Spontaneous Discharge Rate Research Articles

The bed nucleus of the stria terminalis: electrophysiological properties and responses to amygdaloid and hypothalamic stimulation

Single unit activity was recorded in the bed nucleus of the stria terminalis (BNST) in response to amygdaloid and hypothalamic stimulation. BNST neurons were identified by their spontaneous discharge rate, spike duration, orthodromic and antidromic responses and conergence properties. The results indicate that these neurons have characteristic electrophysiological features and that they are organized to receive amygdaloid and hypothalamic inputs with increasing convergence along a dorsal to ventral continuum.

Mugineic acid: Non-selective enhancement of excitatory amino acid actions on rat central neurones

The effects of mugineic acid upon excitations induced by quisqualic acid (quis), N-methyl-D-aspartic acid (NMDA) and kainic acid (kain) on rat central neurones were examined in vivo through microiontophoretic drug administration in anaesthetized rats. Mugineic acid usually caused a non-selective enhancement of drug-induced excitations, occasionally producing direct excitation itself or increasing the rate of spontaneous discharge. Mugineic acid-induced effects were not blocked by the NMDA selective antagonist, 2-amino-5-phosphonovaleric acid (AP5).

Responses of feline medial medullary reticulospinal neurons to cardiac input.

1. Responses of medial medullary reticulospinal (RS) neurons to electrical stimulation of cardiac sympathetic afferents, probing the epicardium and epicardial application of bradykinin, were determined in cats anesthetized with alpha-chloralose. Conduction velocity of RS cells averaged 67 m/s; these neurons were probably part of the RS motor pathway and the bulbospinal pathway that modulates ascending information. Fifty-three RS neurons had unilateral projections and 18 neurons bilateral projections to the thoracic spinal cord. 2. Maximal electrical stimulation of the left stellate ganglion excited 69% of 97 RS neurons with a mean latency of 15 +/- 1.0 ms. Mean spike discharge rate increased from 4 +/- 1.2 to 93 +/- 8.0 spikes/s for responsive neurons. 3. Epicardial bradykinin (0.04 mg) excited 34%, inhibited 2%, and did not affect 64% of 44 RS cells tested. Excited neurons increased their mean discharge rate from 12.3 +/- 3.6 to 18.2 +/- 4.3 spikes/s, with a latency of 24 +/- 3.0 s, in response to bradykinin. Response duration averaged 43 +/- 2.3 s. Neurons responsive to bradykinin had greater spontaneous discharge rates than unresponsive neurons. Thirteen of 16 RS cells excited by bradykinin were located in the gigantocellular tegmental field (FTG); the other three cells were in the paramedian nucleus (PR). 4. Epicardial bradykinin often elicited changes in aortic pressure. Although some neurons responded to altered blood pressure alone, these responses could not account for responses to bradykinin. Furthermore, the percentage of responsive neurons was similar in experiments with intact nerves as well as those with vagotomy and barodenervation. 5. Touching the epicardium with a blunt probe excited 19 of 60 (32%) RS neurons, and visceral receptive fields were mapped for 12 of these cells. Neurons responded with one to three spikes to probing. RS neurons responsive to probing were scattered throughout the medial reticular formation. 6. RS cells were also tested for somatic, auditory, and visual input. Of 63 neurons responsive to sympathetic afferent stimulation, only one did not receive convergent input from at least one of these sources; 51% received input from each tested source. Neurons responsive to bradykinin were more likely to receive visual input than the general population of neurons. RS neurons unresponsive to sympathetic afferent stimulation were less likely to receive convergent inputs from other sensory modalities.(ABSTRACT TRUNCATED AT 400 WORDS)

Models of synchronized hippocampal bursts in the presence of inhibition. II. Ongoing spontaneous population events.

