Decerebrate Rats Research Articles

Azimuthal directional sensitivity of prepulse inhibition of the pinna startle reflex in decerebrate rats

Previous studies have indicated that the auditory midbrain, the inferior colliculus, is important for both sound localization and mediation of prepulse inhibition of the startle reflex. The present study investigated the azimuthal directional sensitivity of prepulse inhibition of the pinna startle reflex in decerebrate rats. The pinna startle reflex was measured by recording multi-unit action potentials from the cervicoauricular muscles. The startling noise burst (94 dB SPL) was produced by a stationary speaker at 0° azimuth, and the non-startling prepulse noise burst (46 dB SPL) was produced by a movable speaker whose direction was changed in the frontal azimuthal plane. The interval between the onset of the prepulse sound and the onset of the startling sound was 100 ms. The pinna reflex to the startling sound was strongly inhibited by the prepulse sound, and the inhibited startle response exhibited a flat azimuthal directional curve. In addition to further confirming that the neural pathways mediating prepulse inhibition are located in the brainstem, the present results indicate that interaural disparities of binaural inputs used for sound localization are not capable of modulating prepulse inhibition of the startle reflex.

Abnormal air-righting reflex in striatal rats.

To understand dynamic postural control of the higher brain, we compared air-righting reflexes in various decerebrate rats. Post-operative 3-5 d thalamic and mesencephalic rats displayed almost similar righting movements as intact. However, in striatal animals, coordination of righting movements was disrupted. The higher brain without cortical control could interfere with the brainstem center of the air-righting reflex.

Kinematic analyses of air-stepping in normal and decerebrate preweanling rats

We studied the ability of l-DOPA (100 mg/kg, subcutaneous) to elicit air-stepping in decerebrate and sham-operated Sprague-Dawley rats from postnatal Day 5 through postnatal Day 20. The most common gait consisted of fore- and hindlimb alternation, but between 10 and 20 days of age, patterns of coordination resembling swimming, in which the forelimbs remained adducted, and galloping became more frequent in both decerebrate and sham-operated rats. Because episodes of galloping were rarely more than two or three step cycles in length, our analyses focused on episodes of stepping in which limbs within the girdles stepped in alternation and diagonal pairs of limbs moved in synchrony (“trot”). The rate of stepping of both decerebrate and sham-operated rats increased from about 2.9 steps/s at Day 5 to about 4 steps/s at Day 20. In both groups, this increase was found to result from a decrease in the duration of the retraction phase of the step cycle. Amplitudes of movement at the wrist, knee, and ankle increased with age in both decerebrate and sham-operated neonates, whereas those of the shoulder, elbow, and hip did not change in either group. The timing of movements at joints within each limb also changed similarly with age in sham-operated and decerebrate pups. During development, forelimb movement was increasingly led by the wrist, which was followed by the elbow and then finally by the shoulder. Hindlimb movements were increasingly led by the knee, followed by the ankle, and finally by the hip. At all ages, diagonal limbs moved in synchrony, and heterolateral limbs within each girdle moved in antiphase. However, the phase relationship between hindlimb and forelimb movements changed both in sham-operated rats and in decerebrate rats during ontogeny. On Day 5, movement of each hindlimb was phase-delayed relative to that of the diagonal forelimb whereas on Days 15 and 20, the hindlimb was phase-advanced. The parallel emergence of different gaits and the similarity of coordination during diagonal progression in sham-operated and decerebrate pups show that age-related changes in gait are mediated no more rostrally than the midbrain. © 2000 John Wiley & Sons, Inc. Dev Psychobiol 36: 1–8, 2000

Fos-like immunoreactivity in the brain stem following oral quinine stimulation in decerebrate rats.

The present study compared the distribution of Fos-like immunoreactivity (FLI) following intraoral stimulation with quinine monohydrochloride (QHCl) in awake intact rats to the pattern obtained in chronic supracollicular decerebrate (CD) rats. Because the behavioral rejection response to QHCl is evident in the CD rat, it was hypothesized that the pattern of FLI in the lower brain stem should be similar in both groups. Overall, the distribution of FLI in the brain stem was quite similar in both intact and CD groups, and QHCl stimulation increased FLI in the rostral (gustatory) nucleus of the solitary tract, the parabrachial nucleus (PBN), and the lateral reticular formation (RF) compared with an unstimulated control group. The CD group differed from the intact group, however, with a trend toward less FLI in the RF and a shift in the pattern of label away from the external subdivision of the PBN. CD rats also had increased FLI in the caudal nucleus of the solitary tract, with or without intraoral infusions. The distribution of QHCl-induced FLI in the brain stem of intact rats thus indicates both local sensorimotor processing as well as the influence of forebrain structures.

