Nociceptive quality of the laser-evoked blink reflex in humans

Laser radiant-heat pulses selectively excite the free nerve endings in the superficial layers of the skin and activate mechano-thermal nociceptive afferents; when directed to the perioral or supraorbital skin, high-intensity laser pulses evoke a blink-like response in the orbicularis oculi muscle (the laser blink reflex, LBR). We investigated the functional properties (startle or nociceptive origin) of the LBR and sought to characterize its central pathways. Using high-intensity CO(2)-laser stimulation of the perioral or supraorbital regions and electromyographic (EMG) recordings from the orbicularis oculi muscles, we did five experiments in 20 healthy volunteers. First, to investigate whether the LBR is a startle response, we studied its habituation to expected rhythmic stimuli and to unexpected arrhythmic stimuli. To assess its possible nociceptive quality, we studied changes in the LBR and the R2 component of the electrical blink reflex after a lidocaine-induced supraorbital nerve block and after intramuscular injection of the opiate fentanyl and the opiate-antagonist naloxone. To characterize the central pathways for the LBR, we investigated the interaction between the LBR and the three components of the blink reflex (R1, R2, and R3) by delivering laser pulses to the perioral or supraorbital regions before or after electrical stimulation of the supraorbital nerve at various interstimulus intervals. Finally, to gain further information on the central LBR pathways, using two identical CO(2)-laser stimulators, we studied the LBR recovery curves with paired laser pulses delivered to adjacent forehead points at interstimulus intervals from 250 ms to 1.5 s. The LBR withstood relatively high-frequency rhythmic stimulations, and unexpected laser pulses failed to evoke larger responses. When lidocaine began to induce hypoalgesia (about 5 min after the injection), the LBR was abolished, whereas R2 was only partly suppressed 10 min after the injection. Fentanyl injection induced strong, naloxone-reversible, LBR suppression (the response decreased to 25.3% of predrug values at 10 min and to 4% at 20 min), whereas R2 remained appreciably unchanged. Whether directed to the perioral or supraorbital regions, preceding laser pulses strongly suppressed R2 and R3 though not R1. Conversely, preceding electrical stimuli to the supraorbital nerve suppressed the LBR. In response to paired stimuli, the LBR recovered significantly faster than R2. These findings indicate that the LBR is a nociceptive reflex, which shares part of the interneuron chain mediating the nonnociceptive R2 blink reflex, probably in the medullary reticular formation. The LBR may prove useful for studying the pathophysiology of orofacial pain syndromes.     

Narcolepsy-cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

Hypocretin (orexin) deficiency plays a major role in the pathophysiology of narcolepsy–cataplexy. In animal models, hypocretinergic projections to the pedunculopontine nucleus are directly involved in muscle tone regulation mediating muscle atonia – a hallmark of cataplexy. We hypothesized that pedunculopontine nucleus function, tested with prepulse inhibition of the blink reflex, is altered in human narcolepsy–cataplexy. Twenty patients with narcolepsy–cataplexy and 20 healthy controls underwent a neurophysiological study of pedunculopontine nucleus function. Blink reflex, prepulse inhibition of the blink reflex and blink reflex excitability recovery were measured. Blink reflex characteristics (R1 latency and amplitude, and R2 and R2c latency and area under the curve) did not differ between patients and controls (P > 0.05). Prepulse stimulation significantly increased R2 and R2c latencies and reduced R2 and R2c areas in patients and controls. However, the R2 and R2c area suppression was significantly less in patients than in controls (to 69.8 ± 14.4 and 74.9 ± 12.6%, respectively, versus 34.5 ± 28.6 and 43.3 ± 29.5%, respectively; each P < 0.001). Blink reflex excitability recovery, as measured by paired‐pulse stimulation, which is not mediated via the pedunculopontine nucleus, did not differ between patients and controls (P > 0.05). Our data showed that prepulse inhibition is reduced in narcolepsy–cataplexy, whereas unconditioned blink reflex and its excitability recovery are normal. Because the pedunculopontine nucleus is important for prepulse inhibition, these results suggest its functional involvement in narcolepsy–cataplexy.     

