10-Hz Rhythm Research Articles

Propofol Reversibly Attenuates Short-Range Microstate Ordering and 20Hz Microstate Oscillations.

Microstate sequences summarize the changing voltage patterns measured by electroencephalography, using a clustering approach to reduce the high dimensionality of the underlying data. A common approach is to restrict the pattern matching step to local maxima of the global field power (GFP) and to interpolate the microstate fit in between. In this study, we investigate how the anesthetic propofol affects microstate sequence periodicity and predictability, and how these metrics are changed by interpolation. We performed two frequency analyses on microstate sequences, one based on time-lagged mutual information, the other based on Fourier transform methodology, and quantified the effects of interpolation. Resting-state microstate sequences had a 20Hz frequency peak related to dominant 10Hz (alpha) rhythms, and the Fourier approach demonstrated that all five microstate classes followed this frequency. The 20Hz periodicity was reversibly attenuated under moderate propofol sedation, as shown by mutual information and Fourier analysis. Characteristic microstate frequencies could only be observed in non-interpolated microstate sequences and were masked by smoothing effects of interpolation. Information-theoretic analysis revealed faster microstate dynamics and larger entropy rates under propofol, whereas Shannon entropy did not change significantly. In moderate sedation, active information storage decreased for non-interpolated sequences. Signatures of non-equilibrium dynamics were observed in non-interpolated sequences, but no changes were observed between sedation levels. All changes occurred while subjects were able to perform an auditory perception task. In summary, we show that low dose propofol reversibly increases the randomness of microstate sequences and attenuates microstate oscillations without correlation to cognitive task performance. Microstate dynamics between GFP peaks reflect physiological processes that are not accessible in interpolated sequences.

Conscious perception and perceptual echoes: a binocular rivalry study.

Alpha rhythms (∼10Hz) in the human brain are classically associated with idling activities, being predominantly observed during quiet restfulness with closed eyes. However, recent studies demonstrated that alpha (∼10Hz) rhythms can directly relate to visual stimulation, resulting in oscillations, which can last for as long as one second. This alpha reverberation, dubbed perceptual echoes (PE), suggests that the visual system actively samples and processes visual information within the alpha-band frequency. Although PE have been linked to various visual functions, their underlying mechanisms and functional role are not completely understood. In this study, we investigated the relationship between conscious perception and the generation and the amplitude of PE. Specifically, we displayed two coloured Gabor patches with different orientations on opposite sides of the screen, and using a set of dichoptic mirrors, we induced a binocular rivalry between the two stimuli. We asked participants to continuously report which one of two Gabor patches they consciously perceived, while recording their EEG signals. Importantly, the luminance of each patch fluctuated randomly over time, generating random sequences from which we estimated two impulse-response functions (IRFs) reflecting the PE generated by the perceived (dominant) and non-perceived (suppressed) stimulus, respectively. We found that the alpha power of the PE generated by the consciously perceived stimulus was comparable with that of the PE generated during monocular vision (control condition) and higher than the PE induced by the suppressed stimulus. Moreover, confirming previous findings, we found that all PEs propagated as a travelling wave from posterior to frontal brain regions, irrespective of conscious perception. All in all our results demonstrate a correlation between conscious perception and PE, suggesting that the synchronization of neural activity plays an important role in visual sampling and conscious perception.

Systemic administration of two different anxiolytic drugs decreases local field potential theta frequency in the medial entorhinal cortex without affecting grid cell firing fields

Neurons coding spatial location (grid cells) are found in medial entorhinal cortex (MEC) and demonstrate increasing size of firing fields and spacing between fields (grid scale) along the dorsoventral axis. This change in grid scale correlates with differences in theta frequency, a 6–10Hz rhythm in the local field potential (LFP) and rhythmic firing of cells. A relationship between theta frequency and grid scale can be found when examining grid cells recorded in different locations along the dorsoventral axis of MEC.When describing the relationship between theta frequency and grid scale, it is important to account for the strong positive correlation between theta frequency and running speed. Plotting LFP theta frequency across running speeds dissociates two components of this relationship: slope and intercept of the linear fit. Change in theta frequency through a change in the slope component has been modeled and shown experimentally to affect grid scale, but the prediction that change in the intercept component would not affect grid scale has not been tested experimentally. This prediction about the relationship of intercept to grid scale is the primary hypothesis tested in the experiments presented here.All known anxiolytic drugs decrease hippocampal theta frequency despite their differing mechanisms of action. Specifically, anxiolytics decrease the intercept of the theta frequency-running speed relationship in the hippocampus. Here we demonstrate that anxiolytics decrease the intercept of the theta frequency-running speed relationship in the MEC, similar to hippocampus, and the decrease in frequency through this change in intercept does not affect grid scale.