Pontine carbachol elicits multiple rapid eye movementsleep-like neural events in urethane-anaesthetized rats

Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. We recorded cortical and hippocampal electroencephalograms and genioglossus and inspiratory intercostal muscle activities in 13 urethane-anaesthetized, spontaneously breathing, tracheotomized and vagotomized rats. In steady-state periods with high-voltage/low-frequency electroencephalogram activity, carbachol microinjections (15–40 nl, 10 mM) were placed in the medial pontine reticular formation. In 12 rats, carbachol elicited episodes of stereotyped hypotonia of genioglossus but not intercostal muscle activity, typical of rapid eye movement sleep, with a latency and duration of 2.2±0.3 min (mean±S.E.M.) and 11.0±2.9 min, respectively. In four of these rats, also similar to rapid eye movement sleep, the major suppression of genioglossus activity (−74±9%) was accompanied by electroencephalogram desynchronization, appearance of hippocampal theta rhythm, and a respiratory rate increase (+14±3%). In the remaining eight rats, the stereotyped suppression of genioglossus activity (−48±3%) occurred without electroencephalogram desynchronization and hippocampal theta, and was accompanied by a respiratory rate decrease (−6±2%); a pattern of response typical of decerebrate animals. Within a rat, similar patterns of response to repeated carbachol injections at the same anatomical site were obtained. Pontine atropine prevented responses to subsequent carbachol injections. Thus, in urethane-anaesthetized rats, pontine carbachol consistently produced a differential suppression of pharyngeal versus respiratory pump muscle activity, and in a subset of animals, this was also accompanied by cortical and hippocampal electrographic changes typical of rapid eye movement sleep. This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.

The posterior basal diencephalon of rats enhances expression of an activated state.

Various ablation studies have implicated the posterior basal diencephalon in the promotion of wakefulness. Although many studies have examined the role of this structure in promotion of cortical arousal, few investigations have attempted to examine its importance in regulation of motor activation (behavioral arousal). In the current study, recordings of freely moving decerebrate rats with and without a posterior basal diencephalon were performed. These studies allowed determination of the behavioral states expressed by the preparations and whether removal of the posterior basal diencephalon completely eliminated expression of both activated state with and activated state without limb movements. Muscle activity was recorded from limb and neck muscles. Eye movements and heart rate were also monitored. The percentage of time spent in various behavioral states and the proportion of limb movements expressed in each of these states were determined. Rats with an intact posterior basal diencephalon cycled between all behavioral states. However, they spent most of the recording time in an activated state. In contrast, removal of the posterior basal diencephalon produced rats that spent most of the recording period in a quiescent state. Limb movements were expressed mainly by animals with an intact posterior basal diencephalon, and only when these animals were in the activated state. The results of this study suggest that the posterior basal diencephalon is required for expression of an activated state and specifically provide evidence for a descending projection from this region required for expression of this state and associated motor activation.

Mutual inhibition between Bötzinger-complex bulbospinal expiratory neurons detected with cross-correlation in the decerebrate rat

We examined the synaptic connections between pairs of Bötzinger-complex, bulbospinal expiratory neurons in decerebrate rats. All were antidromically activated from the spinal cord at the C2-C3 border. Cross-correlation histograms of 18 ipsilateral pairs showed troughs on both sides of time zero (8) and to one side of time zero (4); most (12) were accompanied by peaks at time zero. Similarly, cross-correlation histograms of the contralateral pairs (12) showed troughs on both sides of time zero (3) and to one side of time zero (3); few (2) were accompanied by peaks at time zero. We considered the troughs in these cross-correlation histograms to be evidence of inhibition between the neurons and sought confirmation of the inhibitory connection. First, using the antidromic activation stimulus, we computed post-stimulus histograms of the extracellularly recorded discharge for six neurons and found that three showed troughs. Then, we continued this approach, computing post-stimulus averages of the membrane potentials recorded intracellularly from these neurons after iontophoresis of chloride to reverse inhibitory synaptic potentials. Depolarising potentials were observed in 15 of 16 of these averages. We interpreted these as reversed inhibitory post-synaptic potentials and concluded that Bötzinger-complex, bulbospinal expiratory neurons inhibit one another in rats as they do in cats.