Modulation of trigeminal reflex excitability in migraine: effects of attention and habituation on the blink reflex.

The modulation of trigeminal reflex excitability in migraine patients was evaluated during the asymptomatic phase by studying the effects of attention, habituation and preconditioning stimulus on the R2 and R3 components of the blink reflex (BR). Fifty patients suffering from migraine without aura, 20 affected by migraine with aura and 35 sex- and age-matched controls were selected. In subgroups of migraine with-aura and without-aura patients, and normal controls, the blink reflex was elicited during different cognitive situations: (a) spontaneous mental activity; (b) stimulus anticipation; (c) recognition of target numbers. In the remaining subjects, R2 and R3 habituation was evaluated by repetitive stimulation at 1, 5, 10, 15, 20, 25 and 30 s intervals. The R2 and R3 recovery curves were also computed. A reduced R3 threshold with a normal pain threshold was found in migraine with-aura and without-aura patients; the R3 component was not significantly correlated with the pain thresholds in patients and controls. The R2 and R3 components were less influenced by the warning of the stimulus in migraine without-aura and migraine with-aura patients, in comparison with the control group. A slight increase of both R2 and R3 recovery after preconditioning stimulus was also observed in migraine patients, probably caused by a phenomenon of trigeminal hyperexcitability persisting after the last attack. The abnormal BR modulation by alerting expresses in migraine a dysfunction of adaptation capacity to environmental conditions, probably predisposing to migraine.     

Midbrain 6-hydroxydopamine lesions modulate blink reflex excitability

The blink reflex abnormalities present in the 6 hydroxydopamine (6-OHDA) lesioned rat model of parkinsonism mimicked those of the human with Parkinon's disease. In alert rats, we monitored the long and short latency components of the orbicularis oculi electromyographic (OOemg) response evoked by electrical stimulation of the supraorbital branch of the trigeminal nerve (SO). Two paradigms, habituation and double pulse, provided a measure of blink reflex excitability. In normal rats, repeated stimulation of the SO produced habituation of the R2 component of the blink. In the double pulse paradigm, presentation of two identical SO stimuli resulted in a reduced or suppressed OOemg response to the second stimulus relative to the first. In rats with complete, unilateral lesions of midbrain dopamine neurons, repeated SO stimulation produced facilitation rather than habituation of the R2 component of the blink reflex. This facilitation occurred only with the eyelid contralateral to the lesion. In the double pulse paradigm, the lesioned rats showed increased excitability rather than suppression. This effect occurred bilaterally, although the increased excitability was strongest contralateral to the lesion. Rats with partial lesions of midbrain dopamine neurons exhibited qualitatively similar, but less pronounced blink reflex abnormalities. The R1 component of the blink reflex was unaffected by either the complete or partial lesions. Thus, modification of the blink reflex by 6-OHDA lesions provides a reproducible parkinsonian-like symptom which is amenable to investigations of increases in reflex excitability.     

A role for the basal ganglia in nicotinic modulation of the blink reflex

Summary In humans and rats we found that nicotine transiently modifies the blink reflex. For blinks elicited by stimulation of the supraorbital branch of the trigeminal nerve, nicotine decreased the magnitude of the orbicularis oculi electromyogram (OOemg) and increased the latency of only the long-latency (R2) component. For blinks elicited by electrical stimulation of the cornea, nicotine decreased the magnitude and increased the latency of the single component of OOemg response. Since nicotine modified only one component of the supraorbitally elicited blink reflex, nicotine must act primarily on the central nervous system rather than at the muscle. The effects of nicotine could be caused by direct action on lower brainstem interneurons or indirectly by modulating descending systems impinging on blink interneurons. Since precollicular decerebration eliminated nicotine's effects on the blink reflex, nicotine must act through descending systems. Three lines of evidence suggest that nicotine affects the blink reflex through the basal ganglia by causing dopamine release in the striatum. First, stimulation of the substantia nigra mimicked the effects of nicotine on the blink reflex. Second, haloperidol, a dopamine (D₂) receptor antagonist, blocked the effect of nicotine on the blink reflex. Third, apomorphine, a D₂ receptor agonist, mimicked the effects of nicotine on the blink reflex.     

