maintained with LPS switch to IgG3. The simultaneous stimulation of splenic B cells with LPS and helper cells results in additive IgM and IgG2 responses, but in the selective suppression of IgG3 PFC with a concomitant synergic enhancement of IgG1 responses. These results are interpreted to indicate that the expression of IgG C genes in proliferating B lymphocytes is directed by the quality of nonspecific stimuli.

Animals↗

PubMed2001

The I' potential of the human auditory brainstem response to paired click stimuli.

When stimulated with an appropriate stimulus, the hair cells of the organ of Corti depolarize, causing the release of a neurotransmitter substance, which excites afferent VIIIth nerve dendrites. It is reasonable to hypothesize that excitatory postsynaptic potentials (EPSPs) generated by the dendrites of the auditory nerve in turn initiate a compound action potential (CAP). The EPSP is thought to be the generator potential for the CAP, and may be recorded in auditory brainstem responses (ABRs) as the I' potential. Determining the anatomical origin of I' may enhance the sensitivity of the ABR technique in hair cell/dendrite/auditory nerve evaluations. Whether I' is of sensory or of neural origin is equivocal, and therefore I' is not well understood. To investigate this dilemma, ABRs were recorded from human subjects using standard and paired-click stimuli, and using subtraction methods to generate a derived ABR. Two early peaks, designated as I degree and I', occurred before wave I in the derived ABR. It was hypothesized that peaks I degrees and I' represent the summating potential and the generator potential, generated by the cochlea and VIIIth nerve dendrites, respectively.

Acoustic Stimulation↗

PubMed1978

Urethral striated sphincter responses to electro-bulbocavernosus stimulation.

Electric stimuli of known strength, duration and frequency were applied to the glans penis, and the cystosphincterometric and electromyographic responses of the urethral striated sphincter were recorded. Studies performed on male subjects, including normal men, patients with a neurologic deficit and patients who had undergone prostatectomy, indicate the usefulness of this technique in evaluating the striated sphincter excitability via the pudendal reflex arc. The intravenous administration of diazepam produced a notable increase in the striated sphincter threshold, indicating the applicability of this technique to evaluate the effect of various neuropharmacologic agents on the striated sphincter activity. In addition, the transit time through the pudendal reflex arc was measured with this method to assess the somatic neural integrity of the lower urinary tract. Also, studies on patients with post-radical prostatectomy incontinence have suggested that our technique of striated sphincter evaluation could be applied to the prediction of postoperative urinary incontinence.

Diazepam↗

PubMed1989

Prolongation of cardiac cycle length attenuates negative dromotropic response to selective vagal stimuli.

We stimulated intracardiac parasympathetic nerve fibers that selectively innervated the atrioventricular (AV) nodal area (AV parasympathetic stimulation), and the sinoatrial (SA) nodal area (SA parasympathetic stimulation), in autonomically decentralized, anesthetized dogs. We then compared these responses to those elicited by stimulation of the cervical vagus nerves. We investigated the interactions between the dromotropic and chronotropic responses to simultaneous AV and SA parasympathetic stimulation. AV parasympathetic stimulation increased the AV interval (AV conduction time) but did not alter the interval between atrial depolarizations (sinus cycle length). SA parasympathetic stimulation increased the sinus cycle length and evoked small changes in the AV interval. Simultaneous AV and SA parasympathetic stimulation, at different combinations of frequencies, induced negative dromotropic and chronotropic responses that were similar to those evoked by cervical vagal stimulation. The greater the increase in sinus cycle length, the less did a given parasympathetic stimulation prolong the AV interval. The prolongation of the AV interval by parasympathetic stimulation did not affect the sinus cycle length. These results suggest that the direct pure negative dromotropic response to parasympathetic nerve stimulation is attenuated by the prolongation of the sinus cycle length, e.g. a concomitant negative chronotropic effect of the parasympathetic stimulation, in the dog heart. This attenuation reflects a mechanism that does not depend on the relative timing of the stimulus impulses in the cardiac cycle, i.e. a phase-independent, as well as the previously reported phase-dependent, mechanism.

Animals↗

PubMed1990

Effects of morphine and midazolam on reactivity to peripheral noxious and central aversive stimuli.