Temporal Response Properties of Retinal Ganglion Cells inrd1Mice Evoked by Amplitude-Modulated Electrical Pulse Trains

The electrophysiological properties of degenerated retinas responding to amplitude-modulated electrical pulse trains were investigated to provide a guideline for the development of a stimulation strategy for retinal prostheses. The activities of retinal ganglion cells (RGCs) in response to amplitude-modulated pulse trains were recorded from an in vitro model of retinal prosthesis, which consisted of an rd1 mouse retinal patch attached to a planar multielectrode array. The ability of the population activities of RGCs to effectively represent, or encode, the information on the visual intensity time series, when the intensity of visual input is transformed to pulse amplitudes, was investigated. An optimal pulse amplitude range was selected so that RGC firing rates increased monotonically and linearly. An approximately 10-Hz rhythm was observed in the field potentials from degenerated retinas, which resulted in a rhythmic burst of spontaneous spikes. Multiple peaks were present in poststimulus time histograms, with interpeak intervals corresponding to the oscillation frequency of the field potentials. Phase resetting of the field potential oscillation by stimulation was consistently observed. Despite a prominent alteration of the properties of electrically evoked firing with respect to normal retinas, RGC response strengths could be modulated by pulse amplitude. Accordingly, the temporal information of stimulation could be faithfully represented in the RGC firing patterns by an amplitude-modulated pulse train. The results suggest that pulse amplitude modulation is a feasible means of implementing a stimulation strategy for retinal prostheses, despite the marked change in the physiological properties of RGCs in degenerated retinas.

Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm

We studied the changes in inferior cardiac sympathetic nerve discharge (SND) produced by unilateral microinjections of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Microinjection of the 5-HT2 receptor antagonist LY-53857 (10 mM) into either the rostral or caudal VLM significantly reduced (P < or = 0.05) the 10-Hz rhythmic component of basal SND without affecting its lower-frequency, aperiodic component. The selective depression of 10-Hz power was accompanied by a statistically significant decrease in mean arterial pressure (MAP). Microinjection of LY-53857 into the VLM also attenuated the increase in 10-Hz power that followed tetanic stimulation of depressor sites in the caudal medullary raphé nuclei. Microinjection of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI; 10 microM) into the VLM selectively enhanced 10-Hz SND, and intravenous DOI (1 mg/kg) partially reversed the reduction in 10-Hz SND produced by 5-HT2 receptor blockade in the VLM. Microinjection of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT; 10 mM), into either the rostral or caudal VLM also selectively attenuated 10-Hz SND and significantly reduced MAP. The reduction in 10-Hz SND produced by 8-OHDPAT was partially reversed by intravenous WAY-100635 (1 mg/kg), which selectively blocks 5-HT1A receptors. These results support the view that serotonergic inputs to the VLM play an important role in expression of the 10-Hz rhythm in SND.

Role of 5‐hydroxytryptamine (5‐HT2) receptors in the ventrolateral medulla (VLM) in the expression of the 10‐Hz rhythm in sympathetic nerve discharge (SND)

We have shown that chemical inactivation (muscimol or 8‐OHDPAT microinjections) of the medullary raphe selectively reduces the 10‐Hz rhythmic component in SND of baroreceptor‐denervated, urethane‐anesthetized cats. These data suggest that raphe serotonergic neurons play a role in expression of the 10‐Hz rhythm. The current study was designed to identify the brainstem regions and 5‐HT receptor type acted on by these raphe neurons. For this purpose, power in the 10‐Hz band of left and right inferior cardiac SND was measured before and after unilateral microinjections (50 nl/injection) of a 5‐HT2 receptor antagonist (10 mM LY‐53,857) or agonist (10 uM DOI) into the caudal or rostral VLM, 3.8 − 4.2 mm lateral to the midline. LY‐53,857 significantly (p ≫ 0.05) reduced 10‐Hz power (ipsilateral to the injection site) to 32 +/− 8% and 22 +/− 8% of control when injected into the caudal and rostral VLM, respectively. The 10‐Hz power recorded contralateral to the injection site was reduced to a lesser extent. Power at lower frequencies (&lt; 6 Hz) was not significantly changed in either nerve recording. DOI microinjection into either the caudal or rostral VLM produced a change in 10‐Hz power (an increase) opposite to that produced by the 5‐HT2 receptor antagonist. These results support the view that raphe neurons selectively enhance 10‐Hz SND by activating 5‐HT2 receptors on VLM neurons that comprise the rhythm generator. (Supported by HL‐33266.)