Excitability changes in human peripheral nerve axons in a paradigm mimicking paired-pulse transcranial magnetic stimulation

A peripheral nerve model was developed to determine whether changes in axonal excitability could affect the findings in studies of cortical processes using paired-pulse transcranial magnetic stimulation (TMS). The recovery of axonal excitability from a conditioning stimulus smaller than the test stimulus was qualitatively similar to that with suprathreshold conditioning stimuli. There was an initial decrease in excitability, equivalent to refractoriness at conditioning-test intervals < 4 ms, an increase in excitability, equivalent to supernormality, at intervals of 5–20 ms and a second phase of decreased excitability, equivalent to late subnormality at intervals > 30 ms. H reflex studies using conditioning stimuli below threshold for the H reflex established that these excitability changes could be faithfully translated across an excitatory synapse. Changing membrane potential by injecting polarising current altered axonal excitability in a predictable way, and produced results similar to those reported for many disease states using paired-pulse TMS. Specifically, axonal hyperpolarisation produced a smaller decrease in excitability followed by a greater increase in excitability. This study supports the view that changes in excitability of the stimulated axons should be considered before synaptic mechanisms are invoked in the interpretation of findings from paired-pulse TMS studies.     

Relationship between reflex excitability and symptom duration in hemifacial spasm

Changes in excitability and symmetry characteristics have been analyzed with blink reflex recovery curve method applied with dual stimuli at 200, 600 and 1000 ms in patients with hemifacial spasm (HFS), spasm duration shorter than 1 year (HFS 1), spasm duration longer than 8 years (HFS 2), and control group. When compared with controls, while HFS cases with short symptom duration had significant decreases in inhibition at 200 ms in the spasm and healthy sides, those with long symptom duration had this finding only in the spasm side at the 200 ms interval. When HFS groups were compared with each other, in cases with HFS 1, decreased inhibition in the spasm side was significant at 200 and 600 ms, while this was significant only at 200 ms in HFS 2 cases. HFS groups were not found to be different in terms of R2 recovery grade. In conclusion, in cases with HFS, decreased inhibition attributed to facial motor neuron and brain stem interneurons is more predominant on the side of the spasm and this was shown to be present also, to some extent, in the contralateral side. It can be said from our findings that the abnormalities of the blink reflex recovery do not progress in cases with HFS when the symptom duration becomes longer.     

Abnormal Motoneuronal Excitability in Hyperkinetic Children

To investigate the generality of reported spinal monosynaptic reflex amplitude reductions in hyperkinetic children, H-reflexes were recorded in unmedicated male hyperkinetic and age-matched control children during relaxed wakefulness. Reflex amplitude variations were examined in response to either paired stimuli delivered at varying inter-pair intervals (recovery function procedure) or trains of stimuli delivered at varying rates (homosynaptic depression procedure). As a group, hyperkinetic children demonstrated reflex amplitude reductions in the recovery function region of secondary facilitation (50–300 ms). However, these subjects could be divided into those showing either significantly exaggerated or reduced secondary facilitation relative to controls. Group differences present during paired-stimuli procedures were maintained during repetitive stimulation. Furthermore, response reduction or enhancement in both paradigms extended beyond stimulus intervals encompassing the region of secondary facilitation. The results demonstrate that hyperkinetic children homogeneous for commonly utilized diagnostic criteria may exhibit disparate resting levels of spinal motoneuronal excitability which vary significantly from normal levels. Current thinking regarding bases for secondary facilitation and homosynaptic depression suggests the presence of both neurochemical and neurophysiological disregulation in hyperkinesis.     