Electrical stimulation of the mesencephalic tectum elicits behavioral and autonomic responses similar to those following peripheral noxious stimulation. Benzodiazepine and opioid compounds attenuate escape behavior induced by electrical stimulation of the dorsal periaqueductal gray (PAG) and deep layers of the superior colliculus (SC). The present study determines if microinjections of midazolam and morphine applied to these PAG-SC sites affect both responsiveness to peripheral noxious stimulation and to aversive PAG-SC stimulation. Both aversive brain stimulation or foot-shocks applied at threshold intensities caused running or jumps concomitant with increases in mean arterial blood pressure (MBP) and heart rate (HR). Microinjection of both drugs attenuated the behavioral reaction and increases in MBP and HR induced by mesencephalic tectum stimulation, while attenuating only the increase in heart rate induced by peripheral painful stimulation. These results suggest that the neural substrates of the behavioral and autonomic effects of stimulating the mesencephalic tectum and peripheral nociceptors are different although they may partially overlap.

Animals↗

PubMed1995

Increased sensitivity to ipsilateral cutaneous stimuli following transcranial magnetic stimulation of the parietal lobe.

Transcranial magnetic stimulation of the sensorimotor cortex results in decreased sensitivity of threshold electrical stimuli to fingers of the contralateral hand. It has been suggested that one factor contributing to neglect contralateral to a unilateral parietal lesion is a release of the normal hemisphere from reciprocal interhemispheric inhibition by the damaged hemisphere. Consistent with this account, the current study demonstrated that transcranial magnetic stimulation over the parietal cortex results in increased sensitivity to cutaneous stimulation ipsilateral to the stimulation. The likely mechanism is a transcranial magnetic stimulation-induced transient dysfunction of the ipsilateral parietal cortex that then results in disinhibition of the contralateral parietal cortex.

Adolescent↗

PubMed1976

Electromechanical stimulator for presenting moving cutaneous stimuli.

Recent interest in the neural processing of complex cutaneous stimuli such as moving stimuli has necessitated more versatile stimulating devices. This article describes the construction and application of a relatively inexpensive instrument, utilizing equipment readily available in most neurophysiological laboratories, which provides a variety of moving cutaneous stimuli of selected velocities, excursions, and directions. The electronic portion of the instrument consists of a logically controlled varable rate integrator wired to conform to the electrical and mechanical characteristics of a Grass P5 plug-in. This circuitry operates the remainder of the instrument which consists of a P5 driver amplifier used to drive the pen motor mechanism that provides the moving cutaneous stimulus.

Electric Stimulation↗

PubMed1998

Omega-conotoxin GVIA-resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea-pig vas deferens and its modulation by presynaptic receptors.

1 Intracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea-pig isolated vas deferens. 2 Recently, a component of action potential-evoked release which is insensitive to high concentrations of the selective N-type calcium channel blocker omega-conotoxin GVIA termed 'residual release' has been described. Under these conditions, release of the neurotransmitter ATP evoked by trains of low frequency stimuli is abolished, but at higher frequencies a substantial component of release is revealed. 3 'Residual release' was studied with trains of 5 or 10 stimuli at stimulation frequencies of 10, 20 and 50 Hz. The alpha2-adrenoceptor agonist clonidine (30-100 nM) inhibited 'residual release', the degree of inhibition being most marked at the beginning of a train. 4 The alpha2-adrenoceptor antagonist yohimbine (1 microM) induced a marked increase in 'residual release' which was dependent on both the frequency of stimulation and the number of stimuli in a train. 5 Prostaglandin E2 (30 nM) and neuropeptide Y (100 nM) caused a rapid inhibition of 'residual release' at all stimulation frequencies examined. 6 4-Aminopyridine (100 microM) induced a powerful potential of 'residual release' and could reverse the inhibition of omega-conotoxin GVIA. 7 'Residual release' was modulated through presynaptic alpha2-adrenoceptors suggesting that (i) residual release of ATP is subject to alpha-autoinhibition through the co-release of noradrenaline, (ii) noradrenaline release can be triggered by calcium channels other than the N-type and (iii) when presynaptic receptors are activated, inhibition of transmitter release can occur by mechanisms other than modulation of calcium-entry through N-type calcium channels in postganglionic sympathetic nerves. Prostaglandin E2 and neuropeptide Y also modulated neurotransmitter release.

4-Aminopyridine↗

PubMed1984

Facilitation of vasopressin release from the neurohypophysis by application of electrical stimuli in bursts. Relevant stimulation parameters.

