Unanesthetized Cats Research Articles

Intrathecal blockade of both NMDA and non-NMDA receptors attenuates the exercise pressor reflex in cats.

In decerebrate unanesthetized cats we tested the hypothesis that glutamatergic-receptor blockade in the lumbosacral spinal cord attenuated the reflex increases in mean arterial pressure, inspired minute ventilation, and renal sympathetic nerve activity (RSNA) evoked by static contraction of the triceps surae muscles. Blockade of N-methyl-D-aspartate (NMDA) receptors by intrathecal injection of DL-2-amino-5-phosphonovaleric acid had no effect on the initial phase of the pressor, ventilatory, and RSNA responses to contraction but did attenuate the secondary phase of these responses. Subsequent blockade of non-NMDA receptors in the lumbosacral spinal cord by intrathecal injection of 6-cyano-7-nitroquinoxaline-2,3-dione attenuated both the initial phase of the pressor, RSNA, and ventilatory responses to contraction and the secondary phase of these responses. In addition, NMDA-receptor blockade had no effect on the pressor or RSNA responses to tendon stretch, whereas non-NMDA-receptor blockade abolished these responses. We confirmed that our results were not related to the order of the antagonists injected by performing a series of experiments in which a non-NMDA-receptor antagonist was injected first. Our findings suggest that non-NMDA receptors mediate the spinal transmission of the initial and secondary phases of the pressor, RSNA, and ventilatory responses to contraction and tendon stretch. Therefore, non-NMDA receptors in the dorsal horn appear to be involved in the spinal processing of input from mechanoreceptors and metaboreceptors. Our findings also suggest that NMDA receptors mediate the spinal transmission of the secondary phase of the pressor, RSNA, and ventilatory responses to contraction but do not mediate the spinal transmission of the responses to tendon stretch. Therefore, NMDA receptors in the dorsal horn appear to be involved in the spinal processing of input from metaboreceptors.

Changes in end-expiratory lung volume and diaphragmatic activity during hypoxia and hypercapnia in cats.

To assess the role of diaphragmatic activity at the end of expiration (DE) in the control of end-expiratory lung volume (EELV), 1) these two parameters were correlated in anesthetized cats breathing different gas mixtures; and 2) expiratory flow volume curves in normoxia and hypoxia together with changes in esophageal pressure were measured. The influence of volume feedback on DE control was tested by applying positive end-expiratory pressure (PEEP). The effect of anesthesia was determined by measuring DE in unanesthetized cats. In hyperoxia, DE (but not EELV) decreased. In hypocapnic hypoxia (12, 10, and 8% O2), both DE and EELV gradually increased, and these changes were significantly correlated. When normocapnia was restored in 8% O2, DE and EELV decreased but remained higher than in air. Hypercapnia affected neither DE nor EELV. PEEP blocked the hypoxia-induced increase in DE. Hypoxia decreased expiratory flow and esophageal pressure. Finally, the increases in DE at 12 and 10% O2 were more pronounced when the cats were unanesthetized. These results suggest that the increase in diaphragmatic activity induced by hypocapnic hypoxia during expiration affects expiratory flow and thoracic volume and, therefore, plays a major role in increasing EELV. This phenomenon may also be controlled by volume feedback.

PS-23-8 Treatment of spasticity with repetitive magnetic stimulation; a double-blind placebo-controlled study

The effects of cyclobenzaprine on spinal synaptic transmission were studied in spinal unanesthetized cats. The drug, in cumulative doses up to 20 mg/kg, depressed monosynaptic reflexes evoked by stimulation at 0.2 Hz to a moderate degree. Polysynaptic reflexes were depressed to a similar extent. Monosynaptic reflexes evoked repeatedly at 5 and 10 Hz were depressed even after 5 mg/kg of cyclobenzaprine. Maximum potentiation of monosynaptic responses after tetanization was not affected. Neither direct postsynaptic nor recurrent inhibition was influenced by the drug. Presynaptic inhibition was slightly reduced. It is suggested that direct effects of cyclobenzaprine at the spinal level do not represent the primary site of action responsible for its antispastic activity.