The excitability of human cortical inhibitory circuits responsible for the muscle silent period after transcranial brain stimulation

The silent period after transcranial magnetic brain stimulation mainly reflects the activity of inhibitory circuits in the human motor cortex. To assess the excitability of the cortical inhibitory mechanisms responsible for the silent period after transcranial stimulation, we studied, in 15 healthy human subjects, the recovery cycle of the silent period evoked by transcranial and mixed nerve stimulation delivered with a paired stimulation technique. The recovery cycle is defined as the time course of the changes in the size or duration of a conditioned test response when pairs of stimuli (conditioning and test) are used at different conditioning-test intervals. The recovery cycle of the duration of the silent period in the first dorsal interosseous (FDI) muscle during maximum voluntary contraction after transcranial magnetic stimulation was studied by delivering paired magnetic shocks (a conditioning shock and a test shock) at 120% motor-threshold intensity. Conditioning-test intervals ranged from 20-550 ms. The recovery cycle of the silent period in the FDI muscle during maximum voluntary contraction after nerve stimulation was evaluated by paired, supramaximum bipolar electrical stimulation of the ulnar nerve at the wrist (conditioning-test intervals ranging from 20 to 550 ms). Electromyographic activity was recorded by a pair of surface-disk electrodes over the FDI muscle. The recovery cycle of the silent period after transcranial magnetic stimulation delivered through the large round coil showed two phases of facilitation (lengthening of the silent period), one at 20-40 ms and the other at 180-350 ms conditioning-test intervals, with an interposed phase of inhibition (shortening of the silent period) at 80-160 ms. The conditioning magnetic shock left the size of the test motor-evoked potentials statistically unchanged during maximum voluntary contraction. Paired transcranial stimulation with a figure-of-eight coil increased the duration of the test silent period only at short conditioning-test intervals. Conditioning nerve stimulation left the silent period produced by test nerve stimulation unchanged. In conclusion, after a single transcranial magnetic shock, inhibitory circuits in the human motor cortex undergo distinctive short-term changes in their excitability, probably involving different mechanisms.     

Prepulse modulation of the startle reaction and the blink reflex in normal human subjects

Blink reflexes are usually considered the most representative and consistent response of the auditory startle reaction (ASR), and they are often the only response evaluated in human psychophysiological studies. However, auditory stimuli also induce an auditory blink reflex (ABR), the physiological characteristics and brainstem circuitry of which may be different from those of the ASR. This study aimed to investigate whether there were differences between the orbicularis oculi (OOc) responses elicited with the ABR (OOcABR) and those elicited with the ASR (OOcASR) regarding their behavior to prepulse modulation. For comparison, we also examined the OOc responses to supraorbital nerve stimulation (OOcEBR). Electromyographic responses were simultaneously recorded from the OOc, masseter (MAS) and sternocleidomastoid (SCM) muscles. ABRs were considered when auditory stimuli induced responses limited to the OOc, and ASRs were considered when responses were induced in all muscles recorded from. Prepulse stimuli were either a weak electrical stimulation at the third finger (somatosensory prepulse) or a weak acoustic tone (auditory prepulse) that preceded the response-eliciting stimuli by intervals ranging from 0 to 200 ms. Prepulse effects differed according to prepulse modality, but the OOcABR and the OOcASR were always modulated in the same way. In both responses, somatosensory prepulses induced facilitation from 20 to 50 ms, followed by inhibition beyond 75 ms, and auditory prepulses induced no facilitation but a significant inhibition beyond 30 ms. In the OOcEBR, both somatosensory and acoustic prepulses induced facilitation of R1 and inhibition of R2 beyond 30 ms. Our results suggest that the OOcABR and the OOcASR exhibit the same physiological behavior regarding prepulse modulation. It is hypothesized that prepulse facilitation is due to direct impingement of subthreshold excitatory inputs onto the facial motoneurons while prepulse inhibition results from the engagement of a presynaptic inhibitory circuit in the brainstem. Received: 9 October 1998 / Accepted: 29 April 1999     

F wave measurements detecting changes in motor neuron excitability after ischaemic stroke

