Δ-Tetrahydrocannabinol and the hippocampus: Effects on CA1 field potentials in rats

The effects of Δ⁹-tetiahydrocannabinol (THC) on ortho- and antidromically elicited CA1 field potentials were observed in locally anesthetized rats and in rats anesthetized with urethane. THC augmented amplitudes of population EPSP's as well as orthodromic and antidromic population spikes from pyramidal cells in locally anesthetized animals. Latencies to peak amplitude of these responses were increased. Conditioning-test shock experiments revealed that THC also depressed recurrent inhibition probably mediated by basket cells. In animals under urethane anesthesia THC enhanced test responses, but failed to augment population responses to the conditioning stimulus. It was concluded that THC enhanced postsynaptic excitatory processes but attenuated recurrent inhibition. Urethane anesthesia completely blocked the postsynaptic excitatory effect of THC but had little apparent influence on THC's disinhibitory action.     

Δ9-Tetrahydrocannabinol and the hippocampus: Effects on CA1 field potentials in rats

The effects of Δ⁹-tetiahydrocannabinol (THC) on ortho- and antidromically elicited CA1 field potentials were observed in locally anesthetized rats and in rats anesthetized with urethane. THC augmented amplitudes of population EPSP's as well as orthodromic and antidromic population spikes from pyramidal cells in locally anesthetized animals. Latencies to peak amplitude of these responses were increased. Conditioning-test shock experiments revealed that THC also depressed recurrent inhibition probably mediated by basket cells. In animals under urethane anesthesia THC enhanced test responses, but failed to augment population responses to the conditioning stimulus. It was concluded that THC enhanced postsynaptic excitatory processes but attenuated recurrent inhibition. Urethane anesthesia completely blocked the postsynaptic excitatory effect of THC but had little apparent influence on THC's disinhibitory action.     

Conditioned cortical slow potential responses in urethane anesthetized rats

Cortical slow potential (SP) responses to tone or light stimuli preceding medial forebrain bundle (MFB) stimulation were recorded in urethane anesthetized rats. In the first study, rats were implanted with Ag-AgCl electrodes for recording frontal cortex SPs as well as monopolar electrodes for MFB stimulation. Following recovery, optimum stimulation parameters for SP conditioning were determined for each rat during self-stimulation sessions. These animals were then subjected to extensive associative conditioning in the unanesthetized state. Trials were presented at variable intervals and a 2-sec tone preceded a single 0.5 sec train of MFB stimulation. Negative SP responses developed with training and responses of similar waveform and amplitude were observed in the same animals under urethane anesthesia. Other rats were implanted with MFB stimulating electrodes and, after recovery, stimulation parameters were determined as above but the animals were not subjected to the conditioning procedure prior to urethane administration. Under urethane anesthesia, Ag-AgCl electrodes were placed on the dura over frontal cortex for recording SP responses during pseudoconditioning, conditioning, extinction and retraining trials, using either light or tone stimuli. Negative bilateral SP responses to the tone or light were minimal or nonexistent during pseudoconditioning, developed gradually with pairing, diminished markedly during extinction and returned to maximum amplitude with retraining. The SP responses also reflected discrimination between reinforced and nonreinforced tone and light stimuli as well as reversal conditioning. Furthermore, turning off a light could also serve as the conditioned stimulus for SP response generation. Cortical slow potential responses can be conditioned in urethane anesthetized rats. Therefore, it may be possible to apply additional neurophysiological techniques in these animals to investigate event-related slow potential mechanisms.     

An electrophysiological study of amygdalohypothalamic projections to the ventromedial nucleus of the rat.

