Tectal afferents monosynaptically activate neurons in the pigeon isthmo-optic nucleus

Postsynaptic responses of 105 neurons in brain slices were intracellularly recorded from the isthmo-optic nucleus (ION) in pigeons, and 18 of these neurons were labeled with Lucifer yellow. Excitatory postsynaptic potentials (EPSPs) or spikes were produced in 93 cells, inhibitory postsynaptic potentials (IPSPs) in 10 cells, and EPSPs followed by IPSPs in two cells following electrical stimulation of the tecto-isthmooptic tract. The EPSPs occurred in an all-or-none fashion, with short latencies (1.3 +/- 0.6 ms). Repetitive stimulation increased their amplitude and duration, demonstrating that temporal summation was involved. Neurons producing excitatory responses were distributed throughout cellular layers of the nucleus. Pure IPSPs had a latency of 3.9 +/- 2.3 ms, and cells that responded in this manner were only distributed in the rostral portion of the nucleus. In the remaining two cells with EPSP-IPSP responses, the latency of excitatory responses was 1.5 ms in one cell and 1.4 ms in the other, and that of inhibitory responses was, respectively, 5.1 and 4.1 ms. Thus, it appeared that excitation was monosynaptic, whereas inhibition may be polysynaptic. Four single injections resulted in dye-coupled labeling, and two pairs of closely apposed cells fired spikes, probably resulting from spatial summation of their excitatory responses. The present study suggests that tectal cells directly activate ION neurons and that tectal fibers contact isthmo-optic neurons in a one-to-one fashion. Taken together with previous studies, it appears that the entire tecto-ION-retinal pathway is excitatory.     

Visual responses and afferent connections of the n. ventrolateralis thalami (VLT) in the pigeon (Columba livia)

The nucleus ventrolateralis thalami (VLT) in pigeons receives direct retinal and forebrain projections and has reciprocal connections with the optic tectum. Although VLT is a component of the avian visual system, no study directly examined its connections or its cellular response characteristics. We, therefore, recorded from single units in the pigeon's VLT while visually stimulating the ipsi- and/or contralateral eye. In addition, tracing experiments were conducted to investigate its afferent connections. Electrophysiologically, we discovered three types of neurons, two of which were probably activated via a top-down telencephalotectal system (latencies > 100 ms). Type I neurons responded to uni- and bilateral and type II neurons exclusively to bilateral stimulation. Type III neurons were probably activated by retinal or retinotectal input (latencies < 27 ms) and responded to contra- and bilateral stimulation. Retrograde tracer injections into the VLT revealed an ipsilateral forebrain input from the visual Wulst, from subregions of the arcopallium, and bilateral afferents from the optic tectum. Most intriguing was the direct connection between the VLTs of both hemispheres. We suggest that the avian VLT is part of a system that integrates visuomotor processes which are controlled by both forebrain hemispheres and that VLT contributes to descending tectomotor mechanisms.     

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

The goal of the present study was to determine the effect of activating vagal afferent fibers on the discharge of median preoptic (MnPO) neurons responsive to peripheral angiotensin II (ANG II) and osmotic inputs. Vagal afferents were activated by electrical stimulation of the proximal end of the transected cervical vagus nerve (3 pulses, 100 Hz, 1 ms, 100-500 muA). Of 21 MnPO neurons, 19 were antidromically activated from the hypothalamic paraventricular nucleus (PVH) (latency: 10.3+/-1.3 ms, threshold: 278+/-25 muA). MnPO-PVH cells had an average spontaneous discharge of 2.1+/-0.4 Hz. Injection of ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 mul) through the internal carotid artery significantly (P<0.01) increased the firing rate of most MnPO-PVH neurons (16/19, 84%). Vagus nerve stimulation significantly (P<0.01) decreased discharge (-73+/-9%) in 10 of 16 (63%) neurons with an average onset latency of 108+/-19 ms. Among the remaining 6 MnPO-PVH neurons vagal activation either increased discharge (177+/-100%) with a latency of 115+/-15 ms (n=2) or had no effect (n=4). Pharmacological activation of chemosensitive vagal afferents with phenyl biguanide produced an increase (n=3), decrease (n=2), or no change (n=6) in discharge. These observations indicate that a significant proportion of ANG II- and/or osmo-sensitive MnPO neurons receive convergent vagal input. Although the sensory modalities transmitted by the vagal afferents to MnPO-PVH neurons are not presently known, the presence of inhibitory and excitatory vagal-evoked responses indicates that synaptic processing by these cells integrates humoral and visceral information to subserve potentially important cardiovascular and body fluid homeostatic functions.     