OBJECTIVE: To study mechanisms that are involved in the hyperexcitability of spinal motor neurons in upper motor neuron lesion, by means of F-wave measurements. METHODS: F waves from 44 hospitalized stroke patients and 35 healthy controls were recorded from abductor pollicis brevis muscles in the course of two experiments: (1) single stimuli following high-intensity ipsilateral cutaneous conditioning were used to stimulate the median nerve; (2) paired stimuli were given to the median nerve at gradually increasing interstimulus intervals to assess recovery curves. Mean F-wave amplitudes elicited by the conditioning stimuli were compared with mean F-wave amplitudes elicited by the test stimuli on both the hemiparetic and the unaffected side. RESULTS: There was no reduction on the hemiparetic side of mean F-wave amplitudes elicited following high-intensity ipsilateral cutaneous stimulation. The recovery of mean F-wave amplitude was completed at longer interstimulus intervals on the hemiparetic side than on the unaffected side and in controls. A correlation was found between this delay of recovery and hemiparetic severity. CONCLUSIONS: The results of our study support the role of changes in lower motor neuron membrane excitability in the enhancement of F wave amplitudes after stroke.     

正常学龄儿童瞬目反射的初步研究

应用电刺激法研究４０例正常学龄儿童的瞬目反射。通常能诱发出刺激侧快反应（Ｒ１）、迟反应（Ｒ２）及对侧迟反应（Ｒ２＇）。分析Ｒ１的形态、各波的潜伏期、时程、波幅，制定出正常值。瞬目反对的检查结果可作为诊断多种脑干障碍和三叉神经、面神经病变的方法。     

Jaw-opening reflex after CO2 laser stimulation of the perioral region in man

CO₂ laser pulses selectively excite A-δ and C mechano-thermal nociceptors in the superficial layers of the skin. To study the jaw-opening reflex elicited by a purely nociceptive input, we delivered laser pulses to the perioral region in 15 subjects. Sensory threshold was very low (9 mJ/mm²). High-intensity noxious laser pulses (more than 4 × sensory threshold) evoked a single phase of electromyogram suppression (laser silent period, LSP) at an onset latency of 70 ms in the contracted masseter and temporal muscles, bilaterally. Even maximum-intensity laser pulses failed to activate the suprahyoid muscles. The recovery curves to paired laser stimuli showed that at short interstimulus intervals the test LSP was strongly suppressed. At about 380 ms it recovered to 50%, i.e. its recovery curve resembled that of the masseter late silent period after electrical mental nerve stimulation (SP2). In experiments studying the interaction with heterotopic stimuli and non-nociceptive responses, chin-taps or electrical shocks delivered to the supraorbital, infraorbital or mental nerves before laser stimulation strongly suppressed the LSP. A preceding perioral laser pulse strongly suppressed the masseter SP evoked by supraorbital stimulation and the SP2 evoked by mental stimulation, but left SP1 unaffected. We conclude that the perioral A-δ fibre input elicits a jaw-opening reflex simply by inhibiting the jaw-closers. The LSP response is mediated by a multisynaptic chain of brainstem interneurons and shares with the masseter SP2 part of the central circuit in the ponto-medullary region. We also propose that a common centre processes the various inputs for jaw opening. Received: 18 July 1997 / Accepted: 20 October 1997     

Long latency inhibition of H-reflex recovery by cutaneous tactile stimulation in man: a cutaneous transcortical reflex