1. We extended our computer model of the CA3 region of the hippocampal slice in order to study spontaneous activity occurring in the presence and absence of synaptic inhibition. This was done by providing a steady inward current to the excitatory neurons, whose value was randomly chosen for each cell. With the parameters used, many of the excitatory cells would, if synaptically isolated, remain quiescent, whereas others would burst periodically with periods as brief as 750 ms. Simulations were run for as long as 10 s of neural activity. 2. In the presence of synaptic inhibition, neural activity became organized into recurring, partially synchronized events: clusters of neurons (6% to 12% of the population) would discharge together, with a period averaging 340 ms, shorter than the burst period of any individual neuron. A consequence of periodic clusters of cellular bursts was the widespread occurrence of periodic synchronized synaptic potentials, as have been observed in hippocampal slices and human temporal neocortical slices. The periods between these synaptic potentials are similar in the model to those observed experimentally. 3. The period could be slowed by either increasing the time constant of the slow inhibitory postsynaptic potential (IPSP), or by making the excitatory synapses more powerful. The period seems to be generated in part as follows. Consider those cells with rapid spontaneous discharge rates. An upper bound for the period corresponds to the interval between 1) such a cell's becoming responsive enough to an excitatory synaptic input to burst, and 2) such a cell's bursting spontaneously (i.e., in response to its own intrinsic inward current). For cells with rapid spontaneous discharge rates, the interval defined in this way is approximately 350 ms. 4. Different cells participated in each cluster. A given cluster was initiated by one cell or by two cells bursting together, and spread via excitatory synapses. Excitatory synaptic paths could be traced from the initiating cell(s), directly or through other participants, to all cells participating in a cluster. Spread of activity was limited by two mechanisms, so that not all cells synaptically excited by a participating cell would themselves participate. First, cells might be refractory from having participated in a recent cluster (since the intercluster period was less than the refractory time from a cellular burst to its responsiveness to a synaptic stimulus). Second, some cells might be synaptically inhibited. Synaptic inhibition in this model did not act rapidly enough to suppress the cluster totally.(ABSTRACT TRUNCATED AT 400 WORDS)

Toxic effects of lead in the developing nervous system: in oculo experimental models.

Modern man is chronically exposed to lead in the biosphere at levels several orders of magnitude higher than the natural level that once existed. There is much concern about the possible adverse effects of this population-wide, low-level lead exposure, particularly on the developing organism, wherein the central nervous system may be one primary target. We have developed in oculo test systems, which permit temporal and spatial discrimination of possible effects of lead and other potential neurotoxic agents in the environment on the developing central nervous system as well as on different types of peripheral nerves in the adult. In one experimental protocol, defined areas of the fetal rat brain are grafted to the anterior chamber of the eye of adult rat recipients that are exposed to lead. Such grafts will become vascularized from the host iris and continue developing in oculo. Thus, grafted brain tissue and host brain will share circulation and therefore be exposed to similar amounts of lead. Studies of cerebellar grafts revealed that, although there was a normal gross cytological development in the presence of lead, there was a marked and permanent impairment of spontaneous discharge rates of the grafted Purkinje neurons as observed with electrophysiological techniques long after cessation of lead treatment. The host Purkinje neurons were not affected. A similar, although less dramatic, impairment of cerebellar function could be subsequently demonstrated in intact animals when newborn rats were given lead during the first 20 days of life and studied as adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressure and prolapse--the cause of solitary rectal ulceration.

The cause of solitary rectal ulceration has been investigated using a method that radiologically visualises rectal voiding whilst simultaneously measuring intrarectal pressure and external anal sphincter electromyographic activity. Control subjects and patients with the solitary rectal ulcer syndrome, both with and without mucosal ulceration, have been studied. A high incidence of rectal prolapse (94%) was present in the patients who voided. Overactivity of the anal sphincter during evacuation contributed to the fact that patients with mucosal ulceration required higher intrarectal pressures to void than the controls and the patients without mucosal ulceration. The results indicate that a combination of rectal prolapse and a high voiding pressure may act to cause the mucosal ulceration in this syndrome by exposing the rectal wall to a high transmural pressure gradient.