Cardiovascular responses to microinjections of glutamate into the nucleus tractus solitarii of unanesthetized supracollicular decerebrate rats

In anesthetized rats, microinjections of excitatory amino acids (EAAs) into the nucleus tractus solitarii (nTS), in a region located immediately rostral to the calamus scriptorius (CS), have been generally reported to elicit depressor and bradycardic responses. On the other hand, in conscious freely moving rats, similar microinjections have been reported to elicit pressor and bradycardic responses. These divergent results have been attributed to the effect of anesthetics. A reinvestigation of the effects of EAAs into the nTS in unanesthetized animals became necessary in order to resolve this controversy. The microinjection technique used in freely moving conscious rats suffers from several technical limitations; for example, microinjections cannot be delivered stereotaxically. In order to avoid these limitations, the present experiments were carried out in unanesthetized supracollicular decerebrate rats. A systematic mapping of nTS in these rats, using microinjections of the solutions of EAAs in artificial cerebrospinal (aCSF) fluid, confirmed that depressor and bradycardic responses are elicited from all the sites in the nTS extending from the CS to a level about 1 mm rostral to it. Pressor responses were elicited by microinjections of l-glutamate ( l-Glu) only from the chemoreceptor projection site (a region of the commissural subnucleus, 0.1–0.5 mm caudal to the CS, 0–0.5 mm lateral to the midline and 0.4–0.5 mm deep from the medullary surface). The pressor responses elicited from the aforementioned site were accompanied with bradycardia; this response may be due to diffusion of l-Glu to the dorsal motor nucleus of vagus because the bradycardia disappeared when the depth of the microinjection was reduced to 0.3, instead of 0.5 mm, from the dorsal medullary surface. When urethane was administered intravenously in unanesthetized decerebrate rats, the responses to microinjections of l-Glu remained unchanged, i.e., depressor and bradycardic responses were elicited from all the sites in the nTS extending from the CS to a level about 1 mm rostral to it and pressor and tachycardic responses were elicited from the chemoreceptor projection site. These observations indicated that there is no anesthetic-induced qualitative alteration of the cardiovascular responses to microinjections of EAAs into the nTS.

Prepulse inhibition following lesions of the inferior colliculus: prepulse intensity functions

LI, L., L. M. KORNGUT, B. J. FROST AND R. J. BENINGER. Prepulse inhibition following lesions of the inferior colliculus: Prepulse intensity functions. PHYSIOL BEHAV 65(1) 133–139, 1998.—The magnitude of the acoustic startle response can be reduced by a relatively weak sound presented immediately before the startle-eliciting sound; this phenomenon has been termed prepulse inhibition (PPI). Previous studies reported that PPI was present in the decerebrate rat, indicating that the primary neural pathways mediating PPI are located in the brainstem. The present study investigated the effects of focal excitotoxic lesions of the inferior colliculus (IC) on acoustic PPI in rats. In the first part, startle magnitudes were measured in six normal rats as the interstimulus interval (ISI) between the prepulse and startle-eliciting sounds varied between 10 and 100 ms. Prepulse-inhibited startle changed in an ISI-dependent manner with the most effective ISI at 50 ms. In the second part, 21 rats were assigned to three groups: normal unoperated, cortical lesion, and IC lesion. With the ISI fixed at 50 ms, as the prepulse sound level increased from 29 to 49 dB SPL, startle responses decreased quickly in both normal and cortical lesion rats. However, rats with unilateral IC lesions made with ibotenic acid had significantly lower PPI but did not display any increase in startle magnitude. These data suggest that the IC is an important structure in the neural circuit mediating acoustic PPI.