The effect of cutaneous tactile stimulation on motoneuron excitability was studied in 20 normal subjects and in patients of hemiplegia (n = 14) and paraplegia (n = 15) by plotting H-reflex recovery curves during application of twin pulses alone ("basal" H-reflex recovery curve), and twin pulses synchronized with electrical stimuli evoking tactile sensation in skin over the lateral border of the small toe. The "basal" H-reflex recovery curves from normal subjects showed a significant lateral asymmetry of motoneuron excitability, with an even distribution of subjects showing greater excitability on the left and right sides. However, there was no relation between handedness and the side with greater excitability. The cutaneous stimulation produced a highly significant inhibition of the H-reflex recovery between 600 and 6000 ms, with the maximum inhibition recorded at 1000 and 2000 ms, at which time even a complete inhibition of the test H-reflex was observed in some instances. The effect of cutaneous stimulation before 600 ms was statistically insignificant. The amount of cutaneous inhibition of H-reflex recovery showed a lateral asymmetry. The side with greater motoneuron excitability showed more cutaneous inhibition of the H-reflex recovery. A comparison of the H-reflex recovery at higher frequencies of cutaneous stimulation with that at basal frequency showed a slight but statistically insignificant difference in the amount of cutaneous inhibition of the H-reflex recovery. In hemiplegics, the "basal" H-reflex recovery curves showed greater motoneuron excitability on the affected side as compared to those of the unaffected side or controls, with the late inhibitory phase being completely obliterated. A similar pattern was also observed in paraplegics. Significantly, the lateral asymmetry of motoneuron excitability observed in the control group was absent in paraplegics. The cutaneous stimulation failed to produce any significant effect on the H-reflex recovery curves either in the affected side of hemiplegics or in both sides of paraplegics. The significant long latency inhibition of the H-reflex recovery curve produced by cutaneous tactile stimulation is a new finding.(ABSTRACT TRUNCATED AT 400 WORDS)     

Somatosensory eye blink reflex in peripheral facial palsy

To investigate the association between somatosensory blink reflex (SBR) and peripheral facial palsy (PFP) severity and trigeminal blink reflex (BR) changes in cases with PFP and subsequent postparalytic facial syndrome development (PFS). One hundred and twenty subjects with peripheral facial palsy and post-facial syndrome and 44 age and gender matched healthy volunteers were enrolled to this study. Blink reflexes and somatosensory blink reflex were studied in all. The association between R1 and R2 responses of the BR and SBR positivity was investigated. SBR was elicited in 36.3% of normal subjects, in 18.3% of PFP and in 65.3% of PFS patients. In the paralytic side, the frequency of SBR positivity was significantly lower in PFP group compared to controls and SBR was most frequently observed in patients with PFS. Compared to PFP and control groups, SBR positivity on the non-paralytic side significantly revealed a higher rate in PFS patients. SBR positivity of patients in whom R1 or R2 were absent, was significantly lower than those subjects with prolonged or normal R1 or R2 responses. PFP and successive PFS are good models for the sensory motor gate mechanisms and/or excitability enhancement of brainstem neurons responsible for SBR.     

Unilateral enhancement of early and late blink reflex components in hemidystonia

The side-to-side differences in the EMG activity of the early and late components of blink reflex, regarded as revealing the state of excitability of the brain stem reflex centers, have been analyzed in patients with unilateral dystonia without demonstrable brain lesions. It has been observed that both early and late responses of direct blink reflex were higher on the side affected by hemidystonia than on the contralateral one, while the latency values were in the normal range. Possibility that an abnormal output from the striatum towards the brainstem structures involved in blink reflex appears on the affected side of hemidystonic patients is discussed.     

The Effect of an Acoustic Warning Stimulus Upon the Electrically Elicited Blink Reflex in Humans

In a warned Go/No-Go reaction time experiment blink reflexes were elicited electrically immediately before, at, and shortly after the onset of a low intensity acoustic warning stimulus. This provided the opportunity to study the mutual effects of two stimuli of different modalities arriving at the facial nucleus. The warning stimulus was followed after 3 s by an acoustic response stimulus. Sixteen subjects participated in the experiment. They were informed by the response stimulus if a response (a voluntary blink of the right eye) was required. R1 magnitude was increased from 10 ms to 100 ms after warning stimulus onset, with a pronounced peak at 50 ms. The bilateral late component R2 was enhanced when the reflex eliciting stimulus preceded the warning stimulus. Between 20 ms and 30 ms after warning stimulus onset, R2 returned to control level, whereas an eliciting stimulus presented 40 ms or later after warning stimulus onset produced a pronounced inhibition. R2 latency was facilitated immediately after warning stimulus onset. It was concluded that the mutual effects of stimuli of different modalities can be interpreted only if the moment of arrival at the motor nucleus is taken into consideration.     

