Comprised of the sympathetic nervous system, parasympathetic nervous system, and enteric nervous system, the autonomic nervous system (ANS) provides the neural control of all parts of the body except for skeletal muscles. The ANS has the major responsibility to ensure that the physiological integrity of cells, tissues, and organs throughout the entire body is maintained (homeostasis) in the face of perturbations exerted by both the external and internal environments. Many commonly prescribed drugs, over-the-counter drugs, toxins, and toxicants function by altering transmission within the ANS. Autonomic dysfunction is a signature of many neurological diseases or disorders. Despite the physiological relevance of the ANS, most neuroscience textbooks offer very limited coverage of this portion of the nervous system. This review article provides both historical and current information about the anatomy, physiology, and pharmacology of the sympathetic and parasympathetic divisions of the ANS. The ultimate aim is for this article to be a valuable resource for those interested in learning the basics of these two components of the ANS and to appreciate its importance in both health and disease. Other resources should be consulted for a thorough understanding of the third division of the ANS, the enteric nervous system. © 2016 American Physiological Society. Compr Physiol 6:1239-1278, 2016.

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.

No abstract

We used blockade of excitatory amino acid (EAA) neurotransmission in the medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) to assess the roles of these regions in the control of inferior cardiac sympathetic nerve discharge (SND) and mean arterial pressure (MAP) in urethan-anesthetized, baroreceptor-denervated cats. Bilateral microinjection of a non-N-methyl-D-aspartate (NMDA)-receptor antagonist [1,2,3, 4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide (NBQX)] into the LTF significantly decreased SND to 46 +/- 4% of control (as demonstrated with power-density spectral analysis) and MAP by 16 +/- 6 mmHg. In contrast, bilateral microinjection of an NMDA-receptor antagonist [D(-)-2-amino-5-phosphonopentanoic acid (D-AP5)] into the LTF did not decrease SND or MAP. These results demonstrate that the LTF is an important synaptic relay in the pathway responsible for basal SND in the cat. Bilateral microinjection of NBQX or D-AP5 into the RVLM significantly decreased power in SND to 48 +/- 5 or 61 +/- 5% of control, respectively, and reduced MAP by 15 +/- 2 or 8 +/- 4 mmHg, respectively. These data indicate that EAA-mediated synaptic drive to RVLM-spinal sympathoexcitatory neurons accounts for a significant component of their basal activity.

Partial coherence analysis was used to remove the influences of the central circuits controlling a sympathetic nerve (as reflected by its discharges) on the coherence of the 10-Hz discharges of other sympathetic nerves in unanesthetized decerebrate or urethan-anesthetized cats. In many cases, partialization reduced but did not eliminate the sharp peak near 10 Hz in the coherence functions relating the discharges of sympathetic nerve pairs. This observation implies that the central sources of the 10-Hz rhythmic discharges of any nerve are not identical to those responsible for the rhythm recorded from any other nerve. Partial coherence analysis also revealed differential relationships among the 10-Hz rhythmic discharges of sympathetic nerves with different targets. Importantly, the pattern of differential relationships observed in one experiment could be the reverse of that in the next. Although the basis for the differential relationships is not yet clear, nonuniform coupling of multiple brain stem 10-Hz oscillators and/or nonuniform cross talk between spinal circuits controlling different sympathetic nerves may be involved.

We tested the hypothesis that blockade of N-methyl-D-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 +/- 8 and 24 +/- 6% of control (n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 +/- 22 to 129 +/- 13% of control; n = 4) and vertebral nerves (from 253 +/- 41 to 154 +/- 20% of control; n = 7) and mean arterial pressure (from 39 +/- 7 to 21 +/- 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

1. This is the first study to show that caudal ventrolateral medullary (CVLM) neurons play an important role in governing the 10-Hz rhythm in sympathetic nerve discharge (SND). Spike-triggered averaging showed that the naturally occurring discharges of 66 of 246 CVLM neurons located 0-2.5 mm rostral to the obex, 4-4.25 mm lateral to the midline, and within 2 mm of the ventral surface were correlated to the 10-Hz rhythm in inferior cardiac SND of 17 urethan-anesthetized cats. 2. Frequency domain analysis was used to characterize further the relationships between SND and the discharges of 45 CVLM neurons with activity correlated to the 10-Hz rhythm in inferior cardiac nerve activity. The autospectra of the discharges of 22 of these neurons contained a sharp peak near 10 Hz (corresponding to the peak in the autospectra of SND), although the mean firing rate of these neurons was only 5.9 +/- 0.5 (SE) spikes/s. The peak coherence value relating the 10-Hz discharges of these CVLM neurons and the inferior cardiac nerve was 0.42 +/- 0.03. The autospectra for the other 23 CVLM neurons did not contain a peak near 10 Hz. Their mean firing rate was 2.3 +/- 0.5 spikes/s, and the peak coherence value relating their discharges to the 10-Hz rhythm in SND was 0.08 +/- 0.01. The coherence value was significantly different than zero in all but three cases. 3. Importantly, spike-triggered averaging and coherence analysis demonstrated that CVLM neurons with activity correlated to the 10-Hz rhythm did not have activity correlated 1:1 to the cardiac-related rhythm in SND of baroreceptor-innervated cats. Also, their discharges were not correlated to the irregular 2- to 6-Hz oscillations in SND of baroreceptor-denervated cats. These data support the hypothesis that different pools of brain stem neurons generate the 10-Hz rhythm and the 2- to 6-Hz oscillations (or cardiac-related rhythm) in SND. 4. Despite the fact that CVLM neurons with activity correlated to the 10-Hz rhythm did not have activity correlated 1:1 to the cardiac-related rhythm in SND, these neurons were influenced by baroreceptor afferent nerve activity. First, their firing rates could be decreased (n = 12) or increased (n = 2) during the pressor response induced by inflating a balloon in the aorta (aortic obstruction). Second, on occasion, the discharges of CVLM neurons and the 10-Hz rhythm in SND were entrained to a harmonic of the heart rate.(ABSTRACT TRUNCATED AT 400 WORDS)

No abstract