The influence of the amygdala on the activity of single neurons within the hypothalamic ventromedial nucleus (HVM) was studied in pentobarbital or urethane anesthetized rats. The results are summarized as follows: (1) Stimulation of different amygdaloid nuclei or of the stria terminalis (ST) evoked a prominent field potential within HVM and altered the spike discharge patterns of the majority of HVM neurons. (2) More than 80% of 428 HVM neurons tested with single amygdala shocks exhibited excitation or excitation-inhibition sequences; the remainder displayed inhibitory responses of 100-150 msec duration at latencies slightly longer than for most of the observed excitatory responses. ST stimulation also evoked excitation or excitation-inhibition sequences from 85% of 240 HVM neurons tested; of the remainder, those with spontaneous activity displayed inhibitory responses with durations of 100-150 msec at latencies slightly longer than for most observed excitatory responses. (3) Evoked potential interaction studies suggested that stimulation of either ST or the amygdala activated the same population of HVM neurons. Single cells tested with both amygdala and ST stimulation displayed similar patterns of response. HVM field potentials and single unit responses to amygdala stimulation were markedly diminished by lesions of ST. Thus, in the rat, only one pathway, i.e., the stria terminalis, contains amygdalofugal fibres to the ventromedial hypothalamic nucleus. (4) The orthodromic responses of HVM neurons were dependent on the frequency of amygdala stimulation. Less than 50% of HVM neurons responded to amygdala stimuli at frequencies greater than 33Hz. Many cells could not be activated at stimulation frequencies greater than 10 Hz, and the spontaneous discharges from certain HVM neurons were effectively abolished at this stimulation frequency. (5) Evidence of prominent postsynaptic inhibition was present throughout HVM. Seventeen HVM neurons displayed amygdala evoked unitary activity different from that of the majority of HVM neurons, and these cells were considered to represent possible inhibitory neurons. In contrast to most HVM neurons activated via probable monosynaptic amygdalohypothalamic pathways, these putative inhibitory neurons were apparently activated via polysynaptic pathways. (6) In summary, these results suggest that the amygdala exerts a prominent monosynaptic influence on the activity of many HVM neurons, coupled with polysynaptic activation of powerful local postsynaptic inhibitory mechanism. In the rat, these amygdala evoked events depend on the integrity of the stria terminalis.     

Drastic changes of ventromedial medulla neuronal properties induced by barbiturate anesthesia. I. Comparison of the single-unit types in the same awake and pentobarbital-treated rats.

By means of single-unit recordings, as we have already performed in other studies, we have found that in the awake, drug-free, freely moving rat, there is only one neuronal class potentially involved in nociception and its control at the ventromedial medulla level (VMM, a structure involved in the spinal descending control systems of nociception): the 'multireceptive multimodal' units. These neurons are always activated by very light mechanical (air puff, light touch) and mechanical (pinch, pin-prick) or thermal noxious stimuli, in addition to an auditory stimulus. During identical VMM penetrations, performed in the same animals tested first awake and then anesthetized a few days later with 30 mg/kg of i.p. pentobarbital, we once again found the 'multireceptive multimodal' units, but this time with physiological properties that were strongly modified: in particular, we noted a disappearance of the nociceptive responses consecutive to a strong noxious heat pulse application (36-51 degrees C), associated sometimes with a reduction of the responses due to innocuous stimulation. This is in agreement with the classical effects of barbiturates. In light of previous observations reported in the literature devoted to the VMM physiology in the anesthetized rat, the most important observation in our study was that, with pentobarbital anesthesia, we recorded 'new' neuronal classes as compared to the awake condition. In these classes, which appeared to be qualitatively similar to those already reported under anesthesia, we found the units exclusively driven by innocuous stimulation (excited for the majority), the units specifically driven by noxious stimulation (half excited, half inhibited) and a 'multireceptive multimodal' group inhibited or excited-inhibited by non-noxious and noxious stimuli (half of the multireceptive group). All these data demonstrate that barbiturate anesthesia strongly modifies the VMM physiology in relation to nociception. Furthermore, since our results, that were obtained in anesthetized rats, were qualitatively identical to those described in the literature under similar experimental conditions, they raise the question of the appropriateness of using a barbiturate anesthetic in order to study the cellular mechanisms related to nociception at this level. In addition, these findings indicate that the obtention of only one neuronal class in the awake, drug-free, freely moving rat (the excited 'multireceptive' neurons) is not due to an experimental bias, which strongly emphasizes the reliability of using awake animals. However, it remains to be determined by which mechanisms pentobarbital 'distorts' the VMM physiology as compared to the normal, standard physiological conditions of the awake animal.     