Nonlinear systems analysis of the hippocampal perforant path-dentate projection. III. Comparison of random train and paired impulse stimulation

1. The transformational properties of the network of hippocampal neurons activated monosynaptically and polysynaptically by electrical stimulation of the perforant path were analyzed using random impulse train and paired impulse stimuli. In response to both types of input, the amplitudes of granule cell population spikes evoked in the dentate gyrus were used as the measure of network output. The random stimulus train consisted of a series of 4,064 electrical impulses, with interimpulse intervals determined by a Poisson distribution; the mean interimpulse interval of the train was 500 ms, and the range was 1-5,000 ms. Paired impulse stimuli consisted of pairs of impulses separated by 10-1,200 ms; impulses pairs were delivered once every 20 s. The procedures were applied to both anesthetized and chronically implanted, unanesthetized preparations. 2. Nonlinear systems analysis of population spike responses evoked during random train stimulation revealed that dentate granule cell output to any impulse was highly dependent on the interval since a prior impulse. Data from anesthetized animals showed that population spike amplitudes were markedly suppressed in response to intervals less than 50 ms, facilitated in response to intervals of approximately 100 ms, suppressed slightly in response to intervals of 300-700 ms, and unaffected by intervals greater than 700 ms. Data from unanesthetized animals showed similar results except that facilitation rather than suppression of spike amplitude was observed in response to intervals of 300-700 ms, and could extend to intervals as great as 1,000 ms. 3. The results of paired impulse stimulation applied to the same preparations also showed that granule cell response was highly dependent on interimpulse interval. However, nonlinearities observed with paired impulse stimulation differed from those revealed by a random impulse signal. Compared to results of random train stimulation, a paired impulse format produced greater magnitude spike suppression in response to short interimpulse intervals (e.g., 10-20 ms), maximum facilitation in response to shorter interstimulus intervals (50 ms rather than 100 ms), greater magnitude spike facilitation, and greater suppression in response to intervals greater than or equal to 300 ms. Furthermore, there were virtually no differences in the nonlinearities of granule cell response recorded from anesthetized and unanesthetized animals when a paired impulse format was used, whereas several differences were observed with random train stimuli. 4.(ABSTRACT TRUNCATED AT 400 WORDS)     

Influence of the medial septal nucleus on the excitability of the commissural path-CA1 pyramidal cell synapse in the hippocampus of freely moving mice

Changes in the excitability of the commissural path-CA1 pyramidal cell synapse were studied by varying the interval between the application of a conditioning pulse in the medial septal nucleus and a test pulse in the contralateral hippocampus in freely moving mice. The results showed that septal prestimulation results in marked changes in the excitability of pyramidal cells (population spikes) without any associated changes in the averaged evoked excitatory post synaptic potentials. Thus, as a result of septal stimulation, population spikes were first potentiated for interpulse intervals ranging from 10 to 30 ms; this was followed by inhibition at intervals between 40 and 60 ms and then by another phase of hyperexcitability between 100 and 160 ms.Possible mechanisms underlying this phenomenon are discussed and these successive changes in excitability are compared to the phase-locked ones which occur spontaneously during theta waves.     

Lead stimulus modality change and the attentional modulation of the acoustic and electrical blink reflex

Two experiments investigated the effects of the sensory modality of the lead and of the blink-eliciting stimulus during lead stimulus modality change on blink modulation at lead intervals of 2500 and 3500 ms. Participants were presented with acoustic, visual, or tactile change stimuli after habituation training with lead stimuli from the same or a different sensory modality. In Experiment 1, latency and magnitude of the acoustic blink were facilitated during a change to acoustic or visual lead stimuli, but not during a change to tactile lead stimuli. After habituation to acoustic lead stimuli, blink magnitude was smaller during tactile change stimuli than during habituation stimuli. The latter finding was replicated in Experiment 2 in which blink was elicited by electrical stimulation of the trigeminal nerve. The consistency of the findings across different combinations of lead stimulus and blink-eliciting stimulus modalities does not support a modality-specific account of attentional blink modulation. Rather, blink modulation during generalized orienting reflects modality non-specific processes, although modulation may not always be found during tactile lead stimuli.