Electrophysiological evidence for axonal branching of ambiguous laryngeal motoneurons

Laryngeal motoneurons in the nucleus ambiguous (NA) were identified antidromically by stimulation of the ipsilateral superior laryngeal nerve (S) and/or the recurrent laryngeal nerve (R). In some NA motoneurons, antidromic spikes elicited by both S and R stimulation collided with the spontaneously occurring discharges. In the same neuron, spikes evoked antidromically by stimulation of one laryngeal nerve always collided with antidromic spikes elicited by stimulation of the other laryngeal nerve. Of 105 NA neurons activated by S and R stimulation, 36 neurons satisfied the criteria, and were classified as NA neurons with branching axons (branching NA (B-NA) neurons). Those neurons activated by either S or R stimulation but not both were classified as NA neurons without branching axons (unbranched NA (UB-NA) neurons). Mean antidromic latencies of B-NA neurons were 0.79 +/- 0.20 ms to S stimulation and 1.91 +/- 0.45 ms to R stimulation and those values for UB-NA neurons were 0.84 +/- 0.17 ms to S stimulation and 2.10 +/- 0.53 ms to R stimulation respectively. None of these mean values were significantly different from one another. Conduction time in the unbranched portion of the branching axon was estimated according to the equation reported by Anderson and Yoshida. The mean conduction time for 20 B-NA neurons was 0.45 +/- 0.35 ms. The branching point in B-NA neurons was estimated on the basis of the conduction time in the unbranched stem portion and those times in two branches of a branching axon measured electrophysiologically. The results suggest that the majority of B-NA neurons bifurcate within a half axonal length.(ABSTRACT TRUNCATED AT 250 WORDS)     

Secondary functional properties of lumbar visceral preganglionic neurons

Preganglionic visceral vasoconstrictor (VVC) neurons and motility-regulating (MR) neurons and other visceral preganglionic neurons, which project in the lumbar splanchnic nerves, were analyzed for their segmental distribution, the conduction velocity of their axons, ongoing activity and reflexes elicited by electrical stimulation of visceral afferents in white rami and of somatic afferents in spinal nerves. Identified preganglionic neurons and neurons without ongoing and reflex activity were distributed over segments L1-L5. VVC neurons were distributed over segments L1-L4 and MR neurons over segments L3-L5. VVC axons conducted at 2.8 +/- 2.5 m/s (mean +/- 1 S.D., n = 49), MR axons at 8.1 +/- 4.7 m/s (n = 131). The ongoing activity of VVC neurons was 1.6 +/- 0.7 imp/s (n = 46), that of MR neurons 0.8 +/- 0.7 imp/s (n = 91). There was no correlation between the conduction velocity of preganglionic axons and the rate of ongoing activity for VVC and MR neurons. (4) Electrical stimulation of visceral afferents in white rami and of somatic afferents in spinal nerves elicited short-latency (less than 50 ms) and long-latency (greater than 50 ms) reflexes in practically all VVC neurons, but preferentially short-latency reflexes in only 50 to 60% of the MR neurons. These results show that VVC and MR neurons are not only different in their reflex patterns, elicited by stimulation of visceral receptors and of arterial baro- and chemoreceptors, but also in the 4 properties analyzed in this paper.     