Brain Fos-like immunoreactivity in chronic decerebrate and neurologically intact rats given 2,5-anhydro- d-mannitol

Injection of the fructose analogue, 2,5-anhydro- d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures. Because of the interconnections between brainstem and forebrain areas, it has not been possible to determine whether or to what extent induction of Fos-li in a given region reflects brainstem–forebrain interactions. We addressed this issue using chronic decerebrate (CD) rats with complete transections of the neuroaxis at the meso-diencephalic juncture. CD and neurologically intact control rats were injected (i.p.) with saline or 400 mg/kg 2,5-AM and brains were examined for Fos-li. Both intact and CD rats showed increased Fos-li in the nucleus of the solitary tract (NTS) after injection of 2,5-AM as compared with saline. 2,5-AM treatment increased Fos-li in the external lateral division of parabrachial nucleus (PBNel) in intact but not in CD rats, suggesting that descending projections from the forebrain may play a role in the activation of PBNel neurons after 2,5-AM injection. Decerebration eliminated significant 2,5-AM-induced Fos-li responses in forebrain structures, including the paraventricular nucleus, supraoptic nucleus, bed nucleus of the stria terminalis and central nucleus of the amygdala. The results are consistent with the hypothesis that the activation of forebrain structures after 2,5-AM treatment is due to stimulation by ascending projections from the brainstem.

The role of dorsal respiratory group neurons studied with cross-correlation in the decerebrate rat.

We examined the role of dorsal respiratory group (DRG) inspiratory neurons as transmitters of respiratory drive to phrenic and intercostal motoneurons and as relays of afferent information to ventral respiratory group (VRG) bulbospinal, inspiratory neurons. Attempts to antidromically activate 76 DRG neurons from the spinal cord at the C7 segment resulted in only 4 (5.3%) successes (3 contralateral, 1 ipsilateral). Cross-correlating DRG neuron discharge with that of the ipsilateral (56) and contralateral (20) phrenic nerve detected common activation peaks in 2 and 3 cases respectively, with no evidence for monosynaptic connections. Cross-correlating DRG neuron discharge with that of bulbospinal, inspiratory VRG neurons found some evidence for interaction. Peaks in 7 of 73 (10%) cross-correlation histograms were attributed to a monosynaptic excitation of DRG neurons by VRG neurons, although a common activation cannot be ruled out; troughs, some with an accompanying peak, in 9 (12.3%) histograms were interpreted as a combined excitation of the DRG neuron and delayed inhibition of the VRG neuron. In addition, 2 cross-correlation histograms showed peaks with latencies and half-amplitude widths consistent with a disynaptic excitation of a DRG neuron by a bulbospinal inspiratory VRG neuron. Cross-correlating the discharge of 57 pairs of DRG inspiratory neurons (6 contralateral) detected common activation peaks in 7 (12.3%) cases (none contralateral) and one case interpreted as evidence for a disynaptic excitation. These findings suggest that the role of the DRG inspiratory neurons in rats differs from that in cats, primarily because they do not act to transmit respiratory rhythmic drive directly to phrenic and intercostal motoneurons. The results offer some support for an excitation of DRG neurons by VRG inspiratory neurons, but no support for a role of DRG inspiratory neurons as mediators of afferent information transfer to VRG bulbospinal inspiratory neurons.

Bilaterally independent respiratory rhythms in the decerebrate rat

In rats, respiratory neurons in the medulla oblongata are arranged in longitudinally distributed groups that are duplicated on each side of the neuraxis. Our aim was to determine whether respiratory rhythm is generated independently by each side. We made a complete mid-saggital section of the medulla oblongata, 3.5 mm rostral and 3.5 mm caudal to the obex, in decerebrate, vagotomized, and paralysed adult rats. Respiratory rhythm, monitored by recording the activity of both left and right phrenic nerves, was maintained and became asynchronous between the left and right sides. We concluded that in the adult rat each half of the medulla oblongata is capable of generating respiratory rhythm independently.

Serotonin receptors in the caudal brainstem are necessary and sufficient for the anorectic effect of peripherally administered mCPP.