Pertussis toxin-sensitive G proteins mediate carbachol-induced REM sleep and respiratory depression.

Microinjecting cholinomimetics into the medial pontine reticular formation (mPRF) of conscious cats causes a rapid eye movement (REM) sleep-like state and state-dependent respiratory depression. Muscarinic receptors within the mPRF have been shown to mediate this state-dependent respiratory depression, but the specific signal transduction mechanisms remain poorly understood. This study tested the hypothesis that the cholinergically induced REM sleep-like state and state-dependent respiratory depression are mediated by guanine nucleotide binding proteins (G proteins). Cholera toxin, pertussis toxin, 5'-guanylylimidodiphosphate, and forskolin were microinjected alone and in combination with carbachol into the mPRF of intact unanesthetized cats. All of the G protein-altering compounds significantly reduced the ability of carbachol to produce the REM sleep-like state. Pertussis toxin caused the greatest decrease in the percent of time spent in the carbachol-evoked REM sleep-like state, showing for the first time mediation by a pertussis toxin-sensitive (Gi- or G(o)-like) G protein. Cholera toxin blocked the carbachol-induced respiratory depression, indicating mediation by a Gs-like G protein. Forskolin significantly decreased carbachol-evoked REM sleep. These data provide the first demonstration that adenylyl cyclase within the mPRF contributes to the carbachol induction of REM sleep and respiratory depression.

Activity of rostral trigeminal sensory neurons in the cat during wakefulness and sleep.

1. Relatively little is known about the activity of trigeminal sensory neurons during naturally occurring behavioral states of sleep and wakefulness. Accordingly, experiments were performed in chronic unanesthetized behaving cats in which neuronal activity in the rostral trigeminal sensory nuclear complex (TSNC) was recorded extracellularly in response to low-intensity stimulation of mandibular and maxillary divisions of cranial V nerve. The peripheral responses of TSNC neurons were evaluated during naturally occurring episodes of wakefulness, quiet sleep, and active sleep. 2. The location of the rostral TSNC was confirmed by recording characteristic orthodromic field potentials generated in response to afferent volleys from tooth pulp and inferior alveolar (IAN) nerve stimuli. Antidromic fields from the trigeminal (MotV) and facial (MotVII) motor pools were used to demarcate the anterior and posterior limits of the rostral TSNC (i.e., main sensory nucleus and nucleus oralis pars gamma). 3. In the absence of peripherally applied stimuli, individual rostral TSNC neurons recorded in the chronic, unanesthetized cat during the behavioral state of wakefulness did not display ongoing spike activity. 4. The response characteristics of individual TSNC neurons to low-intensity stimuli delivered to V afferents emanating from the canine tooth pulps during the behavioral state of drowsy wakefulness consisted of a short train of action potentials characterized by a short latency-to-onset (7.2 +/- 0.4 ms, mean +/- SE, n = 51). TSNC neurons fell into two categories on the basis of their response to graded intensities of tooth pulp stimuli. "Stimulus intensity-dependent" neurons demonstrated evoked responses that had a response profile that increased with stimulus intensity. In contrast, the response profile of "stimulus intensity-independent" neurons remained stable irrespective of the stimulus intensity used. 5. During episodes of wakefulness and quiet sleep, IAN-evoked orthodromic fields did not differ in their amplitude or other waveform parameters. However, during active sleep, the IAN-evoked orthodromic field potential was suppressed by an average of 28% as compared with wakefulness. 6. The number of action potentials evoked by consecutive presentation of low-intensity tooth pulp stimuli were compared during sleep and wakefulness. The evoked responses were suppressed during active sleep (29%, n = 42). Suppression observed during active sleep occurred in both ("stimulus-dependent" and "stimulus-independent") groups of TSNC neurons. During the phasic rapid-eye-movement (REM) episodes of active sleep, both the orthodromic field potentials and unitary action potentials were further suppressed or abolished. 7. The conclusion is reached that synaptic transmission through the rostral trigeminal sensory nucleus is dependent on the behavioral state of the animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Respiratory nuclei share synaptic connectivity with pontine reticular regions regulating REM sleep.