Anesthesia effects: auditory brain-stem response

Auditory brain-stem responses (ABRs) were measured in the awake state and with ketamine and xylazine anesthesia in adult gerbils. Surface recorded vertex-positive components of the ABR were analyzed with respect to the awake and anesthetized states as a function of stimulus frequency. ABR thresholds were not altered with ketamine/xylazine. Small increases in peak latency were associated with anesthesia for all components except wave P1. Increases in absolute latency were progressively greater for successive peaks, reaching an average shift of 0.41 msec for wave P6. Amplitude changes with anesthesia were more variable, with increases generally seen for waves P4 and P6. Significant anesthesia effects on peak latency and amplitude were independent of stimulus frequency. These data confirm previously reported ABR sensitivity to non-barbiturate anesthesia. Direct comparisons of ABR interpeak intervals or amplitude ratios from awake versus anesthetized animals must account for the effects of barbiturate and non-barbiturate agents. However, the stability of response threshold and the small magnitude of latency and amplitude changes with a ketamine and xylazine regimen demonstrate that accurate electrophysiological measures of hearing sensitivity and auditory brain-stem activity can be obtained in anesthetized animals, provided that temperature and other parameters are maintained within normal physiological limits.     

Relationship between heterosynaptic reflex facilitation and acquisition of the nictitating membrane response in control and scopolamine-injected rabbits

Classical conditioning of the rabbit nictitating membrane response was accomplished by presenting a 100-msec tone conditioned stimulus at intervals of 0, 100, 200, 400, and 800 msec before the presentation of a 100-msec shock unconditioned stimulus. In addition, tone-alone and shock-alone trials were interspersed during conditioning. On the first day of conditioning, during which there was no evidence of acquisition of conditioned responses to the tone conditioned stimulus, the amplitudes of the nictitating membrane response evoked on paired tone-shock trials were compared with the amplitudes obtained on shock-alone trials to provide a measure of reflex facilitation. There was a significant correlation (+0.86) in control animals between the degree of reflex facilitation and the degree of learning demonstrated at the various tone-shock intervals. Both reflex facilitation and learning were absent at the 0-msec tone-shock interval, increased at the 100-msec interval, reached a maximum at the 200-msec interval, and then declined at the longer intervals. Scopolamine (0.4 mg/kg) did not affect the amplitude of the nictitating membrane response elicited on shock-alone trials but eliminated any evidence of reflex facilitation or learning at the 100- and 800-msec intervals and significantly reduced both reflex facilitation and learning at the 200- and 400-msec intervals. The comparable effects of scopolamine on both reflex facilitation and learning were reflected by a significant correlation (+0.95) between these two measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of pentobarbital anesthesia on nociceptive processing in the medial and lateral pain pathways in rats

Objective

To investigate the effects of pentobarbital anesthesia on nociceptive processing in the medial and lateral pain pathways.

Methods

Laser stimulation was employed to evoke nociceptive responses in rats under awake or anesthetic conditions. Pain-related neuronal activities were simultaneously recorded from the primary somatosensory cortex (SI), ventral posterolateral thalamus (VPL), anterior cingulate cortex (ACC), and medial dorsal thalamus (MD) with 4 eight-wire microelectrode arrays.

Results

Compared with the awake state, pentobarbital anesthesia significantly suppressed the neural activities induced by noxious laser stimulation. Meanwhile, the pain-evoked changes in the neuronal correlations between cortex and thalamus were suppressed in both medial and lateral pain pathways. In addition, the spontaneous firing rates in all the 4 areas were altered (including inhibition and excitation) under the condition of anesthesia.

Conclusion

The nociceptive processing in the brain can be dramatically changed by anesthesia, which indicates that there are considerable differences in the brain activities between awake and anesthetized states. It is better to employ awake animals for recording neural activity when investigating the sensory coding mechanisms, especially pain coding, in order to obtain data that precisely reflect the physiological state.     

Differential impact of hypothermia and pentobarbital on brain-stem auditory evoked responses.