Contrasting thermal sensitivity of spontaneously active A- and C-fibers in experimental nerve-end neuromas

Injured afferent A- and C-fibers ending in experimental neuromas in the rat sciatic nerve generate a substantial spontaneous discharge. We show that for individual axons the rate and percent incidence of spontaneous discharge are sensitive to neuroma temperature. Within the range of 14–43°C, firing rate of all of the myelinated fibers examined increased as temperature rose, and decreased as temperature fell. For fibers with a tonic rhythmic discharge pattern, Q 10 averaged 1.64 at 34–42°C. Some fibers that were initially silent began to fire as the neuroma was warmed, and some fibers active at baseline temperature fell silent when the neuroma was cooled. Unmyelinated fibers behaved quite differently, showing either no response to temperature changes (44% of fibers sampled), or an increase in discharge rate upon cooling (56%). These effects are probably not secondary to vascular changes, but rather reflect thermal sensitivity of the ectopic neuroma impulse generator sites. This thermal sensitivity may account for the aggravation of phantom limb pain and other neuralgias during cold weather (i.e., post-traumatic cold intolerance).

Effects of pentobarbital and flurazepam on respiratory neurons in undrugged cats.

Two hypnotic drugs known to enhance GABAergic transmission, a barbiturate (pentobarbital) and a benzodiazepine (flurazepam), were applied locally to respiratory-related neurons (RN) located in the ventral respiratory area in the medulla of non-anaesthetized cats which were either decerebrated or chronically implanted. Pentobarbital applied iontophoretically depressed the spontaneous discharge rate of most RN tested as well as the increase in firing of RN discharge induced by iontophoretic application of glutamate; pentobarbital also potentiated inhibition induced by iontophoresed GABA. Flurazepam applied by iontophoresis or pressure pulses depressed a minority of RN tested and did not enhance GABA-induced inhibition. These results suggest: that inhibition of RN activity through GABAergic mechanisms can be affected by drugs which act at the chloride ionophore but not those acting indirectly through the benzodiazepine binding site, and the effects of the agents on medullary neuronal activity are independent of an effect on the states of consciousness or on structures rostral to the medulla.

Investigations differentiating the mechanism of specific bradycardic agents from that of calcium channel blockers.

The effects of two "specific bradycardic agents", falipamil (AQ-A 39) and the alinidine-congener STH 2148 (2-[N-(cyclopropylmethyl)-N-(2,6-dibromophenyl)amino]-2-imidazolin e), on the spontaneous electrical discharge rate of intact guinea-pig sinus node preparations were investigated in comparison to that of the "calcium channel blocker" verapamil. Addition of falipamil (10 micrograms/ml) to a maximally rate lowering concentration of STH 2148 (30 micrograms/ml) exerted no further bradycardic effect. In contrast, verapamil (0.1 microgram/ml) added to either STH 2148 (30 micrograms/ml) or a maximally effective concentration of falipamil (30 micrograms/ml) resulted in a further, significant reduction of sinus rate. The results are compatible with the idea of a common mechanism of the two specific bradycardic agents, different from that of calcium channel blockers.

Carbachol-induced increases in locus coeruleus spontaneous activity are associated with an altered pattern of response to sensory stimuli

In order to evaluate the relationship between locus coeruleus (LC) spontaneous activity and LC activity in response to sensory stimuli, the effects of carbachol on both types of LC neuronal activity were investigated in anesthetized rats. Carbachol increased LC spontaneous discharge rate and altered the pattern of LC discharge in response to sciatic nerve stimulation, while saline had no effect. Moreover, the magnitudes of increases in LC spontaneous discharge rate produced by carbachol were highly correlated ( r=0.79) with a measure of simultaneous effects on LC sensory responses. These results suggest that drugs which increase LC spontaneous activity will also disrupt the pattern of LC discharge to sensory stimuli.