Injection of cholinomimetics into the medial pontine reticular formation (mPRF) of intact, unanesthetized cat causes a rapid eye movement (REM) sleep-like state and respiratory depression. The mPRF contains no concentrations of respiratory neurons, and this study examined the hypothesis that respiratory depression evoked from the mPRF is synaptically mediated. The mPRF of conscious cats was injected with bethanechol to define an mPRF zone causing state-dependent respiratory depression. Bethanechol caused a 361% increase in the REM sleep-like state and a 37% decrease in minute ventilation. Additional cats were injected with the retrograde fluorescent tracers True Blue and either Fluoro-Gold or Diamidino Yellow aimed for the cholinoceptive mPRF or for the pontine respiratory group (PRG). After mPRF dye injection, 1) labeling was observed in the PRG, dorsal respiratory group (DRG), and ventral respiratory group (VRG); and 2) double-labeled cells were observed in the VRG and PRG. Dye injections into the PRG produced contralateral and ipsilateral fluorescent labeling of the mPRF, DRG, and VRG. Thus cholinoceptive regions of the mPRF involved in REM sleep generation have reciprocal monosynaptic connections with the PRG and receive monosynaptic projections from the DRG and VRG.

Coordination of the cardiac-related discharges of sympathetic nerves with different targets

Partial coherence analysis was used to remove the influences of pulse-synchronous baroreceptor nerve activity (as reflected by the arterial pulse) on the coherence of the cardiac-related discharges of sympathetic nerve pairs in unanesthetized decerebrate cats. It can be predicted that the peak at the heart rate frequency in the ordinary coherence function relating the discharges of two nerves will be eliminated by either partialization using the arterial pulse or surgical baroreceptor denervation, if the central circuits controlling the nerves share baroreceptor inputs but are not interconnected. Contrary to this prediction, in many experiments the peak was not eliminated by partialization using the arterial pulse. Moreover, partialization often nonuniformly reduced the peaks at the heart rate frequency in the coherence functions for different nerve pairs. These results are consistent with a model of multiple routes over which baroreceptor influences are distributed to the central circuits controlling different sympathetic nerves. Specifically, we propose that the direct route from the baroreceptors to each of the central circuits is complemented by cross talk among the central circuits.

Plasticity in spinal opioid control of lower urinary tract function in paraplegic cats.

Spinal cord injury disrupts micturition reflexes, which produces morbidity. The contribution of endogenous opioid systems to urinary retention were assessed in chronic spinal cats by administering the opioid receptor antagonist, naloxone (5-500 micrograms kg-1, i.p.), to unanesthetized paraplegic cats while monitoring lower urinary tract function and observing hind limb reflexes. While naloxone had no overt effect in acute spinal cats, in chronic spinal cats naloxone induced the release of large volumes of urine and produced marked hind limb hyper-reflexia. Prominent tachyphylaxis and tolerance to the effects of naloxone were evident. Immunohistochemical studies indicated a marked increase in leucine enkephalin and dynorphin in sacral spinal neurons. Together, these data indicate hyperactivity of the endogenous spinal opioid system following recovery from spinal cord injury and, furthermore, suggest that the spinal neural circuitry may become 'dependent' upon elevated levels of endogenous opioid peptides.

Pontine cholinergic reticular mechanisms cause state-dependent changes in the discharge of parabrachial neurons

The present study examined the hypothesis that cholinoceptive reticular mechanisms in the gigantocellular tegmental field (FTG) of the medial pontine reticular formation cause state-dependent changes in the discharge of parabrachial neurons. In chronically implanted, unanesthetized cats, extracellular recordings were made from nonrespiratory and respiratory neurons in the parabrachial nuclear complex (PBNC) during the natural sleep-wake cycle and during the rapid eye movement (REM) sleeplike state caused by FTG microinjection of carbachol or neostigmine. PBNC cells that increased discharge during natural REM sleep (REM-on cells) revealed similar increased discharge during the carbachol-induced REM sleeplike state (DCarb). Cells that decreased discharge in natural REM sleep (REM-off cells) displayed decreased discharge during both DCarb and the neostigmine-induced REM sleeplike states. The limited sample of parabrachial respiratory neurons revealed significantly diminished discharge during the cholinergically induced REM sleeplike state. Thus cholinoceptive mechanisms localized to specific regions of the pontine reticular formation can cause state-dependent changes in the firing rates of respiratory and nonrespiratory neurons in the PBNC.