The role of caudal brainstem 5-HT receptors in mediating the anorectic effect of the direct 5-HT2C/1B agonist, mCPP [1-(3-chlorophenyl)piperazine dihydrochloride], was evaluated. We demonstrated, first, that systemic injections of mCPP yielded a dose-related suppression of intra-oral intake of 12.5% glucose in intact rats and in chronically maintained supracollicular decerebrate rats. The results of the decerebrate experiment suggest that 5-HT receptors in the caudal brainstem are sufficient for mediating the drug's intake effect. We also showed a dose-related intake suppression when mCPP was delivered to the fourth ventricle of intact rats, with potent suppression obtained at doses well below threshold for systemic administration. Whether and to what extent the 5-HT2C/2A antagonist, mesulergine reverses the intake suppression that follows systemic or 4th i.c.v. injection of mCPP was examined. Fourth i.c.v. co-administration of mesulergine (60 microg) and mCPP (40 microg) eliminated the approximately 50% intake suppression observed when mCPP was delivered alone, a result that affirms the receptor selectivity of the 4th i.c.v. agonist effect. We showed, further, that 4th i.c.v.mesulergine (60 microg) completely reversed the intake suppression produced by systemic mCPP (2 mg/kg). The latter result indicates that stimulation of 5-HT receptors in the caudal brainstem is necessary for the intake suppression produced by systemic administration of this 5-HT agonist in the intact rat.

Synaptic connections to phrenic motoneurons in the decerebrate rat.

Phrenic motoneuron membrane potential trajectories in decerebrate rats exhibit three stages; depolarisation during inspiration, a decreased depolarisation during early expiration and hyperpolarization during late expiration. These trajectories are a result of excitation by ventral-group medullary inspiratory neurons and upper-cervical inspiratory neurons during inspiration and the early part of expiration, and inhibition from Bötzinger-complex expiratory neurons during the late part of expiration.

Heart rate, blood pressure, and running speed responses to mesencephalic locomotor region stimulation in anesthetized rats.

The decerebrate rat locomotor preparation described in a previous study requires extensive brain surgery with the possibility of significant blood loss. The purpose of this study was to improve on the previous model by using lightly anesthetized instead of decerebrated rats. After initial surgery consisting of boring a small hole through the parietal bone, the animals were maintained on low levels of halothane anesthetic. The mesencephalic locomotor region was then located by physiological criteria using stereotaxic coordinates from the previous study. Locomotor speed, blood pressure and heart rate responses were then measured over a wide range of stimulation currents that elicited a maximal running speed. Stimulation currents ranged from 36 microA for walking to 82 microA for fast galloping. Locomotor speeds ranged from 20 m/min for walking to 64 m/min for fast galloping. Some animals easily achieved galloping speeds beyond 100 m/min. Blood pressure and heart rate increased with increasing stimulation currents. Blood pressure also increased during stimulation after muscular paralysis. This was not due to current spread, suggesting that the mesencephalic locomotor region might be involved in central command mechanisms. Heart rate did not increase after paralysis. This supports other multi-joint dynamic studies suggesting that movement per se may be necessary to induce heart rate changes, presumably via joint mechanoreceptors. The range of locomotor patterns and cardiovascular responses were obtained under self-supported conditions. By defining the mesencephalic locomotor region via physiological criteria, and by grouping blood pressure and heart rate measurements by gait rather than by stimulation currents, the potential use of the intact model for cardiovascular control studies was demonstrated. The animals were able to run and gallop at high speeds considering they were anesthetized. The simplified preparation will be useful for more complex cardiovascular experiments requiring intact and self-supported conditions.

Effects of extensor muscle afferents on the timing of locomotor activity during walking in adult rats

The influence of hind leg extensor muscle afferents on the timing of locomotor phase transitions was examined in adult, decerebrate rats, walking on a treadwheel. Walking occurred either spontaneously or was induced by stimulation of the mesencephalic locomotor region. Large diameter muscle afferents innervating the lateral or medial gastrocnemius were electrically stimulated during walking. A stimulus was delivered either at the onset of extensor muscle activity, or randomly during the step cycle. Stimulation with a train duration of 300 ms at the onset of extension increased the duration of the extensor bursts. The subsequent flexion phase was delayed. Stimulation with a shorter stimulus train (150 ms) early in extension had little effect on the extension phase duration. However when delivered at the end of extension the same stimulus significantly increased the duration of the extension phase and decreased the duration of the following flexion phase. Stimulating near the end of the flexion phase delayed onset and decreased duration of the subsequent extension phase. The effects of stimulating extensor afferents during the extension phase were weaker but qualitatively similar, to those in cats, suggesting similar mechanisms. The results of this study also show major differences in the integration of extensor muscle afferents between adult and neonatal rats.