Coherent Motor Unit Rhythms in the 6–10 Hz Range During Time-Varying Voluntary Muscle Contractions: Neural Mechanism and Relation to Rhythmical Motor Control

In quasi-sinusoidal (0.5-3.0 Hz) voluntary muscle contractions, we studied the 6- to 10-Hz motor unit (MU) firing synchrony and muscle force oscillation with emphasis on their neural substrate and relation to rhythmical motor control. Our analyses were performed on data from 121 contractions of a finger muscle in 24 human subjects. They demonstrate that coherent 6- to 10-Hz components of MU discharges coexist with carrier components and coherent modulation components underlying the voluntary force variations. The 6- to 10-Hz synchrony has the frequency of the tremor synchrony in steady contractions and is also widespread and in-phase. Its strength ranges from very small to very large (MU/MU coherence >0.50) among contractions; moreover, it is not related to the contraction parameters, in accord with the notion of a distinct 6- to 10-Hz synaptic input to the MUs. Unlike the coherent MU modulations and the voluntary force variations, the in-phase 6- to 10-Hz MU components are suppressed or even eliminated during ischemia, while the respective force component is drastically reduced. These findings agree with the widely assumed supraspinal origin of the MU modulations, but they also strongly suggest a key role for muscle spindle feedback in the generation of the 6- to 10-Hz synaptic input. They therefore provide important information for the study of generators of the 6- to 10-Hz rhythm which subserves the postulated rhythmical control and is manifested as force and movement components. Moreover, they argue for a participation of oscillating spinal stretch reflex loops in the rhythm generation, possibly in interaction with supraspinal oscillators.

Actor's and observer's primary motor cortices stabilize similarly after seen or heard motor actions.

We quantified rhythmic brain activity, recorded with whole-scalp magnetoencephalography (MEG), of 13 healthy subjects who were performing, seeing, or hearing the tapping of a drum membrane with the right index finger. In the actor's primary motor (M1) cortex, the level of the approximately 20-Hz brain rhythms started to decrease, as a sign of M1 activation, approximately 2 s before the action and then increased, with a clear rebound approximately 0.6 s after the tapping, as a sign of M1 stabilization. A very similar time course occurred in the M1 cortex of the observer: the activation, although less vigorous than in the actor, started approximately 0.8 s before the action and was followed by a rebound. When the subject just heard the tapping sound, no preaction activation was visible, but a rebound followed the sound. The approximately 10-Hz somatosensory rhythm, which also started to decrease before own and viewed actions, returned to the baseline level approximately 0.6 s later after own actions than observed actions. This delay likely reflects proprioceptive input to the cortex, available only during own actions, and therefore could be related to the brain signature of the sense of agency. The strikingly similar motor cortex reactivity during the first and third person actions expands previous data on brain mechanisms of intersubjective understanding. Besides motor cortex activation before own and observed (predicted) actions, the M1 cortex of both the viewer and the listener stabilized in a very similar manner after brisk motor actions.

Role of ventrolateral medulla in generating the 10-Hz rhythm in sympathetic nerve discharge

We recorded changes in right inferior cardiac and either left inferior cardiac or left vertebral sympathetic nerve discharge (SND) produced by unilateral microinjections of GABA-A and excitatory amino acid (EAA) receptor antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Unilateral microinjections of GABA-A receptor antagonists, SR-95531 or bicuculline, into single tracks in VLM anywhere between 1 and 5 mm rostral to the obex eliminated or markedly reduced 10-Hz power in SND on both sides of the body. Low-frequency components (<6 Hz) of SND were unaffected. Complete blockade of the 10-Hz rhythm occurred with a dose of SR-95531 as low as 6.25 pmol in a 50-nl volume. Unilateral microinjections of the nonselective EAA receptor antagonist, kynurenate (KYN; 7.5 nmol), into the caudal or rostral VLM significantly reduced, but did not eliminate, 10-Hz SND ipsilateral to the injection sites, while 10-Hz SND contralateral to the injection sites was not significantly changed. These observations suggest that 1) GABAergic transmission in VLM is critical for generation of the 10-Hz rhythm, 2) the caudal and rostral portions of VLM act together to generate the 10-Hz rhythm, and 3) 10-Hz rhythm generation depends, at least in part, on tonic or phasic excitatory drive to GABAergic interneurons in caudal VLM and presympathetic neurons in rostral VLM. The data also suggest that pathways interconnecting the two halves of the brain stem play an important role in promoting 10-Hz rhythm generation.