Changes of laryngeal reflex after cough reflex in unanesthetized decerebrate cats

Changes of laryngeal reflex after cough reflex in unanesthetized decerebrate cats

Effect of electrical stimulation of the hypoglossal nerve on airflow mechanics in the isolated upper airway.

To determine the influence of electrical hypoglossal (HG) nerve stimulation on upper airway airflow mechanics, we analyzed pressure-flow relationships obtained during bilateral supramaximal HG nerve stimulation over a range of frequencies from 0 to 100 Hz in the isolated feline upper airway. Inspiratory airflow (VI), hypopharyngeal pressure (Php), and pharyngeal pressure (Pph) immediately upstream from the flow-limiting site (FLS) were recorded while Php was rapidly lowered to achieve inspiratory flow limitation in the isolated upper airway. Pressure-flow relationships were analyzed to determine the maximum in VI (VImax) and the mechanical determinants of VImax, the upper airway critical pressure (Pcrit) and the nasal resistance (RN) upstream to the FLS. In groups of decerebrate spinally anesthetized (n = 6) and unanesthetized (n = 6) cats, graded increases in VImax (p < 0.05) and decreases in Pcrit (p < 0.001) were observed as the stimulation frequency of the intact HG nerves was increased. In the cats with and without spinal anesthesia, VImax increased by 139 and 201%, and Pcrit decreased by 159 and 280%, respectively. RN was also correlated with stimulation frequency in the cats without spinal anesthesia (p = 0.01) and increased in four of six cats with spinal anesthesia. In an additional six decerebrate cats, significant increases in VImax (p < 0.001) and decreases in Pcrit (p = 0.01) were elicited by stimulating the distal cut HG nerve ends (50 Hz), whereas no changes were noted in these parameters when the proximal ends were stimulated. The findings suggest that HG stimulation increases VImax by decreasing Pcrit, which indicates a decrease in upper airway collapsibility at the FLS.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscarinic cholinoceptive reticular mechanisms and parabrachial neuron discharge: a novel experimental approach.

This study examined the hypothesis that cholinergic receptor mechanisms within the gigantocellular tegmental field (FTG) of the medial pontine reticular formation can cause state-dependent changes in the firing rates of parabrachial nuclear complex (PBNC) neurons. Using intact, unanesthetized cats, long-term recordings were obtained from single PBNC neurons following FTG administration of cholinergic agonists and antagonists. We show that the state-dependent decrease in PBNC cell discharge reported in this study can be attributed to muscarinic mechanisms within the FTG. Our pharmacological blocking results further suggest that diminished PBNC discharge was mediated by non-M1 muscarinic receptors in the FTG. This study demonstrates the usefulness of combining long-term neuronal recordings in the PBNC with multiple pharmacological manipulations within the FTG.

Pedunculopontine stimulation alters respiration and increases ACh release in the pontine reticular formation.

The present study examined the hypothesis that cholinergic neurons in the pedunculopontine tegmental nucleus (PPT) can cause the release of acetylcholine (ACh) in the pontine reticular formation and contribute to respiratory depression. In vivo microdialysis of the gigantocellular tegmental field (FTG) was performed in 10 adult male cats while respiration was being measured. In four intact, unanesthetized cats these measurements were obtained during states of quiet wakefulness and during the rapid eye movement (REM) sleeplike state caused by FTG microinjections of carbachol. The results demonstrate a simultaneous time course of enhanced ACh release in the FTG and respiratory rate depression. In six barbiturate-anesthetized cats similar measurements were obtained while PPT regions containing NADPH-positive neurons were electrically stimulated. PPT stimulation caused increased ACh release in the FTG and caused respiratory rate depression. Together, these findings are consistent with the hypothesis of a causal relationship between ACh release in the FTG and respiratory depression.

Medullary respiratory neuronal activity during augmented breaths in intact unanesthetized cats.