Two experiments were conducted to determine the effects of hypothermia and pentobarbital anesthesia, alone and in combination, on the brain-stem auditory evoked responses (BAERs) of rats. In experiment I, unanesthetized rats were cooled to colonic temperatures 0.5 and 1.0 degrees C below normal. In experiment II, 2 groups of rats were cooled and tested at 37.5, 36.0, 34.5 and 31.5 degrees C. One group was anesthetized during testing and the other group was awake. The rat BAER was sensitive to cooling of 1 degree C or less. Peak latencies were prolonged and peak-to-peak amplitudes were increased by hypothermia alone. The effect on amplitude may be related to the time course of temperature change or to stimulus level. Pentobarbital significantly affected both latencies and amplitudes over and above the effects of cooling. The specific effects of pentobarbital differed by BAER peak and by temperature. The findings point up the importance of the potential confound of anesthetic drugs in most of the evoked potential literature on hypothermia and, for the first time, quantify the complex interactions between pentobarbital and temperature which affect the BAER wave form.     

Direct demonstration of the effect of lorazepam on the excitability of the human motor cortex.

OBJECTIVES: The present study explored the effects of lorazepam, a benzodiazepine with agonist action at the GABA(A) receptor, on human motor cortex excitability as tested using transcranial magnetic stimulation. METHODS: We recorded directly the descending volley evoked by single and paired transcranial magnetic stimulation from the spinal cord of a conscious subject with a cervical epidural electrode before and after a single oral dose of lorazepam. We evaluated the effects of lorazepam on the descending volleys evoked by a single magnetic stimulation and paired cortical stimulation using the intracortical inhibition paradigm (subthreshold conditioning stimulus) and the short latency intracortical facilitation paradigm (suprathreshold conditioning stimulus). RESULTS: Using a single magnetic stimulus lorazepam decreased the amplitude of the later I waves in the descending volley; this was accompanied by a decrease in the amplitude of the evoked EMG response. Using the intracortical inhibition paradigm lorazepam increased the amount of corticocortical inhibition, particularly at 4 and 5 ms interstimulus intervals. There was no effect on the amount of facilitation observed in the short latency intracortical facilitation paradigm. CONCLUSIONS: The present findings provide direct evidence that lorazepam increases the excitability of inhibitory circuits in the human motor cortex.     

Idazoxan increases perforant path-evoked EPSP slope paired pulse inhibition and reduces perforant path-evoked population spike paired pulse facilitation in rat dentate gyrus

Norepinephrine, acting via beta-adrenoceptors, enhances the perforant path-evoked potential in dentate gyrus. Using systemic idazoxan to increase norepinephrine, and paired perforant path pulses to probe early inhibition, previous investigators reported that idazoxan increased initial spike amplitude and increased somatic feedback inhibition. Here, feedback inhibition was re-examined in idazoxan-treated (5 mg/kg) rats under urethane anesthesia. To control for initial increased spike amplitude after idazoxan, evoked potentials were matched, pre- and post-idazoxan, on initial population spike. Input-output current profiles were also compared pre- and post-idazoxan. Saline- and timolol-filled micropipettes permitted evaluation of a contribution of local beta-adrenoceptors. As previously observed, initial spike amplitude was potentiated by idazoxan. Comparable spike potentiation was not seen on the timolol micropipette. Paired pulse inhibition of spike amplitude apparently increased, but input-output curve comparisons revealed a loss of feedback facilitation rather than an increase in feedback inhibition. Initial EPSP slopes were depressed after idazoxan in input-output curve data. EPSP slope feedback ratios were significantly reduced following idazoxan.These data suggest idazoxan has multiple effects on perforant path input to the dentate gyrus. Spike potentiation following idazoxan has previously been shown to depend on intact norepinephrine input. Here, the reduction in spike potentiation on the timolol pipette is consistent with other evidence that norepinephrine-mediated potentiation of the perforant path-evoked potential is dependent on local beta-adrenoceptor activation. The input-output data suggest a decrease in feedback facilitation after idazoxan is likely to account for the apparent increase in feedback inhibition previously reported. Decreased EPSP slope ratios with similar paired pulse intervals have been reported in novel environments. Since exposure to novel environments activates locus coeruleus neurons, norepinephrine may mediate the change in EPSP slope inhibition reported in awake rats.In summary, these results are consistent with the hypothesis that idazoxan potentiates granule cell responses to perforant path input in the dentate gyrus via increases in norepinephrine that lead to beta-adrenoceptor activation, and, further, that idazoxan reduces paired pulse feedback spike facilitation and enhances EPSP slope, but not spike, feedback inhibition.     