Clozapine and prazosin slow the rhythm of head movements during focused stereotypy induced by d-amphetamine in rats

Clozapine is an efficacious, symptom-ameliorating, atypical antipsychotic drug with few extrapyramidal side effects. Clozapine has been reported either not to affect or to increase d-amphetamine-induced stereotypy, a behavior that is blocked by typical antipsychotic drugs. This work used a high-resolution measurement system to reassess clozapine's effects on d-amphetamine-induced focused stereotypy (FS) in rats. A force-plate actometer permitted the quantitation of the rhythm and vigor of movements during FS. Eight rats received a sensitizing series of doses of 5.0 mg/kg d-amphetamine sulfate, and this dosing regimen induced head movements with a rhythm near 10 Hz. Thirty minutes after d-amphetamine treatment, rats received acute clozapine (2.5-10.0 mg/kg), followed by eight, daily clozapine injections (5.0 mg/kg) given with d-amphetamine on days 2, 5, and 8. Effects of acute doses of the alpha1-noradrenergic antagonist prazosin (0.5-2.0 mg/kg) on the d-amphetamine response were also examined. Clozapine dose-dependently slowed the near 10-Hz rhythm and reduced the vigor of the d-amphetamine-induced FS. Clozapine significantly lengthened the duration of the FS phase, but the rhythm remained slowed. No evidence for tolerance to clozapine's rhythm-slowing effects was seen in the subchronic phase. Prazosin dose-dependently reduced the near 10-Hz rhythm induced by d-amphetamine, but prazosin did not lengthen the FS phase. The results show that clozapine diminished the rhythm and vigor of d-amphetamine-induced stereotyped head movements but, at the same time, lengthened the duration of the expression of the stereotypy. alpha1 antagonism is a likely contributor to the rhythm-modulating effects of clozapine.

Role of GABA in generating the 10‐Hz rhythm in sympathetic nerve discharge

The 10-Hz rhythm in SND of the cat is dependent on neurons located in the caudal and rostral ventral lateral medulla (VLM) and medullary raphe (Barman and Gebber, J Biol Rhythms 15: –379, 2000). We sought to determine whether GABA-mediated synaptic transmission in these regions is involved in 10-Hz rhythm generation. For this purpose, we recorded the discharges of the left and right inferior cardiac or the left vertebral and right inferior cardiac postganglionic sympathetic nerves in baroreceptor-denervated cats anesthetized with urethane. Unilateral microinjection of GABA-A receptor antagonists (50 nl of 1- mM solution of either SR-95531 or bicuculline) into the VLM eliminated the 10-Hz rhythm bilaterally. This was the case for injections made in single or multiple tracks in the VLM between the obex and 6 mm rostral. Recovery occurred within 3 h, and 10-Hz SND was unchanged after microinjection of vehicle (phosphate buffered saline). In contrast, the 10-Hz rhythm in SND was enhanced by multiple microinjections of the GABA antagonists into the raphe from 0 to 6 mm rostral to the obex. These results indicate that GABA-mediated synaptic inhibition in the VLM is critical for 10-Hz rhythm generation. Moreover, the data support the view that networks of neurons located bilaterally throughout the VLM act as a unit to generate the 10-Hz rhythm in SND. (Supported by NIH grant HL33266.)

Role of medullary excitatory amino acid receptors in mediating the 10-Hz rhythm in sympathetic nerve discharge of cats

We tested the hypothesis that excitatory amino acid (EAA)-mediated transmission plays a role in generating the 10-Hz rhythm in sympathetic nerve discharge (SND) of baroreceptor-denervated, urethane-anesthetized cats. Microinjection of either an N-methyl- d-aspartate (NMDA) or non-NMDA receptor antagonist into any one of three medullary regions (lateral tegmental field, rostral, or caudal ventrolateral medulla) essentially eliminated the 10-Hz rhythm in inferior cardiac SND. We conclude that EAA receptors in the medulla are critical for generation of the 10-Hz rhythm.