Is the pontine pneumotaxic center necessary for eupneic respiration?

Respiration consists of three phases – inspiration (I), post-inspiration (post-I), and late expiration (E2). Pre-I is a subphase occurring at the end of E2. Hypoglossal (XII) discharge contains I and occasionally pre-I activity. Functionally, XII pre-I underlies tongue muscle contraction and expansion of the upper airway, causing a decrease in airway resistance in anticipation of the succeeding inspiratory effort. It has been shown that vagotomy causes an increase in pre-I activity in XII in anesthetized animals. Also, in anesthetized artificially-ventilated animals, XII onset is synchronized with that of inspiratory phrenic nerve (PhN) activity. Therefore, we sought to systematically test the hypothesis that XII pre-I is present in vagus-intact unanesthetized decerebrate animals and vagal afferents negatively modulate XII pre-I discharge in decerebrate rats, in the absence of confounding anesthesia. Experiments were performed on seven Sprague-Dawley unanesthetized decerebrate adult male rats and bilateral PhN and XII recordings performed. In three animals, vagotomy was performed during PhN recordings and one animal was vagotomized during initial surgical preparation prior to recordings. In vagus-intact animals, XII pre-I duration averaged 12.4 ms. Vagotomy was associated with greater XII pre-I duration, expressed in absolute time (89.5 vs. 12.4 ms; p < 0.01) as well as relative to the XII bursting period (18.9 vs. 3.4%; p < 0.01). Vagal deafferentation was also associated with a larger relative amplitude of the pre-I XII activity relative to total XII discharge (12.4 vs. 2.1%; p < 0.01). We conclude that pre-I discharge is present in vagus-intact artificially-ventilated unanesthetized decerebrate animals and is negatively modulated by vagal afferents.

Spontaneous activity of otolith-related vestibular nuclear neurons in the decerebrate rat

The discharge properties of lateral and descending vestibular neurons responsive to constant velocity off-vertical axis rotations (OVAR) in the clockwise (CW) and counterclockwise (CCW) directions, were studied at the stationary and earth-horizontal position of decerebrate adult rats. From the coefficient of variation (CV), the spontaneous activities of OVAR-responsive neurons were classified into regular and irregular patterns. Of the neurons (n = 36) that showed symmetric and stable bidirectional response sensitivity (δ defined as CW gain over CCW gain) to OVAR (10° tilt), some exhibited progressive phase shift with velocity (1.75–15°/s) while others exhibited stable response phase. Most neurons of the former group (93% or 1213) showed regular discharge pattern while only 22% (n = 523) of the latter group showed such a pattern. Though the phase-stable neurons showed a significantly higher average CV than the phase-shifted neurons, there was no significant difference between the mean spontaneous firing rates of these neurons. The neurons (n = 17) that showed asymmetric and variable δ to OVAR velocity can also be grouped - those that exhibited a greater gain with rotations directed towards the side of recording (I neurons) showed irregular discharge pattern while those that exhibited a greater gain with rotations directed towards the side contralateral to recording (C neurons) showed regular discharge pattern. The I and C neurons also exhibited significant difference in mean firing rates. The relationship between the response characteristics of the OVAR-responsive neurons and their spontaneous activity at the stationary and earth-horizontal position is discussed.

Spinal connections of ventral-group bulbospinal inspiratory neurons studied with cross-correlation in the decerebrate rat.