The physiological significance of the 'bursting' pattern of firing exhibited by activated vasopressin-secreting neurones was investigated by delivering bursts of electrical stimuli to isolated rat neurohypophyses incubated in vitro and by determining vasopressin release. The stimuli were delivered in bursts at three different average frequencies (2.5, 5.0, and 7.5 Hz). For each average frequency, stimuli were delivered at a constant 10 Hz, and the durations of the burst and silence periods were altered, so that the stimulator was switched on for 25, 50 or 75% of the total time. The burst duration varied from 2.5 to 30 s. The vasopressin release generally increased with the average frequency of stimulation, but varied widely for different burst durations. The vasopressin release per stimulus pulse was found to correlate extremely well (r2 = 0.91) with burst durations of up to 20 s, regardless of the average frequency. If it is assumed that complete recovery from the effects of each burst of stimuli took place during the intervening silence periods, it can be shown that vasopressin release per burst increased as the square of burst duration. By analogy with other neurosecretory systems, facilitation of calcium entry during the bursts may be responsible.

Animals↗

PubMed1994

Neuronal responses in cat primary auditory cortex to electrical cochlear stimulation. I. Intensity dependence of firing rate and response latency.

1. Responses of neurons in primary auditory cortex (AI) of the barbiturate anesthetized adult cat were studied using cochlear stimulation with electrical and acoustic stimuli. Acoustic stimulation of the ear ipsilateral to the studied cortical hemisphere with brief biphasic clicks was compared with electrical stimulation of the contralateral cochlea with brief biphasic electrical pulses delivered via a feline cochlear prosthesis. The contralateral ear was deafened immediately before implantation of the cochlear prosthesis. The feline cochlear prosthesis consisted of four bipolar electrode pairs and was placed in the scala tympani. Two bipolar electrode conditions were used for stimulation: one near radial pair with electrode spacing of approximately 0.5 mm, and one longitudinal pair with electrode spacing of approximately 6 mm. 2. The firing rates obtained from single- and multiple-neuron recordings were measured as a function of stimulus intensity for single electrical and acoustic pulses. Resulting rate/level functions were characterized by a fast growing low-level segment and a more slowly growing, saturating, or decreasing high-level segment. The slopes of these two segments as well as the stimulus level and firing rate at the juncture of these two segments (the transition point) provide a complete characterization of the response magnitude behavior as a function of stimulus intensity. 3. The main characteristics of rate/level functions obtained with electrical and acoustic cochlear stimulation were quite similar. However, for any given neuron, differences in the primary growth behavior, such as monotonic or nonmonotonic growth, could be observed between the different stimulation modes. 4. Response latencies from single- and multiple-neuron recordings were obtained as a function of stimulus intensity for electrical and acoustic pulses. Resulting latency/level functions were characterized by a rapidly decreasing low-level segment and a more slowly decreasing high-level segment. The slopes of these two segments as well as the stimulus level and response latency at the juncture of these two segments (the transition point) provide a complete characterization of the response latency behavior as a function of stimulus intensity. Transition point levels for the rate/level function and the latency/level were nearly identical. 5. The characteristic latency behavior for each neuronal response was found to be very similar for acoustic and electrical stimulation. Correlation analysis revealed a close relationship between latency parameters of the two electrical stimulation conditions, a weaker relationship between the longitudinal electrical and the acoustic conditions, and the weakest relationship between the radial electrical and acoustic conditions. 6. Correlation analysis for rate and latency parameters revealed several relationships between these response aspects.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗

PubMed1986

Ipsilateral and contralateral SEP components following median nerve stimulation: effects of interfering stimuli applied to the contralateral hand.

Somatosensory evoked potentials (SEPs) recorded over the hemisphere ipsilateral and contralateral to the electrically stimulated median nerve were analysed in the presence or absence of interfering movement, tactile and vibratory activity in the contralateral hand. In the control wave forms the early potentials recorded over the ipsilateral frontal region, P19 and N25, showed apparent phase reversal with N19 and P25 respectively in the contralateral parietal region and were therefore considered to be produced by the same generator in the primary sensory cortex. All other potentials recorded over the ipsilateral hemisphere were of the same polarity and similar latency to potentials present contralaterally, and their amplitude diminished progressively with distance from the contralateral hemisphere. They were therefore believed to be volume-conducted from the contralateral hemisphere, rather than originating in the ipsilateral hemisphere through uncrossed ascending pathways or interhemispheric connections. The distribution of effects produced by interfering activity in the contralateral hand was demonstrated by subtracting the 'interference' from the 'control' response to derive a 'difference' wave form. Difference potentials present over the contralateral scalp were consistent with influence on generators in the contralateral hemisphere. In particular, voluntary movement of the contralateral hand resulted in difference potentials distributed in accordance with a proposed generator in area 3a or 4. No consistent difference potentials were found in the ipsilateral parietal region. In the ipsilateral frontal region, however, an upward potential whose latency was around 55 msec was proposed to be due to a generator in the supplementary motor area of the contralateral hemisphere.