A comparison of the electrophysiological and pharmacological properties of serotonin-containing neurons in the nucleus raphe dorsalis, raphe medianus and raphe pallidus recorded from mouse brain slices In Vitro : Role of autoreceptors

The potential role of autoreceptors in regulating the activity of serotonin-containing nucleus raphe dorsalis (RD), raphe medianus (RM) and raphe pallidus (RPA) neurons was examined by recording the activity of these neurons under a variety of conditions both in vivo and in vitro. Raphe neurons recorded in vivo displayed the characteristic slow, rhythmic discharge pattern previously described for rat and cat raphe cells. The activity of these neurons was suppressed in a dose-dependent manner by tryptophan, LSD and chlorimipramine administered intravenously. There were no significant changes in the spontaneous discharge rate of raphe neurons over time when recorded in vitro, even though tissue serotonin and its metabolite, 5-hydroxyindoleacetic acid, decreased dramatically. RPA neurons fired significantly faster than either RD or RM neurons both in vivo and in vitro. Prior depletion of brain serotonin by p-chlorophenylalanine administration resulted in no significant change in raphe unit activity recorded in vitro. Elevation of brain serotonin by monoamine oxidase inhibition produced a total inhibition of raphe unit activity in vitro. Similarly, increasing the concentration of serotonin in the tissue slice by adding serotonin directly to the incubation medium resulted in a profound, though transitory, depression of unit activity. This depressant effect of serotonin was rapidly reversible upon drug wash-out. Serotonin receptor blockers, methiothepin, cypoheptadine, and methysergide, produced no significant change in unit activity. The serotonin reuptake blocker, fluoxetine, produced a total inhibition of raphe unit activity in all three nuclei in vitro. These data suggest that excess serotonin suppresses the activity of raphe neurons, apparently by an action on autoreceptors, but that a deficiency, or normal concentration, of serotonin does not influence the spontaneous activity of these cells. The data also show that RD and RM are much more sensitive to the depressant effects of serotonin than the caudal RPA neurons. More generally, these studies provide a data base for examining the electrophysiological and pharmacological characteristics of serotonergic neurons in the three major serotonin-containing nuclei in mouse brain. The mouse has proven to be a much easier species than the rat to use in these types of studies, based on the finding that mouse brain slices are more viable in vitro than are rat brain slices.

か牛外電気刺激によるか牛神経興奮性に対するキシロカイン静注の影響について

It is not yet well understood where are the acting sites of the lidocaine in the auditory system. Our previous study has shown that injection of lidocaine reduced the spontaneous discharge rate transiently in guinea pigs.This study was further aimed to elucidate the effects of lidocaine on the cochlear nerve by recording the single nerve action potentials which were evoked by electrical pulse applied to the cochlea through the round window membrane before and after intravenous injection of lidocaine.One minute after intravenous injection of lidocaine, the threshold of spikes responding to the electrical stimuli was twice as much as that of preinjection. It decreased linearly and took 36 min. for full recovery.Decrease of spontaneous discharge rate started about 10 seconds earlier than prolongation of latency of the spikes by the electrical stimuli after initiation of lidocaine injection. These results indicate that intravenous injection of lidocaine acts directly on the cochlear nerve and causes transient decrease of its excitability.