Current generators and properties of early components evoked in rat olfactory cortex

Depth-profile, current-source-density (CSD) and impedance analysis were used to determine the current generators of secondary waves "a" and "b" in the response evoked in pyriform cortex (PC) of the urethane anesthetized rat following OB or LOT stimulation. Positive peaks (sinks) in the second-derivative curves of the "a" and "b" waves were localized at 50-75 and 225-250 microns deep, respectively. Cortical impedance was significantly (p less than 0.01) correlated with the cell packing density of PC layers, being maximal close to the zero dipole point of the gross evoked response; magnitude of conductivity gradients was, however, insufficient to alter the interpretation of positive and negative peaks in terms of net membrane currents. Post-tetanic and/or frequency potentiation of PC responses but not long-term potentiation were found in the majority of animals tested. Recovery of the test "b" wave was faster when using paired-shock stimulation at 3.0 Hz than at 0.3 Hz; suppression of this component following a conditioning OB volley could be overcome and the "b" wave facilitated if either a long-latency component (i.e., 65-100 msec) was present in the priming response, or if the conditioning stimulus was delivered to the mediodorsal thalamic nucleus (MDT). These results confirm and extend similar ones in other species, suggesting that following OB or LOT stimulation three successive excitatory processes take place in PC neural elements of the rat under urethane anesthesia: an initial monosynaptic excitation of distal segments of apical dendrites of layer II cells, and to a lesser extent, also of layer III neurons ("a" wave), followed by action potentials in their respective somas (PS wave); subsequently, long association axons give rise to a di or polysynaptic compound EPSP in proximal apical and possibly also, in basal pyramidal dendrites ("b" wave; early reactivation process). Finally, a "late" reactivation takes place in PC involving neurons which participated in the early reactivation process (late component). In addition, heterosynaptic facilitation of the "b" wave in the PC evoked response follows MDT conditioning stimulation.     

Interhemispheric interaction between the hand motor areas in patients with cortical myoclonus.

OBJECTIVE: To study interhemispheric interaction between the hand motor areas of both hemispheres through the corpus callosum in myoclonus epilepsy. SUBJECTS: Five patients with benign myoclonus epilepsy and ten age matched normal volunteers. METHODS: We studied effects of a medially directed conditioning stimulus over the right hand motor area on responses in the right first dorsal interosseous muscle to a posteriorly directed test stimulus over the left hand motor area. RESULTS: In normal subjects, inhibition was evoked at interstimulus intervals (ISIs) of 8-20ms (late inhibition). In contrast, facilitation occurred in patients at ISIs of 4-6ms (early facilitation) with no late inhibition. CONCLUSIONS: The lack of late inhibition in the patients is consistent with the idea that cortical inhibitory interneurones are affected in myoclonus epilepsy. We propose that this releases interhemispheric facilitation from powerful surround inhibition. The consequence is a predominant early facilitation between the hemispheres in patients with myoclonus epilepsy.     

Drastic changes of ventromedial medulla neuronal properties induced by barbiturate anesthesia. II. Modifications of the single-unit activity produced by Brevital, a short-acting barbiturate in the awake, freely moving rat

In the preceding study, we have found that pentobarbital, a powerful barbiturate substance, strongly modified the ventromedial medulla (VMM) physiology in relation to nociception: indeed, in the same rats, during time-separated similar VMM penetrations, we have recorded, under pentobarbital, 'new' neuronal groups as compared to the awake state, such as the units exclusively driven (excited or inhibited) by cutaneous innocuous or noxious stimulations and the multimodal multireceptive neurons inhibited by non-noxious and noxious stimuli. Still under pentobarbital, we have also recorded the same units found as the rats were awake, i.e., the multimodal multireceptive neurons exclusively excited by various innocuous and noxious stimuli. However, the spontaneous and nociceptive activities of these units were strongly modified as compared to awake animals. Using Brevital (a short-acting barbiturate substance) administration, we have, in the present study, tried to understand the mechanisms underlying these drastic modifications. In particular, one of the questions was whether or not the 'new' neuronal classes recorded under anesthesia resulted from a modification of the physiological properties of the unique VMM neuronal group potentially involved in nociception in awake animals: the multimodal multireceptive units. By following the VMM neuronal activities either before and after or after Brevital administration until recovery from anesthesia, we have determined that the units exclusively driven by innocuous stimulation might result from a modification of the multimodal multireceptive neurons. Alternatively, the multireceptive units inhibited by peripheral stimulations are possibly totally different neurons, silent when the animals are awake.     