The ventrolateral medulla of the cat mediates vestibulosympathetic reflexes

Extracellular recordings were made from 94 neurons located in the ventrolateral medulla (VLM) whose firing rate was affected by vestibular nerve (VN) stimulation; 50 of these units were in the subretrofacial (SRF) nucleus, which contains cells that make direct excitatory connections with sympathetic preganglionic neurons. The sample included 12 SRF cells which were antidromically driven from the upper thoracic spinal cord and had conduction velocities of 10 m/s or less; the effect of VN stimulation on all but one of these units was inhibition. The onset latency of the response to VN stimulation was long [20.3 +/- 3.7 (S.E.M.) ms, n = 9, for the antidromically activated neurons and 12.1 +/- 1.2 ms, n = 73, for the others], suggesting that the effects were predominantly polysynaptic. In addition, most of the spontaneously active units tested (33/36) received convergent inputs from the carotid sinus nerve (CSN), as would be expected for neurons which influence sympathetic outflow. Vestibular-elicited inhibition of SRF neurons with projections to the intermediolateral cell column could account for late, long duration inhibition of sympathetic discharges produced by labyrinth stimulation.     

Different cardiovascular neuron groups in the ventral reticular formation of the rostral medulla in rabbits: single neurone studies

To examine whether the cardiovascular neurons of the ventral medulla consist of functionally different kinds of neurons, single neuronal activity of the ventral medulla, activity of the renal sympathetic nerves (RSNA), blood flow of the ear (EarBF) and arterial pressure (AP) were recorded in urethane-anesthetized, vagotomized and immobilized rabbits during electrical stimulation of the aortic nerve (AN, baroreceptor afferent fibers) and electrical stimulation of the dorsomedial hypothalamus (DMH) that reduced EarBF but less affected on AP and RSNA. The dorsolateral funiculus of the second cervical cord was stimulated to evoke antidromic spikes of medullary neurons. Two kinds of reticulo-spinal neurons were identified. Activities of one kind of neurons were facilitated by stimulation of DMH (latency 48.6+/-27.6 ms, n=11) but they did not respond to stimulation of the AN. Therefore, it was presumed that these neurons controlled vasomotion of the ear through the vasoconstrictor neurons in the spinal cord but did not participate in regulation of systemic AP. Activities of the other neurons were inhibited by stimulation of the AN (latency 47.8+/-8 4 ms, n=16) but they did not respond to the DMH stimulation. These neurons were identical to those reported previously as the RVLM neurons, and they contributed to regulate systemic AP but might not participate in control of cutaneous vascular movement. The former neurons were located medially to the latter in the reticular formation of the rostral ventral medulla. These results provided evidence at the single neuronal level that the cardiovascular neurons in the ventral medulla were consisted of functionally different sympatho-excitatory neurons and they were located at the different sites in the rostral ventral medulla.     

Responses of rat lateral hypothalamic neuron activity to vestibular nuclei stimulation

Effects of lateral vestibular nucleus (LVN) stimulation on neuronal activity in the rat lateral hypothalamic area (LHA), including specific glucose-sensitive neurons, were investigated by extracellular and intracellular recordings in vivo. Stimulation of the contralateral LVN evoked 3 types of response in 46% (111/240) of the neurons recorded extracellularly: long latency (38.1 +/- 23.6 ms) excitation (62/111, 56%), short latency (6.9 +/- 3.1 ms) excitation-inhibition (33/111, 30%), and inhibition with 20.1 +/- 11.1 ms latency (16/111, 14%). Glucose-sensitive neurons, which were identified by electrophoretic application of glucose, did not respond specifically to such stimulation. Neuronal activity was recorded intracellularly from 31 LHA neurons, of which 13 responded to LVN stimulation. Seven of the 13 neurons showed a long latency EPSP (10.4 +/- 5.5 ms) and the remaining 6 exhibited an EPSP-IPSP sequence with shorter latency (4.5 +/- 3.0 ms). The amplitude of these responses was graded with a change in stimulus intensity. The EPSPs of both types of response were considered to be polysynaptic because of shortening of latencies by higher current stimulation. Since the LHA is implicated in the regulation of autonomic nerve activity, the present results showing polysynaptic pathways from the LVN to the LHA suggest functional involvement of the LHA in vestibulo-autonomic responses.     