We examined the synaptic connections from ventral-group bulbospinal inspiratory neurons to upper-cervical inspiratory neurons and phrenic and intercostal motoneurons in decerebrate rats using cross-correlation. Inspiratory neurons were recorded in the medulla (n = 28) at the level of the obex and from the upper-cervical segments (C1 and C2) of the spinal cord (n = 29) in 18 vagotomized, paralyzed, ventilated, and decerebrated rats. The neurons were identified by their inspiratory firing pattern and antidromic activation from the spinal cord at C7. Whole-nerve recordings were made using bipolar electrodes from the central cut ends of the C5 phrenic nerve and the external and internal intercostal nerves at various thoracic levels. Cross-correlation histograms were computed between these recordings to detect short time scale synchronizations indicative of synaptic connections. Cross-correlation histograms (n = 20), computed between the activities of ventral-group bulbospinal inspiratory neurons and the phrenic nerve, all showed peaks (mean half-amplitude width +/- SD, 1.1 +/- 0.3 ms) at short latencies (mean latency +/- SD, 2.0 +/- 0.6 ms) suggestive of monosynaptic excitation. Cross-correlation histograms (n = 33), computed between the activities of ventral-group bulbospinal inspiratory neurons and upper-cervical inspiratory neurons, displayed four (12%) peaks (mean half-amplitude width +/- SD, 0.9 +/- 0.1 ms) at short latencies (mean latency +/- SD, 1.8 +/- 0.6 ms) suggestive of monosynaptic excitation, and six (18%) peaks (mean half-amplitude width +/- SD, 1.4 +/- 0.4 ms) at latencies near zero suggestive of excitation from a common source. Cross-correlation histograms (n = 34), computed between the activities of ventral-group bulbospinal inspiratory neurons and the internal and external intercostal nerves at various thoracic levels (T2-8), showed six (18%) peaks (mean half-amplitude width +/- SD, 2.5 +/- 0.5 ms) at short latency (mean latency +/- SD, 4.5 +/- 1.1 ms) suggestive of oligosynaptic connections. Cross-correlation histograms (n = 42) computed between activities of intercostal nerves at various levels of the thoracic spinal cord showed central peaks suggestive of excitation from a common source. Although the size of the peaks decreased with segmental separation, the displacement of the peaks from time zero did not increase with segmental separation (mean displacement +/- SD, 0.6 +/- 0.6 ms) as would be expected if the common excitation resulted from a descending monosynaptic excitation by a source such as the ventral-group bulbospinal inspiratory neurons. We conclude that all ventral-group bulbospinal inspiratory neurons make monosynaptic connections to phrenic motoneurons, a few make monosynaptic connections to upper-cervical, inspiratory neurons, but connections to intercostal motoneurons are made via interneurons.

Connections from upper cervical inspiratory neurons to phrenic and intercostal motoneurons studied with cross-correlation in the decerebrate rat.

We examined the synaptic connections from upper cervical inspiratory neurons to phrenic and intercostal motoneurons in decerebrate rats using cross-correlation. Upper cervical inspiratory neurons (n = 79) were recorded from the C1 and C2 segments of the spinal cord in 38 vagotomized, paralyzed, ventilated, and decerebrate rats. The neurons were identified by their inspiratory firing pattern and antidromic activation from the ipsilateral spinal cord at C7. Whole-nerve recordings were made using bipolar electrodes from the central cut ends of the C5 phrenic nerve and the external and internal intercostal nerves at various thoracic levels. Cross-correlation histograms were computed between these recordings to detect short time-scale synchronizations indicative of synaptic connections. The 55 cross-correlation histograms computed between the upper cervical inspiratory neurons and the ipsilateral phrenic nerve showed seven (13%) narrow peaks (mean half-amplitude width +/- SD, 1.09 +/- 0.15 ms) at short latencies (mean latency +/- SD, 1.29 +/- 0.26 ms) suggestive of monosynaptic excitation, and four (7%) broader peaks (mean half-amplitude width +/- SD, 1.50 +/- 0.17 ms) at short latencies (mean latency +/- SD, 1.40 +/- 0.24 ms) suggestive of oligosynaptic excitation. Another 14 (25%) cross-correlation histograms displayed a central broad peak (mean half-amplitude width +/- SD, 1.59 +/- 0.23 ms) suggestive of common activation. The eight cross-correlation histograms computed between the upper cervical inspiratory neurons and the contralateral phrenic nerve were featureless. The 77 cross-correlation histograms computed between the upper cervical inspiratory neurons and the internal and external intercostal nerves at various thoracic levels (T2-8) showed no peaks suggestive of synaptic connections. We conclude that some upper cervical inspiratory neurons make monosynaptic and paucisynaptic connections to phrenic motoneurons but not to intercostal motoneurons.