Inhibition of hand muscle motoneurones by peripheral nerve stimulation in the relaxed human subject. Antidromic versus orthodromic input

In active muscle, a supramaximal conditioning stimulus to peripheral nerve produces a classic silent period in the EMG. The present experiments examined the effect of this type of conditioning stimulus on motoneurone excitability in relaxed muscle.EMG responses evoked by transcranial magnetic stimulation of the brain were recorded from the first dorsal interosseus muscle (FDI) in 10 healthy subjects and 5 patients with sensory neuropathy. These responses (motor evoked potentials) were conditioned by supramaximal peripheral nerve stimuli given 0–150 msec beforehand. In the normal subjects, the classic silent period in the FDI lasted about 100 msec. The same conditioning stimulus only abolished motor evoked potentials when the conditioning-test interval was so short that the antidromic peripheral nerve volley collided with the orthodromic volley set up by magnetic brain stimulation. At longer conditioning-test intervals, although remarkably inhibited (65% mean suppression between 10 and 40 msec), the test motor potential was never completely abolished and gradually recovered by 100 msec.Inhibition of cortically evoked motor potentials did not depend upon activity set up by the conditioning stimulus in peripheral nerve sensory fibres. The patients with complete peripheral sensory neuropathy had the same extent and time-course of inhibition as the normal subjects. We conclude that in relaxed subjects the inhibitory effect of peripheral conditioning results almost exclusively from the motoneuronal inhibitory mechanisms consequent to antidromic invasion.     

Intracortical inhibition and facilitation in paired-pulse transcranial magnetic stimulation: effect of conditioning stimulus intensity on sizes and latencies of motor evoked potentials.

The influence of the intensity of the conditioning stimulus on intracortical inhibition (ICI) and intracortical facilitation (ICF) was assessed in a study using paired-pulse transcranial magnetic stimulation. Interstimulus intervals (ISIs) between conditioning and test stimuli were 3 msec and 13 msec. Latencies and areas of motor evoked potentials in response to the test stimulus were measured in the right extensor carpi radialis muscle. Motor evoked potential areas with ISIs of 3 msec and 13 msec showed a different dependence on the intensity of the conditioning stimulus. In contrast, the changes of motor evoked potential latencies were fairly similar with both ISIs. The findings point to a parallel action of ICI and ICF. Furthermore, the latencies seem to be a more sensitive indicator for ICF action than the size parameters of motor evoked potentials.     

Conditioning stimulation techniques for enhancement of transcranially elicited evoked motor responses

INTRODUCTION: In spite of the use of multipulse, transcranial electrical stimulation (TES) is still insufficient in a subgroup of patients to elicit motor-evoked potentials during intraoperative neurophysiological monitoring (IONM). Classic facilitation methods used in awake patients are precluded under general anaesthesia. Conditioning techniques can be used in this situation. OBJECTIVE: To present clinical experimental data and models of motor-neuron (MN) excitability for homonymous and heteronymous conditioning and discuss their applications in IONM. MATERIAL AND METHODS: Data were obtained in a prospective study on multipulse TES-conditioning of the monosynaptic H-reflex and double multipulse TES. DISCUSSION: The principle of facilitation by conditioning stimulation is to apply a test stimulus when motor neurons (MNs) have been made maximally excitable by a conditioning stimulus. Both conditioning and test stimuli recruit separate populations of MNs. The overlapping fraction of MNs controls the efficacy of facilitation. Heteronymous conditioning stimulation, which is performed at a different site from the test stimulus, is illustrated by the TES-conditioned H-reflex (HR). Autonomous conditioning stimulation, which is performed at the same stimulation site, is illustrated by double-train TES (dt-TES). The facilitating curves obtained by conditioning stimulation are often 3-modal and show peaks of facilitation at short intertrain intervals (S-ITIs) of 10ms and between 15 and 20ms and at longer intertrain intervals (L-ITI) of over 100ms. The facilitation curves from HR and dt-TES are not always identical since different alphaMN pools are involved. Dt-TES is often successful in neurologically impaired patients whereas facilitation of the HR can be used when conditioned by TES at subthreshold levels allowing continuous IONM without movement in the surgical field. Alternatively, facilitation by conditioning from peripheral-nerve stimulation can be used for selective transmission of subthreshold TES motor responses to peripheral muscles, permitting motor-monitoring by a so-called selective motor-gating technique. CONCLUSIONS: Facilitation techniques offer many possibilities in IONM by enhancing low-amplitude TES-MEP responses. They can also selectively enhance responses in a few muscle groups for the reduction of movement.     