Changes in mechanoreceptive field properties of trigeminal somatosensory brainstem neurons induced by stimulation of nucleus raphe magnus in cats

Experiments were carried out on adult anesthetized cats in which the effects of nucleus raphe magnus (NRM) conditioning stimulation (20 ms) were tested on the responses evoked by orofacial stimuli in single brainstem neurons of trigeminal (V) subnucleus oralis. The NRM stimulation induced inhibition of the responses of 57 of 77 low-threshold mechanoreceptive (LTM) neurons and the one wide-dynamic range (WDR) neuron tested. The duration of the neuronal inhibition ranged from 300-600 ms and the mean threshold for inhibition ranged from 47.8 +/- 4.8 to 102.7 +/- 15 microA depending on the orofacial stimulation site (skin or tooth pulp) and form (mechanical or electrical) of cutaneous stimuli used to evoke neuronal responses. In 20 LTM neurons showing NRM-induced inhibition that were specifically examined for the effects of NRM stimulation on the mechanoreceptive field, one population (n = 11) showed shrinkage (mean 55 +/- 4.4% from control area) of the mechanoreceptive field while the remaining neurons (n = 9) showed no change in mechanoreceptive field size during NRM stimulation. The former group of neurons were also distinguished from the latter neurons by their significantly larger mechanoreceptive field and the activation of the majority of them by electrical stimuli applied outside their mechanoreceptive field. The responses of these neurons evoked by low-threshold inputs from the edge of the mechanoreceptive field were more sensitive to NRM conditioning stimulation than responses evoked from the mechanoreceptive field center, as judged by threshold, magnitude and duration of the NRM-induced inhibition. These findings underscore the sensitivity of LTM neurons to NRM influences. They also reveal a particular population of oralis neurons which have a differential sensitivity of low-threshold inputs evoked from the edge compared to the center of the mechanoreceptive field.     

Electrophysiological analysis of the ascending and descending components of the micturition reflex pathway in the rat

Electrophysiological techniques were used to examine the organization of the spinobulbospinal micturition reflex pathway in the rat. Electrical stimulation of afferent axons in the pelvic nerve evoked a long latency (136 +/- 41 ms) response on bladder postganglionic nerves, whereas stimulation in the dorsal pontine tegmentum elicited shorter latency firing (72 +/- 25 ms) on these nerves. Transection of the pelvic nerve eliminated these responses. Firing on the bladder postganglionic nerves was evoked by stimulation in a relatively limited area of the pons within and close to the laterodorsal tegmental nucleus (LDT) and adjacent ventral periaqueductal gray. Stimulation at sites ventral to this excitatory area inhibited at latencies of 107 +/- 11 ms the asynchronous firing on the bladder postganglionic nerves elicited by bladder distension. Electrical stimulation of afferents in the pelvic nerve evoked short latency (13 +/- 3 ms) negative field potentials in the dorsal part of the periaqueductal gray as well as long latency (42 +/- 7 ms) field potentials in and adjacent to the LDT. The responses were not altered by neuromuscular blockade. Similar responses were elicited by stimulation of afferent axons in the bladder nerves. The sum of the latencies of the ascending and descending pathways between the LDT and the pelvic nerve (i.e. 72 ms plus 42 ms = 114 ms) is comparable although somewhat shorter (22 ms) than the latency of the entire micturition reflex. These results provide further evidence that the micturition reflex in the rat is mediated by a spinobulbospinal pathway which passes through the dorsal pontine tegmentum, and that neurons in the periaqueductal gray as well as the LDT may play as important role in the regulation of the micturition.     

Effects of lingual nerve and chewing cortex stimulation upon activity of the swallowing neurons located in the region of the hypoglossal motor nucleus