In intact unanesthetized cats, we studied the behavior of five medullary respiratory cell types during augmented breaths: 1) decrementing, 2) augmenting, and 3) late-onset inspiratory cells and 4) decrementing and 5) augmenting expiratory cells. Certain features of their behavior were inconsistent with either their proposed role in rhythmogenesis or the proposed nature of augmented breaths. For example, decrementing inspiratory cells switched to an augmenting pattern during the second part of the augmented breath. This behavior is inconsistent with mechanisms proposed to account for their decrementing pattern and with their postulated inhibitory actions on augmenting inspiratory cells, which are intensely active at the same time. In addition, augmenting expiratory cells discharged intensely at the end of inspiration and then throughout expiration, indicating that their discharge profiles (and, therefore, their inhibitory actions) are more labile than previously assumed. The behavior of inspiratory cells gave mixed evidence of the idea that the augmented breath comprises two inspiratory phases: decrementing and late-onset inspiratory cells discharged in two bursts during the inspiratory phase, but other inspiratory cells discharged without interruption throughout it. These results reveal that current theories do not account for the behavior of medullary respiratory cells during augmented breaths.

Changes in membrane potential and postsynaptic potentials evoked by strychnine in neocortical neurons

Intracellular responses of neurons of the suprasylvian fissure to intracortical stimulation before and during topical cortical strychnine application was studied in experiments on immobilized, unanesthetized cats (a local anesthetic was used). Untreated cortical neurons responded to intracortical stimulation with a monosynaptic excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). Application of strychnine evoked epileptiform population activity and paroxysmal depolarizations of neuronal membrane potentials (MPs), followed by hyperpolarization. Increased hyperpolarizations, and the prolonged duration of their summation were responsible for an increased MP and reduced or abolished tonic spike activity. Intracellular application (as a result of diffusion from the microelectrode) of ethyleneglycoltetraacetate (EGTA) that blocked the calcium-dependent potassium membrane conductance (gK(Ca)) abolished the hyperpolarization. The development of epileptiform activity was accompanied by reduction of the IPSP, and an increase in the monosynaptic EPSP. The role of gK(Ca) and postsynaptic inhibition in epileptogenesis is discussed.

Control of torque direction by spinal pathways at the cat ankle joint.

To study the biomechanics of the calcaneal tendon's complex insertion onto the calcaneus, we measured torque-time trajectories exerted by the triceps surae and tibialis anterior muscles in eight unanesthetized decerebrate cats using a multi-axis force-moment sensor placed at the ankle joint. The ankle was constrained to an angle of 110 degrees plantarflexion. Muscles were activated using crossed-extension (XER), flexion (FWR), and caudal cutaneous sural nerve (SNR) reflexes. Torque contributions of other muscles activated by these reflexes were eliminated by denervation or tenotomy. In two animals, miniature pressure transducers were implanted among tendon fibers from the lateral gastrocnemius (LG) muscle that insert straight into the calcaneus or among tendon fibers from the medial gastrocnemius (MG) that cross over and insert on the lateral aspect of calcaneus. Reflexively evoked torques had the following directions: FWR, dorsiflexion and adduction; SNR, plantarflexion and abduction; and XER, plantarflexion and modest abduction or adduction. The proportion of abduction torque to plantarflexion torque was always greater for SNR than XER; this difference was about 50% of the magnitude of abduction torque generated by tetanic stimulation of the peronei. During SNR, pressures were higher in regions of the calcaneal tendon originating from MG than regions originating from LG. Similarly, pressures within the MG portion of the calcaneal tendon were higher during SNR than during XER, although these two reflexes produced matched ankle plantarflexion forces. Selective tenotomies and electromyographic recordings further demonstrated that MG generated most of the torque in response to SNR, while soleus, LG, and MG all generated torques in response to XER.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of vagal afferents inhibits locomotion in mesencephalic cats

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7-25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.

Short-term modulation of cerebellar Purkinje cell activity after spontaneous climbing fiber input.