Adult↗

PubMed1985

Antidiuretic hormone involvement in the release of alpha-melanocyte-stimulating hormone by hyperosmotic stimuli.

In the normal Wistar rat, the plasma alpha-MSH level was raised by hypertonic saline injection (as compared with control rats injected with isotonic saline). No such rise in alpha-MSH followed hypertonic saline administration in the Brattleboro (hereditary diabetes insipidus) animal (compared to isotonic saline injected controls). It is suggested that, in the rat, endogenous antidiuretic hormone is involved in the secretory response of the pars intermedia to osmotic stimuli.

Animals↗

PubMedDate not supplied

Stereoselective electrophysiological effects of propafenone in Langendorff perfused guinea pig hearts.

The present study was focused on the stereoselective electrophysiological effects of (R)- and (S)-propafenone.HCl evaluated in isolated Langendorff perfused guinea pig hearts. Conduction intervals were measured using an ECG-recording method of high resolution. Refractory periods of the different parts of the myocardium were determined by stimulation with premature stimuli, as well as by stimulation with increasing pacing rate (rate-dependent/refractory periods). Drug concentrations of 0.1, 1 and 3 microM were tested. Both compounds induced a dose-dependent increase in AV-nodal, His-bundle, and intraventricular conduction time which reached significance (p less than 0.01) following 3 microM of either compound. Sinus rate was also dose-dependently and significantly reduced. (R)- and (S)-propafenone.HCl induced a marked prolongation of the rate-dependent refractory period of sino-atrial (by 140 +/- 22%, p less than 0.01 and by 141 +/- 14%, p less than 0.01, respectively) and AV-nodal (by 34 +/- 22%, p less than 0.01 and by 42 +/- 15%, p less than 0.01, respectively) conduction and of the atrial (by 182 +/- 21%, p less than 0.01 and by 195 +/- 15%, p less than 0.01, respectively) and ventricular (by 93 +/- 16%, p less than 0.01 and by 88 +/- 16%, p less than 0.01, respectively) myocardium. The effective refractory periods evaluated by stimulation with premature stimuli were also significantly prolonged under the influence of (R)- and (S)-propafenone.HCl, except the ventricular myocardial refractoriness by (R)-propafenone.HCl (increase to 114 +/- 23%, n.s.). Both compounds showed a strong rate-dependence of their effects and, thus, the refractory periods evaluated by stimulation with increasing pacing rate were significantly more prolonged than the refractory periods evaluated by stimulation with premature stimuli. The main difference between the effects of (R)- and (S)-propafenone.HCl on the cardiac electrical activity is the lack of effect of (R)-propafenone.HCl on the ventricular myocardial refractoriness evaluated by stimulation with premature stimuli.

Animals↗

PubMed1985

Response of serotonin-containing neurons in nucleus raphe magnus to morphine, noxious stimuli, and periaqueductal gray stimulation in freely moving cats.

Extracellular single-unit recordings were made in nucleus raphe magnus in unanesthetized, unrestrained cats. Discharge of serotonergic neurons in this region was increased when animals were aroused by noxious stimuli such as pinch and radiant heating of the tail, but these cells were not specifically nociceptive. Peristimulus time histograms indicated that stimulation in the periaqueductal gray was excitatory but alveolar nerve stimulation at a noxious current intensity was no more effective than nonnoxious nerve stimulation in activating serotonergic unit discharge: Similarly, stressful treatments such as physical restraint increased the discharge of some serotonergic neurons, but these cells were activated during any period of behavioral arousal whether or not arousal was the result of aversive treatment. Injection of Formalin into the paw produced pain lasting about 30 min without increasing serotonergic unit discharge above rates observed during undisturbed active waking behavior. The activity of serotonergic neurons was not increased by an analgesic dose of morphine (2 mg/kg, i.p.). These results then are not consistent with the hypothesis that morphine analgesia depends on activation of serotonergic neurons in nucleus raphe magnus or that these cells are specifically involved in modulation of nociception. These neurons may, however, be involved in nociceptive control within the context of a general modulation of sensorimotor processes by serotonin in the central nervous system. We did observe neurochemically unidentified neurons in the medulla whose discharge was more specifically activated by aversive stimuli and also by morphine. It is possible that these neurons are more directly involved in the mediation of opiate and/or stress-induced analgesia.

Analgesia↗

PubMed1984

Effect of maleimide derivatives on superoxide-generating system of guinea-pig neutrophils stimulated by different soluble stimuli.