Functional relationship between human rolandic oscillations and motor cortical excitability: an MEG study

Synchronization and desynchronization of the neural rhythm in the brain play an important role in the orchestration of perception, motor action and conscious experience. Based on the results of electrocorticographic and magnetoencephalographic (MEG) recordings, it has been considered that human rolandic oscillations originate in the anterior bank of the central sulcus (20-Hz rhythm) and the postcentral cortex (10-Hz rhythm): the 20-Hz oscillation is closely related to motor function, while the 10-Hz rhythm is attributed mainly to sensory function. To test whether the rolandic oscillations are functionally relevant to the motor cortical excitability, we examined effects of 1-Hz repetitive transcranial magnetic stimulation (rTMS) of the left primary motor cortex (M1) on movement-related changes of the rolandic oscillations in 12 normal subjects. MEG data recorded during brisk extension of the right index finger in two different sessions (with and without rTMS conditioning) were compared. Motor-evoked potential (MEP) of the right hand muscle was also measured before and after rTMS to assess the motor cortical excitability. We found that 1-Hz rTMS over M1 significantly reduced the movement-related rebound of the 20-Hz oscillation in association with decreased motor cortical excitability. In particular, movement-related rebound of the 20-Hz rhythm was closely tied with motor cortical excitability. These findings further strengthen the notion of functional relevance of 20-Hz cortical oscillation to motor cortical excitability. In the framework of previous studies, the decrease in movement-related rebound may be regarded as a compensatory reaction to the inhibited cortical activity.

An Unusual Form of Phase Walk in a System of Coupled Oscillators

The authors describe an unusual form of phase walk (i.e., a progressive change in phase angle between coupled oscillators) using the 10-Hz rhythmic discharges of the inferior cardiac and vertebral postganglionic sympathetic nerves (CN and VN, respectively) in hypercapnic, baroreceptor-denervated, and vagotomized cats anesthetized with urethane. Unlike phase walk ascribable to weakened coupling (desynchronization of oscillators), the phase walk of VN 10- Hz activity relative to CN10-Hz activity 1) recurred on the time scale of the respiratory cycle, 2) was bidirectional with CN-VN phase angle increasing during expiration and decreasing during inspiration, and 3) occurred over a range equivalent to one-half the period of the 10-Hz rhythm rather than a full cycle. Moreover, this form of phase walk occurred during strong coupling of the 10-Hz oscillators, as reflected by CN-VN coherence values approaching 1.0. The authors propose that the bidirectional phase walk reflects a state of strong coupling of the 10-Hz oscillators controlling the CN and VN, the angle of which is reset from cycle to cycle by the continuously changing level of activity in their respiratory inputs. In addition, the data demonstrate that frequency and amplitude modulation of sympathetic nerve discharge can be independently regulated by respiratory inputs.

Activation of the 10-Hz sympathetic generator during the second phase of severe hypoxia–hypercapnia and Cushing reaction

Under urethane anesthesia, as in freely moving cats, the sympathetic nerve discharge (SND) contains a 10-Hz component, either as a single peak in the autospectra or in addition to the cardiac-related or 2–6-Hz rhythm. In this study, we examined the changes in these rhythmic SND components during the reaction to asphyxia and to sudden elevation in the intracranial pressure (Cushing reaction). In all cats included in this study, resting SND was dominated by 2–6-Hz rhythm, but a peak at 10 Hz was also present in the coherence functions. During asphyxia or Cushing reaction, the 2–6-Hz component exhibited the usual two-phase pattern of activation followed by suppression. In phase 2, however, the SND did not desynchronize, as in chloralose–urethane anesthetized cats [Am. J. Physiol. 256 (1989) R120; J. Physiol. (London) 469 (1993) 37], and the massive SND activation and the resulting pressor reaction was due to strengthening of the 10-Hz rhythm. After the ischemic reaction, the 10-Hz component diminished and 2–6-Hz rhythm recovered. These findings suggest that two-phase response to hypoxia–hypercapnia is not due to hypoxic neuronal damage but represents a physiological sympathetic reaction involving different patterns of SND.

Coupling of arterial pulse and 10-Hz rhythm in sympathetic nerve discharge

We used time series analysis to characterize the relationships among the arterial pulse (AP) and the cardiac-related and 10-Hz rhythms in sympathetic nerve discharge (SND) of urethane-anesthetized cats. We found that 10-Hz activity was more tightly coupled to the AP than to the cardiac-related rhythm. These data support the view that the dynamic coupling of AP and the 10-Hz rhythm in SND involves a direct influence of baroreceptor activity on the 10-Hz oscillator.