1. There are two opposite points of view concerning the way climbing fiber input in a Purkinje cell modifies simple spike (SS) activity transiently: depression versus enhancement of SS activity. The different groups of investigators favored one effect predominating over the other. In the decerebrate unanesthetized cat, we recorded spontaneous activity of single Purkinje cells and investigated time course of SS activity after the complex spike (CS). 2. In the peri-CS time histogram, there was a SS pause lasting, on average, 10.8 ms after onset of the CS in all of the 316 cells recorded. The pause was followed by a rapid increase in SS activity to a maximum, which was on average 175.6% of a pre-CS control level, and a gradual return to around the control level in the majority of the cells recorded (pause-facilitation type, 71.2%). The increase in SS activity was significant (P < 0.01, t test) during 20-100 ms. The SS activity during the 20-100 ms was, on average, 163.7% of the control level. In some cells (pure-pause type, 25.3%), no significant changes were found (P > 0.01) in the post-pause SS firing. In contrast, only 3.5% of the cells (pause-reduction type) showed a significant (P < 0.01) firing decrease (average 54.0% of the control level) lasting 20-60 ms after the pause period. 3. Analysis of the pre-CS time histogram revealed no significant differences (P > 0.01) in the SS activity between pre-CS periods in all of the cells recorded, suggesting that the SS activity enhancement is not due to a coactivated mossy fiber input just preceding the activation of the climbing fiber input. 4. Analysis of the raster diagram revealed variability of individual SS responses after the CS. The probability of occurrence of the increase in SS number during a post-CS period of 0-100 ms with respect to that during a pre-CS period of -100-0 ms in individual raster traces was high (on average 78.2%), medium (57.3%), and low (36.3%) in the pause-facilitation, pure-pause, and pause-reduction types of the cell, respectively. 5. Nonsequential time histograms showing frequency distribution of the pause duration after the CS in individual raster traces and that showing interspike intervals of the SS were constructed.(ABSTRACT TRUNCATED AT 400 WORDS)

Differential inhibition by ethanol of norepinephrine- and clonidine-induced emesis in cats

The effect of acute ethanol administration into the cerebral ventricles on the unanesthetized cat upon emesis produced by norepinephrine and clonidine injected similarly as well as upon emesis evoked by copper sulfate given orally was compared and investigated. Ethanol inhibited the norepinephrine- and clonidine-induced emesis. The inhibitory effect of ethanol occurred after a transient and inconsistent emetic action of the drug. Norepinephrine-induced emesis was about 12 times more sensitive than clonidine-induced emesis to the inhibitory effect of ethanol. In addition, norepinephrine-, but not clonidine-induced emesis was abolished after ablation of the area postrema. On the contrary, intracerebroventricular ethanol had virtually no effect on emesis caused by intragastric copper sulfate. The inhibitory effect of ethanol is ascribed to an action on alpha-2 adrenoceptors within the area postrema and on imidazoline-preferring sites and/or muscarinic cholinoceptors outside the area postrema, but not on the emetic region of the brainstem reticular formation. It follows then that ethanol can differentiate alpha-2 adrenoceptors from imidazoline-preferring sites and/or muscarinic cholinoceptors in the brain of the cat.

The 10-Hz rhythm in sympathetic nerve discharge.

Frequency-domain analysis was used to characterize the relationships among the rhythmic discharges recorded simultaneously from two to four sympathetic nerves in unanesthetized decerebrate cats. The major new findings were as follows. 1) The 10-Hz rhythmic discharges of different nerves cohered strongly in baroreceptor-innervated and -denervated cats. 2) The interval between the discharges of two nerves was frequency dependent in the 10-Hz band in some cats, supporting the view that the 10-Hz rhythm is generated by multiple central circuits that are coupled. 3) In some cases the central circuits responsible for the 10-Hz rhythms nonuniformly affected different nerves. 4) In baroreceptor-innervated cats the coherence values for the cardiac-related discharges of any two nerves were significantly higher than those for the 10-Hz rhythms. 5) In baroreceptor-denervated cats the 10-Hz rhythmic discharges of different nerves cohered more strongly than the 2- to 6-Hz rhythms. 6) The 10-Hz rhythm usually was not a harmonic of the 2- to 6-Hz or cardiac-related rhythm. Thus these rhythms are generated independently.