Cardiovascular responses elicited by stimulation of neurons in the central amygdaloid nucleus in awake but not anesthetized rats resemble conditioned emotional responses

Cardiovascular responses elicited by electrical stimulation of the central amygdaloid nucleus were examined in awake and anesthetized rats. Stimulation through chronically implanted electrodes evoked increases in arterial pressure and heart rate in awake, freely behaving rats. The responses, which were dependent upon the frequency and the intensity of the stimulus, were not consistently related to the presence of evoked amygdaloid afterdischarges or to evoked behavioral reactions. Following induction of anesthesia, stimuli delivered to the same rats through the same fixed electrodes produced decreases in blood pressure and heart rate. Microinjection ofl-glutamate into the amygdala of freely behaving rats also elicited increases in arterial pressure and heart rate, indicating that the cardiovascular changes evoked by electrical stimuli are due to excitation of local neurons rather than fibers of passage. The timing and pattern of the response elicited by electrical stimulation of the amygdala in the awake but not anesthetized rat closely corresponds with that evoked by an acoustic conditioned emotional stimulus.     

Increased inhibition in dentate gyrus granule cells following exposure to GABA-uptake blockers

Rats anesthetized with urethane had stimulating and recording electrodes placed in the perforant pathway and in the dentate gyrus. They were then exposed to increasing doses of either the vehicle control dimethylsulfoxide (DMSO) or one of two gamma-aminobutyric acid (GABA)-uptake blockers (SKF-100330A or SKF-89976A). Analysis of evoked field potentials from dentate granule cells indicated that the only effect of the GABA uptake blockers was to increase the threshold for evoking the field population spikes (PS). No other measure of excitatory postsynaptic potentials (EPSPs) or PS's were significantly affected. The lack of effect on evoked EPSP by these drugs suggests no direct effect on transmitter release at this synapse, while the increase in PS threshold suggests a slight decrease in granule cell excitability. The effects of the two GABA-uptake blockers on synaptically mediated facilitation and inhibition was tested by using paired-pulse paradigms. Both GABA-uptake blockers increased early GABA-mediated inhibition to a greater extent than they reduced synaptically mediated facilitation. Neither GABA uptake blocker appeared to effect the late inhibition seen at paired-pulse intervals of 400-1000 ms which is presumably associated with calcium-activated increases in potassium conductance. These effects on granule cell responses occurred at doses found previously not to be associated with side effects and yet to be anticonvulsant in unanesthetized rats. These data confirm in vivo that SKF-100330A and SKF-89976A increase GABA-mediated inhibition. The effect on granule cell excitability and late inhibition are minimal. Although facilitation was reduced by exposure to these drugs, the mechanism of this reduction (direct or prolongation of early inhibition) cannot be determined.     

Brainstem reticular stimulation facilitates back muscle motoneuronal responses to pudendal nerve input

In urethane or pentobarbital anesthetized female rats, stimulation with bipolar electrodes in the medullary reticular formation evoked activity in lateral longissimus muscle nerves, when trains of pulses were applied. Combined stimulation of the medullary reticular formation and the pudendal nerve revealed a marked mutual facilitation of their two separate effects on the excitability of the lateral longissimus muscle nerves. These results match previous conclusions based on the effects of spinal column transection on the pudendal nerve-evoked response, and are consistent with a role for this mutual facilitation in the control of lordosis behavior.