This study focuses on motoneurons and interneurons in the region of the hypoglossal nucleus (XIIth) related to swallowing and chewing. In sheep anesthetized with halothane, we have used extracellular microelectrodes to study the effects of stimulation of the superior laryngeal nerve (SLN), the lingual nerve (LN) and the chewing cortex (CCx) upon activities of the swallowing neurons (SNs). Ipsilateral stimulation (1-5 pulses at 500 Hz) of the peripheral afferents or CCx did not generally induce a short latency activation of the hypoglossal swallowing motoneurons (Group I SNs) since only 4 motoneurons (69 tested) were activated by the SLN, 4 motoneurons (56 tested) by the LN and none by the CCx. In contrast, the same stimulations were more effective with swallowing interneurons (Group II SNs) located in the reticular formation close to the XIIth motor nucleus since 12 neurons (30 tested) were activated with short latencies (9 +/- 1.8 ms; mean latency +/- S.D.) by the SLN, 9 neurons (21 tested) by the LN (latency; 8 +/- 1.8 ms) and 5 neurons (18 tested) by the CCx (latency: 13 +/- 1.7 ms). Seven neurons were activated by two or three modes of stimulation indicating the existence of convergent inputs upon some Group II SNs. During chewing movements induced by a prolonged stimulation (20-40 Hz) of the CCx, 10 Group I SNs (16 tested) versus only one Group II SN (8 tested) were found to fire in association with the jaw opening. Moreover, 3 motoneurons and 4 interneurons inactive during swallowing discharged during chewing movements.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nucleus entopeduncularis stimulation on thalamic nuclei motor neurons under normal conditions and after injury of the nigrostriatal dopaminergic system produced by the neurotoxin MPTP

Two groups of acute experiments were performed on cats anesthetized by ketamine and immobilized by myorelaxine to study reactions of neurons in ventral anterior (VA) and ventral lateral (VL) thalamic nuclei to stimulation of nucleus entopeduncularis (nEp) in normal animals and in those treated with chronic injections of neurotoxin--N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 5 mg/kg, i.m., daily, for five days). It was established that in normal cats 28% of the neurons studied have responded to nEp stimulation by inhibition with the latency shorter than 7 ms. In a half of inhibiting neurons after the first phase of inhibition which lasted 18 +/- 2 ms, the second inhibitory phase was registered. The duration of the latter was 25 +/- 4 ms. In MPTP-treated cats the number of neurons inhibited after nEp stimulation was practically the same as in normal ones (24.5%). A tendency of the first phase shortening and a statistically significant increase of the second inhibition phase duration up to 50 +/- 11 ms were found. It was suggested that changes in the inhibitory processes in VA-VL neurons receiving afferents from nEp might be explained by hyperpolarization of the nerve cell membrane evoked by increasing pallidothalamic inhibitory influences. That hyperpolarization created conditions for a decrease in Cl(-)-dependent and an increase in Ca(2+)-dependent K(+)-related phases of inhibitory postsynaptic potentials.     

Electrophysiological study of paraventricular nucleus neurons projecting to the dorsomedial medulla and their response to baroreceptor stimulation in rats

In male rats anesthetized with urethane, extracellular recordings were made from 415 neurons in the paraventricular nucleus (PVN) and adjacent areas. Of these neurons 64 were excited antidromically by stimulation of the dorsomedial medulla but not by stimulation of the pituitary stalk (first group). Seventy-three neurons were antidromically excited by stimulation of the pituitary stalk but not of the dorsomedial medulla (second group, neurosecretory cells). The other 2 neurons were antidromically excited by stimulation of both the dorsomedial medulla and the pituitary stalk (third group). Latencies of antidromically evoked action potentials by stimulation of the dorsomedial medulla and of the pituitary stalk ranged between 8 and 60 ms (mean +/- S.D., 38.5 +/- 9.8, n = 66) and from 7 to 24 ms (mean +/- S.D., 13.0 +/- 3.6, n = 75), respectively, suggesting unmyelinated fiber projections in both instances. PVN neurons of these 3 groups were found to be dispersed throughout the PVN and no difference in specific locations between the neuron groups existed. Their characteristics, however, were different. The first group of neurons discharged at a slower rate and showed no phasic pattern of firing, while 28% of the second group of neurons ('identified' neurosecretory cells) showed phasic patterns of firing and their rates of discharge were higher than those of the first group of neurons. The two neurons belonging to the third group showed irregular spontaneous discharges. The areas within the dorsomedial medulla stimulation of which evoked antidromic excitation of PVN neurons were located within and adjacent to the nucleus of the tractus solitarius (NTS) and the dorsal motor nucleus of the vagus (DMV). Among PVN neurons which were antidromically excited by stimulation of dorsomedial medulla, 51 cells were examined for their responses to excitation of baroreceptors. An increase in pressure of the 'isolated' carotid sinus excited 2 neurons, and inhibited 7 (14%). On the other hand, 27% (11 out of 41) of neurosecretory cells (second group) were inhibited by baroreceptor stimulation. From these results, it was concluded that essentially separate populations of PVN neurons project to the neurohypophysis and to the NTS, DMV and their vicinities, and that some of the caudally-projecting PVN neurons receive synaptic input from carotid baroreceptor reflex pathway, suggesting the possible involvement of these PVN neurons in central cardiovascular regulation.     