Responses of Cat Auditory Nerve Fibers to Biphasic Electrical Current Pulses

Discharge patterns of single auditory nerve fibers were recorded from normal-hearing cats implanted with a 12-band intracochlear electrode array. Stimuli were biphasic current pulses of specifiable width, amplitude, and rate. Acoustic tuning curves were obtained to determine the cochlear positions of the fibers. Response latencies to electrical stimuli formed two groups. Short latency (0.3 to 0.7 ms) responses were attributed to direct activation of spiral ganglion neurons. At high stimulus intensities, these often exhibited abrupt shifts toward even shorter latencies. Long latency (> 1.5 ms) responses were probably caused by electrophonic activation of functional hair cells. Response thresholds to electrical stimuli depended on a fiber's proximity to the stimulating electrodes, and they did not depend on a fiber's acoustic response threshold or spontaneous discharge rate. High intensity (> 1.5 mA) stimuli could excite fibers over a wide range of characteristic frequencies, even for the narrowest (0.45 mm) electrode separations. Response threshold was an exponentially decreasing function of pulse width for widths up to 300 μs/phase. Fiber discharges were highly phase-locked at all suprathreshold intensities, and saturation discharge rates usually equaled stimulus pulse rates for rates up to at least 800 pulses/s. Dynamic ranges were small (1 to 6 dB), increased with pulse rate, and were uncorrelated with electrical response threshold. Within the dynamic range, shapes of poststimulus time and interspike interval histograms resembled those obtained in response to acoustic stimuli. Depolarization block caused fiber activity to cease in 2 to 5 seconds for sustained stimuli presented at high (> 600 pulses/s) pulse rates and intensities.

Corticotropin-releasing factor disrupts sensory responses of brain noradrenergic neurons.

In order to elucidate the possible role of noradrenergic neurons of the nucleus locus coeruleus (LC) in stress responses, the effects of corticotropin-releasing factor (CRF) on LC neuronal activity were characterized. In haloth-aneanesthetized rats, intracerebroventricular administration of CRF was found to have two distinct actions: A dose-dependent increase in spontaneous discharge activity was observed 3 min after peptide injection, with 1.0 and 3.0 micrograms CRF increasing activity by 7 +/- 2 and 47 +/- 12%, respectively; Ala14CRF (3.0 micrograms), an inactive analogue of CRF, had no effect on LC spontaneous discharge rates. These results confirm and extend previous studies of CRF activation of LC basal discharge activity; additionally, CRF (1.0 and 3.0 micrograms) disrupted sensory responses of LC cells to sciatic nerve stimulation. As previously reported, responses of LC neurons to electrical stimulation of the sciatic nerve usually consisted of a brief activation beginning 20-40 ms after stimulus followed by a period of relatively suppressed activity lasting 100-200 ms. CRF attenuated both components. Responses plotted as normalized, cumulative histograms became more linear in the presence of CRF (1.0 and 3.0 micrograms), suggesting that discharge rates during phasic responses to sciatic stimulation were similar to spontaneous rates. Statistical comparison using the Kolmogorov-Smirnoff test or correlation coefficients demonstrated that both 1.0 and 3.0 micrograms CRF reduced response components, while 0.3 micrograms and Ala14CRF (3.0 micrograms) had no effect. The degree of attenuation of LC sensory responses by CRF was not linearly related to the magnitude of CRF-induced increases in spontaneous discharge rate, suggesting that these are distinct effects of CRF.(ABSTRACT TRUNCATED AT 250 WORDS)

Postnatal development of auditory nerve and cochlear nucleus neuronal responses in kittens

Neurons located within the auditory periphery of kittens (i.e., primary auditory nerve fibers and neurons of the cochlear nucleus (CN)) exhibit similar response properties throughout the early stages of postnatal development. Neural thresholds to acoustic stimuli are uniformly high, spontaneous and acoustically-evoked discharge rates are low, input/output slopes are shallow, and temporal discharge patterns are markedly immature. Phase-locking abilities are poor in developing mammals and all neurons exhibit broad bandpass tuning curves, with cen0ter frequencies clustering near 1.5 kHz. Throughout the first week, response thresholds, maximum discharge rates, rate-intensity slopes, dynamic ranges and other response indices remain essentially unchanged. Thereafter, between the 7th and 20th postnatal days, peripheral auditory development proceeds rapidly, such that thresholds, tuning properties, temporal discharge patterns, and input/output functions achieve maturity. The role of synaptogenesis in the development of adult response properties has been studied through microionophoresis of neuroactive molecules onto the surface of neurons in the caudal divisions of the cochlear nuclei of developing kittens. Results of preliminary experiments suggest that inhibitory postsynaptic receptor function precedes intrinsic excitatory neurotransmission. Furthermore, during the first two weeks of postnatal development in kittens, GABA microionophoresis onto immature caudal CN neurons, exhibiting sustained responses to acoustic stimuli, converts response patterns to the onset type in the majority of neurons encountered.

