This study was designed to test the hypothesis that the medullary lateral tegmental field (LTF) is an important synaptic relay in the baroreceptor reflex pathway controlling sympathetic nerve discharge (SND) of urethan-anesthetized cats. We determined the effects of blockade of excitatory amino acid-mediated neurotransmission in the LTF on three indexes of baroreceptor reflex function: cardiac-related power in SND, strength of linear correlation (coherence value) of SND to the arterial pulse (AP), and inhibition of SND during increased arterial pressure produced by abrupt obstruction of the abdominal aorta. Bilateral microinjection of D-(-)-2-amino-5-phosphonopentanoic acid, an N-methyl-D-aspartate (NMDA) receptor antagonist, abolished cardiac-related power and coherence of SND to the AP, and it prevented inhibition of SND during aortic obstruction. These data support the view that NMDA receptor-mediated neurotransmission in the LTF is critical for baroreceptor reflex control of SND. Bilateral microinjection of 1,2, 3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]-quinoxaline-7-sulfonamid e, a non-NMDA receptor antagonist, decreased cardiac-related power and total power in the 0- to 6-Hz band of SND; however, the AP-SND coherence value remained high, and inhibition of SND during aortic obstruction was preserved. These data imply that non-NMDA receptor-mediated neurotransmission in the LTF is involved in setting the level of excitatory drive to sympathetic nerves.
We studied the following properties of cat ventrolateral medullary (VLM) neurons that projected to the thoracic spinal cord: the relationship between their spontaneous activity and that in the inferior cardiac postganglionic sympathetic nerve, their responses to baroreceptor-reflex activation, their axonal conduction velocities, the funicular trajectories of their axons, the likely sites of termination of their axons, and their axonal branching patterns. Microstimulation in the second thoracic spinal segment (T2) antidromically activated 67 VLM neurons (as determined with time-controlled collision of spontaneous and evoked action potentials), whose activity was correlated to inferior cardiac sympathetic nerve discharge (as determined with spike-triggered averaging). We tested the effect of baroreceptor-reflex activation on the firing rate of 20 of these VLM-spinal neurons. Because the firing rate decreased in each instance, these neurons apparently subserved a sympathoexcitatory function. The axonal branching patterns of 51 VLM-spinal sympathoexcitatory neurons were studied. Thirty-four neurons were antidromically activated by stimulation in the T2 gray matter and in more caudal thoracic spinal segments (T11 and/or T6). In each case, the antidromic response evoked by stimulation in the T2 gray matter was due to activation of an axonal branch rather than the main axon (via current spread to the white matter). This was demonstrated with tests that included time-controlled collision of the action potentials initiated by stimulation in T2 and a more caudal thoracic spinal segment. Some VLM-spinal axons that projected to T11 branched in T6 as well as in T2. These data indicate that some VLM-spinal neurons exerted widespread excitatory influences on sympathetic outflow. Seventeen VLM sympathoexcitatory neurons that innervated the T2 gray matter could not be antidromically activated by stimulation in T5, T6, and T11 despite an extensive search at each level. Thus the axonal projections of some VLM-spinal neurons were restricted to upper thoracic segments. Antidromic mapping in T2 revealed that the axons of VLM sympathoexcitatory neurons coursed through the dorsolateral or ventrolateral funiculus to innervate the region of the intermediolateral nucleus. Mean axonal conduction velocity was 3.5 +/- 0.3 m/s. Those VLM-spinal axons restricted to upper thoracic segments generally were located dorsally and/or medially to those that innervated widely separated thoracic segments. The discharges of 35 other VLM neurons that were antidromically activated by T2 stimulation were not related to sympathetic nerve activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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.
A study was made of 170 neurons of the lateral tegmental field (LTF) of the cat medulla with spontaneous activity temporally related to the 2- to 6-Hz slow wave in inferior cardiac postganglionic sympathetic nerve discharge (as demonstrated with spike-triggered averaging). LTF neurons were excited by the iontophoresis of L-glutamate, and an inflection on the rising phase of their action potentials was observed. Thus, the site of extracellular unit recording presumably was in the region of the cell body. The lag between LTF unit spike occurrence and the peak of the 2- to 6-Hz slow wave in sympathetic nerve discharge (SND) was unchanged when blood pressure and, thus, baroreceptor nerve activity were lowered to a level at which the phase relationship between the slow wave and the cardiac cycle was disrupted. Thus, the discharges of LTF neurons apparently were more closely associated with those of elements of "efferent" brain stem networks controlling SND than with those of interneurons in the afferent limb of the baroreceptor reflex arc. LTF neurons with sympathetic nerve- and cardiac-related activity were classified into three types depending on their responses to elevated carotid sinus pressure (i.e., baroreceptor reflex activation). Of the 82 neurons tested, 33 were inhibited, 16 were excited, and 33 were unaffected by baroreceptor reflex activation. Using data collected in this and previous studies from our laboratory, we compared the firing times of neurons in the LTF, rostral ventrolateral medulla, and medullary raphe nuclei relative to the peak of the sympathetic nerve slow wave. LTF neurons that were inhibited by baroreceptor reflex activation are presumed to subserve a sympathoexcitatory function. These neurons fired significantly earlier during the sympathetic nerve slow wave than their counterparts in the rostral ventrolateral medulla and medullary raphe nuclei. LTF neurons classified as sympathoinhibitory (i.e., excited by baroreceptor reflex activation) fired significantly earlier than their counterparts in the medullary raphe nuclei. These data raise the possibility that LTF neurons are closer (at least in a temporal sense) to the region of origin of the 2- to 6-Hz component of SND than are ventrolateral medullary and raphe neurons. The firing times of sympathoexcitatory and sympathoinhibitory LTF neurons were not significantly different. These data are discussed relative to potential mechanisms involved in generating SND. Microstimulation of the second thoracic spinal segment was used to determine whether the axons of LTF neurons with sympathetic nerve-related activity projected to this level.(ABSTRACT TRUNCATED AT 400 WORDS)
The coherence function and phase spectrum were used to study the relationships between the discharges of sets of two postganglionic or preganglionic sympathetic nerves in baroreceptor-denervated cats anesthetized with either 5,5-diallylbarbiturate-urethan or alpha-chloralose. Most of the power in sympathetic nerve discharge was contained between 2 and 6 Hz. The coherence values relating the activity of two nerves were significantly different from zero within this frequency band. The phase spectrum was either linear or complex (i.e., showed changes in slope) within the coherent frequency band. We observed three patterns of relationship. The first pattern was characterized by a constant interval between activity in different sympathetic nerves within the coherent frequency band. The second pattern was characterized by a frequency-dependent interval. The third pattern was characterized by uncoupling of the 2- to 6-Hz rhythms in the discharges of different nerves. Switching between these patterns was observed. We suggest that the three patterns reflect different functional states of the central system responsible for the 2- to 6-Hz rhythm. Two models of this system are entertained. The first model is one of a system of coupled oscillators while filtering circuits that receive common inputs are the elements of the second model.
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