Morphology of layer V pyramidal neurons in the cat somatosensory cortex: an intracellular HRP study

Pyramidal tract (PT) or corticopontine neurons of the cat somatosensory cortex (SI) were identified with antidromic activation on stimulation of the bulbar pyramid or pontine nuclei (PN) and stained intracellularly with HRP after examining the electrophysiological properties. Comparison of the conduction velocity of the stem axons and the soma-dendritic morphology revealed that in the cat SI, there exists two types of layer V pyramidal neurons, i.e. one has smooth apical dendrites with larger soma (51.6 +/- 9.5 x 22.7 +/- 2.8 micron) and the other has richly spinous apical dendrites with smaller soma (34.0 +/- 8.8 x 15.3 +/- 3.3 micron). The former group responded antidromically at latencies shorter than 1 ms by PT stimulation or 1.5 ms by PN stimulation, respectively. These values were consistent with the borderline latencies between two similar groups of layer V pyramidal neurons in the motor (fast and slow PTNs) and parietal (aspiny and spiny layer V corticopontine neurons) cortices in the cat.     

Effect of fetal infraorbital nerve transection upon trigeminal primary afferent projections in the rat

Transganglionic tracing with a combination of horseradish peroxidase (HRP) and wheat germ agglutinin-conjugated HRP (WGA-HRP) was employed to compare the trigeminal (V) innervation of the brainstem in adult rats that sustained transection of the infraorbital nerve (ION) on either the day of birth or just prior to the beginning of the 17th embryonic day (E-17). The same methods were also employed to assess the effects of such lesions upon the innervation of the brainstem by the lingual, inferior alveolar, mylohyoid, and auriculotemporal V branches. Previous experiments (Chiaia et al.: Dev. Brain Res. 36:75-88, '87) showed that application of HRP and WGA-HRP to the ION in normal adult rats (N = 3) labelled 12,553 +/- 1,455 (mean +/- s.d.) V ganglion cells while application of these tracers to the regenerated ION after neonatal transection (N = 9) labelled 5,001 +/- 1,287 ganglion cells. Application of HRP and WGA-HRP to the regenerated ION in adulthood (N = 6) after fetal transection labelled 5,476 +/- 3,056 ganglion cells. Thus, the numbers of ganglion cells giving rise to the regenerated ION after fetal and neonatal transection were equivalent (P greater than .05). The central projections of the ION after fetal transection were qualitatively different from those observed after neonatal injury. After neonatal transection, the central terminal field of regenerated ION fibers in adulthood is almost completely restricted to layers I and II of subnucleus caudalis (SpC; Jacquin and Rhoades: Brain Res. 269:137-144, '83; Chiaia et al.: Dev. Brain Res. 36:75-88, '87). After fetal transection, regenerated ION axons terminate heavily in all portions of the V brainstem complex. After neonatal ION transection, we (Jacquin and Rhoades: J. Comp. Neurol. 235:129-143, '85) have been unable to detect central sprouting of undamaged V mandibular axons by means of transganglionic tracing with HRP and WGA-HRP. Such sprouting was evident in both V subnucleus interpolaris (SpI) and SpC after fetal ION transection. We carried out one additional experiment to determine whether ION ganglion cells that survived fetal axotomy were more resistant to axonal damage than the population of neurons that normally contribute to this nerve on the day of birth. Rats (N = 5) sustained transection of the ION on E-17 and again on the day of birth. The regenerated ION was then labelled with HRP and WGA-HRP when the animals reached adulthood.(ABSTRACT TRUNCATED AT 400 WORDS)     

Involvement of reticular neurons located dorsal to the facial nucleus in activation of the jaw-closing muscle in rats