Acute ultrastructural changes in acoustic trauma: serial-section reconstruction of stereocilia and cuticular plates.

Single-unit recordings were made from populations of auditory-nerve fibers in 12 cats before and after acoustic overstimulation. Cats were killed 4 to 16 h after exposure, and the cochleas were analyzed at the light- and electron-microscopic levels. The exposures were designed to create 40 to 60 dB of acute threshold shift. Physiological changes were similar to those seen in cases of permanent threshold shift: tuning curves with elevation of 'tips' and 'tails' were associated with significant decreases in the mean spontaneous discharge rates; tuning curves with elevated tips but hypersensitive tails were associated with clear elevation of the mean spontaneous rates. At the light-microscopic level, none of the ears showed any significant stereociliary pathology. Some of the ears showed no light-microscopic pathology whatsoever, while others showed signs of swelling and vacuolization in both inner and outer hair cell areas in cochlear regions appropriate to the CF regions showing threshold shifts. The presence or absence of these light-microscopic changes was, to some extent, dependent on the nature of the exposure stimulus. At the electron-microscopic level, in addition to apparent swelling of radial afferent terminals, the inner hair cells themselves were swollen. In two cochlear regions (from two ears) which showed acute threshold shifts of 20 to 40 dB, but no light-microscopic changes, serial-section ultrastructural analysis of stereocilia and cuticular plates was performed. In contrast to the situation in ears with permanent threshold shifts [(1986) Hear Res. 26, 65-88], there was no pathology in the intracuticular portion of the stereocilia rootlets. There were, however, significant changes in the lengths of the supracuticular portion of the rootlets. It is suggested that this attenuation of the supracuticular rootlet could decrease the stiffness of the stereocilia tufts and thereby change the tuning properties and sensitivity of the cochlear partition.

か牛神経自発放電に対するキシロカイン静注の影響について

Intravenous injection of lidocaine is used to relieve tinnitus clinically. But the mechanisms of the relief of tinnitus is not yet clearly understood. There are few experiments to know the effect of lidocaine on the cochlea of animals. Since most of them aimed to show the changes of AP and CM as effects of lidocaine on the cochlea, they used much doses of lidocaine to affect the cochlea.This study was undertaken in order to elucidate the effect of this drug on the cochlea by recording the cochlear nerve spontaneous discharges which are related to tinnitus originated from the cochlea.Intravenous administration of lidocaine in the dose of 5mg/kg demonstrated no remarkable changes of the spontaneous discharge rate but that of 10mg/kg caused a temporary decresase of the spike rate of the nerve fibers ranging from 23% to 100%. It was a general tendency that decrease of spike rate in the fibers with higher spike rate was prominent in those with lower spike rate.It was concluded that intravenous administration of lidocaine acted on the cochlear nerve fiber in the way to suppress their discharge rate temorarily.

アスピリンによりか牛障害を呈したモルモットのか牛に対するキシロカインの影響について

Our previous reports showed that the cochlear spontaneous discharge rate and the excitability of the nerve were decreased following injection of 10mg/kg of lidocaine to the guinea pigs with the normal cochlea. This study is aimed to know the effects of lidocaine on the impaired cochlea which was induced by injection of Aspirin.Aspirin impaires the cochlear functions and produces tinnitus and hearing loss clinically. Following injectcion of aspirin we injected 5mg/kg of lidocaine to the same guinea pigs to know the effects of lidocaine on the impaired cochlea. The cochlear spontaneous discharge rate was decreased significantly (p<0.01) following injection of 5mg/kg of lidocaine. But the minimum threshold to the tone stimuli was not changed. This dose, 5mg/kg, is the smallest among the doses which have been reported to be effective on the cochlea.Clinically tinnitus originated from the abnormal temporal pattern of interspike interval of cochlear spontaneous discharge may be relieved by intravenous injection of lidocaine which decreases the cochlear spontaneous discharge rate.