The effect of modification of maleimide derivatives on superoxide production by guinea-pig neutrophils induced by a variety of different soluble stimuli was studied. Pretreatment of neutrophils by showdomycin, a very slowly penetrating-SH reagent, did not affect superoxide production by all of the stimuli used, suggesting no exposure of sulfhydryl groups involved in superoxide-generating system on the cell surface. Pretreatment with N-ethylmaleimide (MalNEt), a considerably penetrating-SH reagent, markedly inhibited superoxide production stimulated by formyl-methionyl-leucyl-phenylalanine (HCO-Met-Leu-Phe), cytochalasin E or digitonin, but not superoxide production stimulated by the ionophore A23187 or sodium fluoride. The oxygen consumption stimulated by HCO-Met-Leu-Phe or cytochalasin E was inhibited by MalNEt pretreatment, whereas the oxygen consumption stimulated by A23187 was not inhibited by MalNEt. The inhibition by MalNEt of superoxide production did not appear to be due to the interference with binding of the affected stimuli, since MalNEt pretreatment did not inhibit the release of lysozyme, granule enzyme, induced by HCO-Met-Leu-Phe, cytochalasin E or digitonin. Particulate fractions from MalNEt-pretreated neutrophils before exposure to the stimulus exhibited the inhibition of the enhancement of NADPH-dependent superoxide production induced by HCO-Met-Leu-Phe, cytochalasin E or digitonin, but not A23187, whereas treatment of neutrophils with MalNEt after activation by these stimuli had no effect on the NADPH oxidase activity in particulate fractions. Direct exposure of particulate fractions from A23187-stimulated neutrophils to MalNEt showed no actual susceptibility of NADPH oxidase to MalNEt inhibition. These findings suggest that the inhibitory effect of MalNEt is caused by the modification of the process of the activation by the affected stimuli of the superoxide system, probably NADPH oxidase and that at least two mechanisms exist for activation of superoxide-generating system in guinea-pig neutrophils on the basis of the susceptibility to MalNEt inhibition.

Animals↗

PubMed1991

Attenuation in detection of somatosensory stimuli by transcranial magnetic stimulation.

Effects of magnetic stimulation (MS) of the scalp and direct cortical electrical stimulation on detection of an electrical stimulus to the index finger (S1) were studied in 7 normal volunteers and a patient with epilepsy. Detection of somatosensory stimuli was attenuated when MS was delivered 200 msec before S1, was blocked when MS was delivered simultaneously to and 20 msec after S1, and was fully recovered when MS was delivered 200 msec after S1. This effect showed topographic specificity, being produced by scalp stimulation of restricted scalp positions contralateral to the finger stimulated, was maximal with low intensities of finger stimulation and high intensities of MS (usually over that required for motor threshold), and could also be produced in the absence of motor evoked responses in a peripheral hand muscle. These results show that a focal cortical stimulus can briefly attenuate detection of somatosensory stimuli before, during, and after cortical arrival of a somatosensory afferent volley. Several different mechanisms probably contribute to this phenomenon.

Adult↗

PubMed1976

Differential effects of male stimuli on follicle-stimulating hormone, luteinizing hormone, and prolactin secretion in prepubertal female mice.

Puberty may be induced rapidly in young female mice by exposing them to adult males. The relevant male stimuli include a urinary pheromone and tactile cues, the latter acting in a potentiating capacity. The specific action of the urinary pheromone on pituitary gonadotropins was the subject of the present research. Immature females of a standard size were either paired with adult males, isolated and their bedding sprayed with male urine, or maintained as isolated controls. Exposure to male urine resulted in a rapid and significant release of LH (30 min) which was maintained at an average of 50% higher than levels in isolated controls throughout the 48 h experiment; no immediate changes were observed in either serum FSH or prolactin, but FSH was depressed and prolactin rose progressively during later sampling periods. Cohabitation with an adult male yielded parallel but decidedly stronger reponses in the concentrations of all three hormones. Exogenous estrogen, administered in a second experiment at a dosage previously found to mimic the puberty-inducing action of a male, suppressed serum FSH and LH while elevating serum prolactin. Thus, the present results suggest a) that the male's urinary stimulus exerts its action on immature females via LH release with no immediate and/or direct effects on the other two tropic hormones, and b) that the delayed alterations in serum FSH and prolactin concentrations accompanying male- and/or urine-exposure are secondary consequences of an LH-induced release of estradiol. Attempts to induce the entire pubertal cycle in intact females with subovulating doses of LH, nevertheless, were unsuccessful.

Animals↗