The location of excitatory premotor neurons for jaw-closing motoneurons was examined by the use of electrical and chemical stimulation and extracellular single-unit recording techniques in the anesthetized rat. Single-pulse electrical stimulation of the supratrigeminal region (SupV) and the reticular formation dorsal to the facial nucleus (RdVII) elicited masseter EMG response at mean (+/-SD) latencies of 2.22 +/- 0.59 ms and 3.10 +/- 1.14 ms, respectively. Microinjection (0.1-0.3 microl) of glutamate (50 mM) or kainate (0.5-100 microM) into RdVII increased masseter nerve activity in artificially ventilated and immobilized rats by 30.2 +/- 40.5% and 50.7 +/- 46.8% compared to baseline values, respectively. Forty reticular neurons were antidromically activated by stimulation of the ipsilateral trigeminal motor nucleus (MoV). Twenty neurons were found in RdVII, and the remaining 20 neurons were located in SupV, or areas adjacent to SupV or RdVII. Eleven neurons in RdVII responded to at least either passive jaw opening or light pressure applied to the teeth or tongue. Nine neurons responded to passive jaw opening. Five of the nine neurons responded to multiple stimulus categories. A monosynaptic excitatory projection from one neuron in RdVII was detected by spike-triggered averaging of the rectified masseter nerve activity. We suggest that reticular neurons in RdVII are involved in increasing masseter muscle activity and that excitatory premotor neurons for masseter motoneurons are likely located in this area. RdVII could be an important candidate for controlling activity of jaw-closing muscles via peripheral inputs.     

Morphological features of layer V pyramidal neurons in the cat parietal cortex: an intracellular HRP study

Layer V pyramidal neurons in the cat parietal cortex (areas 5 and 7) were investigated with intracellular HRP staining. Antidromic responses were recorded intracellularly as well as extracellularly with pontine stimulation under Nembutal anesthesia. The relationship between the latency of antidromic responses and the morphology of HRP-stained neurons was analyzed. A total of 65 neurons were stained with HRP, and sixteen of these neurons were activated antidromically with pontine stimulation. Two distinct groups of layer V pyramidal neurons were detected morphologically by intracellular HRP staining; i.e., one (F type) consisted of neurons with relatively large somata (58.4 +/- 8.1 micron X 24.5 +/- 5.1 micron, N = 11) and aspiny or sparsely spinous apical dendrites, and the other (S type) consisted of neurons with smaller somata (44.6 +/- 7.6 micron X 19.3 +/- 3.9 micron, N = 22) and richly spinous apical dendrites. These two groups showed different electrophysiological properties; i.e., the former responded antidromically to pontine stimulation at a latency shorter than 1.5 ms (namely, with a conduction velocity faster than 18 m/second) and the latter responded at a latency longer than 1.5 ms. The two neuronal types in the parietal cortex corresponded respectively to fast and slow pyramidal tract neurons (PTNs) investigated in the sensorimotor cortex. Although their morphological features were almost similar to those of PTNs, the branching pattern of apical dendrites of the F-type pyramidal neuron seemed to be different from that of fast PTNs. In the parietal cortex, apical dendrites of F-type neurons showed rather frequent branching in layer I. This was similar to the pattern of branching in slow PTNs. Such a characteristic branching pattern suggested that, in the cat parietal cortex, layer V pyramidal neurons of both types are adapted to receive cerebellar inputs through the ventroanterior (VA) thalamic nucleus to the superficial cortical layers.     

Differential changes in axonal conduction following CNS demyelination in two mouse models