Neural mechanisms of tone-on-tone masking: patterns of discharge rate and discharge synchrony related to rates of spontaneous discharge in the chinchilla auditory nerve.

Responses of chinchilla auditory nerve fibers to brief probe tones in the presence of a fixed tonal masker were obtained. The stimulus conditions were analogous to those that have been used in many psychophysical experiments. The relation between previously described response properties of auditory nerve fibers and features of psychophysical tone-on-tone masking was examined. In psychophysical studies, a fixed narrowband masker produces a characteristic pattern of masked thresholds, which becomes broad and asymmetrical at high masker levels. In the present experiment 1, a 5,000-Hz masker was presented at 30, 50, and 70 dB SPL. Masked thresholds based on the average rate of response to probe tones were estimated for single auditory nerve fibers. The lowest of these masked thresholds formed a pattern similar to the psychophysical masking pattern, becoming broader and more asymmetrical as the masker was increased to 70 dB SPL. The masked thresholds of fibers with low and medium rates of spontaneous discharge (SR) were as low as or lower than the masked thresholds of fibers with high SRs. In certain frequency regions, masked thresholds based on responses to cochlear distortion products were lower than the masked thresholds of any fiber responding to the probe tone; this result is also similar to previous psychophysical observations. In experiment 2, responses of chinchilla auditory nerve fibers to probe tones in the presence of a masker at 1,000 Hz and 50 dB SPL were studied. Probe tone thresholds in the presence of this masker have been measured psychophysically in chinchillas. Thus the relation between behavioral and neural masked thresholds in the same species could be examined. Masked thresholds were estimated from average discharge rate responses and also from discharge synchrony. Good quantitative agreement was observed between the probe tone levels at which changes in average discharge rate were observed and the chinchilla's behavioral masked thresholds. For fibers matched for characteristic frequency, the masked thresholds based on average discharge rate of high-SR fibers tended to be elevated compared with the thresholds of medium-SR fibers. Changes in discharge rate synchronized to the probe tone occurred at levels lower than the chinchilla's behavioral masked thresholds. If discharge synchrony can be used for detection, the code would appear to be based on the relative synchrony to the probe tone and to the masking tone. Low synchrony masked thresholds were obtained from fibers with all SRs.(ABSTRACT TRUNCATED AT 400 WORDS)

The modification by systemic morphine of the responses of serotonergic and non-serotonergic neurons in nucleus raphe magnus to heating the tail

In anaesthetised rats, 63 raphe-spinal units in nucleus raphe magnus (NRM) have been identified by means of electrophysiological methods and further classified into serotonergic (5-HT) and non-5-HT units according to their conduction velocity and spontaneous discharge rate. All units, except one, showed either excitatory ( n = 39) or inhibitory ( n = 23) responses to noxious heating of the tail with hot water at 52°C. The threshold temperature was around 44°C and both types of responses increased with stepwise increases in temperature. The excitatory or inhibitory responses of raphe-spinal units induced by noxious heating of the tail correlated well with those elicited by noxious pinching, but did not correlate with the different transmitter populations (5-HT or non-5-HT) of the NRM unit. The effects of morphine or Fentanyl administration on the heat-induced responses of NRM units was observed. The possible involvement of NRM raphe-spinal units in ‘diffuse noxious inhibitory controls’ (DNICs) was discussed, particularly in relation to the ‘lifting of DNICs’ produced by morphine.