"Rapid" rhythmic discharges of sympathetic nerves: sources, mechanisms of generation, and physiological relevance.

Like virtually all other physiological control systems, the sympathetic nervous system controlling cardiovascular function is characterized by the presence of rhythmic activity. These include slow rhythms with frequencies at or below that of the respiration and rapid rhythms with frequencies at or above that of the heart beat. The rapid rhythms are the subject of this review. The specific questions entertained are as follows: (1) Are the rapid cardiac-related and 10-Hz rhythms inherent to central sympathetic networks, or are they imposed on sympathetic nerve discharge (SND) by extrinsic periodic inputs? (2) Does basal SND arise from an anatomically circumscribed "vasomotor center" composed of pacemaker neurons in the rostral ventrolateral medulla or from an anatomically distributed network oscillator composed of different types of brainstem neurons, none of which necessarily have intrinsic pacemaker properties? (3) Are the rapid rhythms generated by single circuits or by systems of coupled oscillators, each with a separate target? (4) Are the rapid rhythms in SND simply by-products of the sympathetic generating mechanisms, or do they subserve selective and special functions, such as the formulation of differential patterns of spinal sympathetic outflow that support particular behaviors? The controversial aspects of these issues and the state-of-the-art analytical methods used to study them are stressed in this review.

Differential pattern of spinal sympathetic outflow in response to stimulation of the caudal medullary raphe.

In urethan-anesthetized cats, frequency domain analysis was used to explore the mechanisms of differential responses of inferior cardiac (CN), vertebral (VN), and renal (RN) sympathetic nerves to electrical stimulation of a discrete region of the medullary raphe (0-2 mm caudal to the obex). Raphe stimulation in baroreceptor-denervated cats at frequencies (7-12 Hz) that entrained the 10-Hz rhythm in nerve activity decreased CN and RN activities but increased VN activity. The reductions in CN and RN discharges were associated with decreased low-frequency (</=6 Hz) power and either increased (low stimulus intensity) or decreased (high stimulus intensity) 10-Hz band power. In contrast, VN 10-Hz band power was increased at all stimulus intensities, without changes in low-frequency power. High-frequency (25 Hz) stimulation decreased low-frequency activity of CN and RN discharges in both baroreceptor-denervated and baroreceptor-intact cats, without decreasing VN low-frequency activity. We propose that the differential pattern produced by raphe stimulation involves resonance at the level of the 10-Hz oscillators and differential inhibition of follower circuits that transmit both 10-Hz and low-frequency activity to sympathetic nerves.

Defenselike patterns of spinal sympathetic outflow involving the 10-Hz and cardiac-related rhythms.

Frequency- and time-domain analyses were used to compare the effects of stimulation of the defense region of the midbrain periaqueductal gray (PAG) on the 10-Hz and cardiac-related discharges of sympathetic nerves with different cardiovascular targets. In baroreceptor-denervated cats anesthetized with urethan, PAG stimulation at frequencies equal to or higher (up to 25 Hz) than that of the free-running 10-Hz rhythm produced an immediate and sustained decrease in vertebral sympathetic nerve (VN) 10-Hz activity but increased the 10-Hz discharges of the inferior cardiac (CN) and renal (RN) nerves. In baroreceptor-innervated cats, VN cardiac-related activity was initially unchanged by high-frequency (25-Hz) PAG stimulation, or it increased along with that in the CN and RN. Later, during high-frequency PAG stimulation, when the rise in blood pressure approached its peak, VN cardiac-related activity usually was reduced below control level. At this time, the increases in CN and RN cardiac-related discharges were largely sustained. The cardiac-related discharges of the three nerves were unaffected by PAG stimulation at frequencies just below or just above that of the heartbeat. We conclude that the defenselike pattern of spinal sympathetic outflow involving the 10-Hz rhythm is different in mechanism and character from that involving the cardiac-related rhythm.

Lateral tegmental field neurons with activity correlated to the 10-Hz rhythm in sympathetic nerve discharge

Neurons in the lateral tegmental field (FTL) has been previously reported to have activity only minimally correlated (<1% of neurons tested) with the 10-Hz rhythm of the slow wave of the sympathetic nerve discharge. We report here that 10% of the neurons recently tested in the FTL could be shown to correlate with the 10-Hz rhythm. The neuron-to-nerve coherence is weaker than in other medullary areas, but is nonetheless significant.