Transgenic and disease model mice have been used to investigate the molecular mechanisms of demyelinating diseases. However, less attention has been given to elucidating changes in nerve conduction in these mice. We established an experimental system to measure the response latency of cortical neurons and examined changes in nerve conduction in cuprizone-induced demyelinating mice and in myelin basic protein-deficient shiverer mice. Stimulating and recording electrodes were placed in the right and left sensori-motor cortices, respectively. Electrical stimulation of the right cortex evoked antidromic responses in left cortical neurons with a latency of 9.38 +/- 0.31 ms (n = 107; mean +/- SEM). While response latency was longer in mice at 7 days and 4 weeks of cuprizone treatment (12.35 +/- 0.35 ms, n = 102; 11.72 +/- 0.29 ms, n = 103, respectively), response latency at 7 days and 4 weeks after removal of cuprizone was partially restored (10.72 +/- 0.45 ms, n = 106; 10.27 +/- 0.34 ms, n = 107, respectively). Likewise, electron microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone removal. We also examined whether the myelin abnormalities in shiverer mice affected their response latencies. But there were no significant differences in response latencies in shiverer (9.83 +/- 0.24 ms, n = 103) and wild-type (9.33 +/- 0.22 ms, n = 112) mice. The results of these electrophysiological assessments imply that different demyelinating mechanisms, differentially affecting axon conduction, are present in the cuprizone-treated and shiverer mice, and may provide new insights to understanding the pathophysiology of demyelination in animal models in the CNS.     

Cardiovascular afferent and fastigial nucleus inputs to paramedian reticulospinal neurons

In chloralose anesthetized, paralyzed and artificially ventilated cats, the region of the paramedian reticular nucleus (PRN) was systematically explored for single units antidromically activated by electrical stimulation of histologically verified sites in the intermediate gray region of the upper thoracic cord (T2). These antidromically identified units were then tested for their orthodromic responses to electrical stimulation of ipsilateral carotid sinus nerve (CSN) and of pressor sites in the contralateral fastigial nucleus (FN). Sixty-two histologically verified single units, located predominantly in the caudal half of the ventral PRN, were antidromically activated with latencies corresponding to a mean conduction velocity of 36.4 +/- 2.1 m/s. Of these units 25 (40%) were excited orthodromically by stimulation of the CSN and/or FN: 5 to stimulation of the CSN only (mean latency, 18.3 +/- 9.9 ms), 6 to stimulation of the FN only (mean latency, 7 +/- 1.7 ms), and 14 to stimulation of both the CSN and FN (mean latencies, 12.3 +/- 2.9 ms and 8.4 +/- 1 ms, respectively). These data provide electrophysiological evidence for the existence of PRN reticulo-spinal neurons that integrate and relay cardiovascular afferent information from the CSN and FN to spinal autonomic neurons.     

Inhibition of cardiopulmonary input to thoracic spinothalamic tract cells by stimulation of the subcoeruleus-parabrachial region in the primate

Effects of electrically stimulating the subcoeruleus-parabrachial (SC-PB) region on 31 spinothalamic tract neurons which receive excitatory input from cardiopulmonary sympathetic afferent fibers were studied in 21 monkeys anesthetized with chloralose. A conditioning stimulus to the SC-PB region inhibited the activity of 5 cells responding to the test stimulus applied to sympathetic afferent fibers. At a conditioning-test interval of 10 ms, test responses were maximally reduced to 47 +/- 6% of the control. Inhibitory effects were present at conditioning-test intervals up to 150 ms. Excitatory effects of both A delta-and C-fiber sympathetic afferents were reduced by stimulation of the SC-PB region; however, C-fiber input was more powerfully inhibited. Intracardiac injection of the algesic agent bradykinin excited 8 of 12 spinothalamic tract neurons tested; the responding cells increased their activity from 12 +/- 13 to 31 +/- 8 impulses/s. SC-PB stimulation (212 +/- 45 microA) reduced the peak activity caused by bradykinin to 6 +/- 2 impulses/s. Aortic occlusion increased the discharge rate of 5 out of 8 neurons from 13 +/- 3 to 21 +/- 4 impulses/s. At the peak of the response of aortic occlusion, SC-PB stimulation (238 +/- 20 microA) decreased neuron activity to 3 +/- 0 impulses/s. Effective sites for inhibition of spinothalamic tract cell activity were located in the lateral and medial parabrachial nuclei and the nucleus subcoeruleus. This study demonstrates that stimulation of the dorsolateral pons can inhibit the responses of upper thoracic spinothalamic tract neurons to cardiopulmonary sympathetic afferent input. Our laboratory previously has shown that stimulation of cardiopulmonary vagal afferents inhibits spinothalamic tract cells via supraspinal mechanisms. The SC-PB region may be a site activated by cardiac vagal afferents during ischemia and therefore, may be involved in the etiology of painless myocardial infarctions.