Sympathetic Afferents Research Articles

Cardiac input to medullary reticular formation: neuronal responses to CAO.

Responses of 46 medullary reticular neurons to coronary arterial occlusions (CAO) of the left anterior descending (LAD) and left circumflex (CX) coronary arteries were determined in chloralose-anesthetized cats paralyzed with pancuronium. Extracellular potentials were recorded from individual neurons, in the medial reticular formation, responsive to electrical stimulation of cardiopulmonary sympathetic afferents. CAO responses were characterized by one of three patterns. Cell activity changed during myocardial ischemia (IS response). Fifteen neurons were excited during ischemia (9 +/- 2.8 to 15 +/- 3.2 spikes/s for CX occlusion and 10 +/- 3.0 to 17 +/- 4.7 spikes/s for LAD occlusion), and two were inhibited (8 +/- 3.0 to 4 +/- 3.0 spikes/s). Cell activity changed at the onset or release of occlusion and rapidly adapted (ON response). Four cells were excited at the onset of LAD occlusion (2 +/- 1.4 to 10 +/- 6.0 spikes/s), 9 cells were excited at onset of CX occlusion (5 +/- 2.5 to 16 +/- 5.6 spikes/s), and 1 cell decreased its rate at onset of CX occlusion. A combination of ON and IS responses occurred in five cells (ON-IS response). Overall, 24 neurons exhibited at least one of these responses, and 22 cells were unaffected by CAO. Thirty neurons were tested for responses to CAO of CX and LAD; neurons most often exhibited different patterns of responses to CAO of each artery. Thirty-one of 34 cells tested exhibited qualitatively, but often not quantitatively, similar responses to cardiac ischemia and to application of bradykinin to epicardium of free wall of left ventricle. Results indicate that medullary neurons often respond differentially to occlusion of different coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory responses to chemical activation of left ventricular receptors

Respiratory responses to chemical activation of receptors in the left ventricle were measured in anesthetized cats. Application of capsaicin (10 μg) or bradykinin (500 ng) to the serosal surface of the left ventricle caused increases in phrenic nerve activity and in arterial pressyre. These responses persisted after cervical vagotomy and after bilateral transection of the carotid sinus nerves. Bilateral stellate ganglionectomy abolished the respiratory responses to capsaicin and bradykinin. In addition, stellate ganglionectomy prevented the arterial pressure response to bradykinin; however, a slight increase in arterial pressure occurred with application of capsaicin. It is concluded that activation of sympathetic afferents orginating in the left ventricle caused an increase in respiratory output.

Effects of propranolol on the impulse activity of cardiovascular sympathetic afferent fibers.

The influence of beta-adrenergic receptor blockade on the impulse activity of 21 cardiovascular sympathetic afferent nerve fibers (11 from the thoracic aorta, 10 from the pulmonary veins), isolated from the left sympathetic rami communicantes T-3 and T-4 was studied in anesthetized, vagotomized cats. Aortic pressure, heart rate, and neural discharge were recorded during control conditions and during brief aortic occlusions of comparable amplitude and duration. Administration of dl-propranolol (0.2-0-4 mg/kg) did not modify aortic pressure or neural discharge of the fibers during control conditions, although, as expected, heart rate was diminished. dl-Propranolol administration did change the response of cardiovascular sympathetic afferents to similar aortic pressure increases. Before drug administration, aortic occlusion caused a significant increase in neural discharge of both aortic and pulmonary vein sympathetic afferent fibers, from 0.52 +/- 0.12 to 1.64 +/- 0.31 and from 0.67 +/- 0.10 to 2.08 +/- 0.25 impulses/sec, respectively (p less than 0.05). After dl-propranolol administration, comparable increases in aortic pressure resulted in slight but not significant increases in neural discharge of aortic and pulmonary vein fibers. Administration of d-propranolol (0.4-0.6 mg/kg), which possesses only membrane-stabilizing properties, did not modify the firing rate of four pulmonary sympathetic afferents, which subsequently decreased their response to pressure rises after administration of dl-propranolol. These results indicate that beta-adrenergic receptor blockade reduces the responsiveness to hemodynamic stimuli of sympathetic cardiovascular afferent fibers that are capable of mediating excitatory pressor reflexes.

Cardiorespiratory changes following chemical applications to gut serosa

Application of 0.2–0.3 ml of 1 M ammonium chloride, 100 mM citric acid, 100 mM hydrochloric acid, 1% potassium chloride, 1% ammonium oxalate, 1% oxalic acid, 0.5% sodium hydroxide, 200 μg% bradykinin or 20 mg% capsaicin to gastrointestinal serosa produced a fall in blood pressure and inhibition of respiration in hypertensive as well as normotensive rats. In 6 (8%) of the animals studied, a fall in heart rate was also seen which was blocked by atropine. The blood pressure changes were independent of changes in heart rate. After acute abdominal vagotomy, while the respiratory inhibition following chemical application on gut serosa was enhanced, the cardiovascular responses were the same as before. In animals subjected to sympathetic denervation by spinal section at T5, celiac ganglionectomy or splanchnicotomy, a similar application produced an augmented respiratory response while the cardiovascular parameters were unaffected. These results show that the above inhibitions were mediated through the sympathetic afferents and a minor stimulation of respiration, via vagal afferents. The efferent pathway for the cardiac changes seems to be via vagus and the vascular changes via the sympathetics. In chronic vagotomized animals, the same stimulation produced a response similar to that seen in animals with intact vagus. An adaptive response may be operating in chronic animals reverting the status back to normal.

Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction.

We have demonstrated previously that sympathetic and vagal afferents travel in an apical-to-basal course in the heart, and can be stimulated selectively with epicardial applications of bradykinin and nicotine, respectively. In this study we tested the hypothesis that transmural myocardial infarction interrupts sympathetic and vagal afferent fibers traveling through the infarction and produces regions of afferent denervation in areas apical to the infarction. In open-chest, chloralose-anesthetized dogs, transmural myocardial infarction was created by embolizing a diagonal branch of the left anterior descending coronary artery with a vinyl latex solution that was injected directly into the artery and hardened rapidly. The transmural nature of the infarction was verified by the nitro blue tetrazolium staining technique for dehydrogenase enzymes. Epicardial applications of bradykinin (5 micrograms) and nicotine (50 micrograms) were used to stimulate chemically sensitive sympathetic and vagal afferent nerve endings, respectively. Twenty-nine dogs were studied before and 90 min after creation of transmural myocardial infarction. In 20 dogs, epicardial bradykinin applied before production of transmural myocardial infarction produced a maximal pressor response of 13 +/- 3 mm Hg 40 sec after application (p less than .01 vs preapplication values), while topical nicotine produced a maximal depressor response of 14 +/- 2 mm Hg (p less than .01 vs preapplication values) 20 sec after application at all sites tested. Ninety minutes after production of transmural myocardial infarction, epicardial sites basal to the infarction continued to respond normally to both drugs, while sites within the area of infarction and apical to the area (noninfarcted myocardium) no longer showed a pressor response to topical bradykinin or a depressor response to topical nicotine.(ABSTRACT TRUNCATED AT 250 WORDS)

Activation of lumbar spinoreticular neurons by stimulation of muscle, cutaneous and sympathetic afferents

Forty-four spinal neurons located mainly in laminae IV–VII of the L7 and S1 segments projected primarily contralaterally and to the lateral reticular nucleus. Muscle and cutaneous input was via group II and III afferents, whereas sympathetic input was via group III or IV afferents. Close-arterial injection of bradykinin and/or caosaicin excited most of the neurons so tested. These responses make these neurons likely candidates for the ascending pathway of the exercise pressor reflex.

Autonomic hyperreflexia: A mortal danger for spinal cord-damaged women in labor

Reproductive care of women with spinal cord damage demands knowledge of such women's reproductive potential and the specific complications to which these women are prone during pregnancy and childbirth, especially autonomic hyperreflexia. Fertility in cord-damaged women of reproductive age is generally undiminished as are libido, ability to have intercourse, and ability to bear children. Frequent complications of cord-damaged pregnant women include urinary tract infection, anemia, pressure sores, sepsis, unattended birth, and autonomic hyperreflexia. Autonomic hyperreflexia or autonomic dysreflexia occurs during labor in up to two thirds of women with cord lesions above T-6. Autonomic hyperreflexia results from noxious stimuli including distention of the bladder, cervix, or rectum, which evokes mass triggering of sympathetic and parasympathetic afferents that are uninhibited by supraspinal centers below the cord lesion. Autonomic hyperreflexia manifests itself with sudden onset of marked hypertension and headache during uterine contractions, as well as bradycardia or tachycardia, various cardiac dysrhythmias, and marked diaphoresis with piloerection and flushing above the level of the cord lesion. We describe the second reported occurrence of intraventricular hemorrhage due to autonomic hyperreflexia during labor and detail recommendations for anticipating and mitigating this potentially lethal complication of parturition in cord-damaged women. Pregnancy and parturition are best carried out with informed cooperation of the patient and of obstetric, cord rehabilitation, anesthetic, and nursing personnel.

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat.

The present study was designed to determine effect of the preganglionic splanchnic nerve activity (SNA) on the brief hypotension accompanied with the occlusion of left circumflex coronary artery (CxCAO) in chloralose anesthetized cats. Following CxCAO in animals with neuraxis intact, no significant alterations of SNA occurred despite the significant fall in mean blood pressure (MBP). A significant fall in MBP also occurred in vagotomized animals with arterial baroreceptors intact, but SNA was significantly augmented from 12.9 +/- 2.7 impulses/sec before CxCAO to 24.4 +/- 4.3 impulses/sec 60 sec after the occlusion. In vagotomized animals, in which their carotid sinuses were isolated and perfused with the constant pressure at a level equal to systemic blood pressure (112 +/- 6 mmHg) and with higher pressure (167 +/- 7 mmHg), SNA was not altered significantly during the hypotension due to CxCAO. When the carotid sinuses were perfused with lower pressure (53 +/- 8 mmHg), a significant increase in SNA occurred simultaneously with the decrease in MBP after CxCAO. The peak decreases in blood pressure during the coronary occlusion were significantly greater in the vagotomized group (-46 +/- 5 mmHg) and in the Low-CSP group (-50 +/- 5 mmHg) than in other groups. Onset of this excitatory efferent sympathetic response to the hypotension due to the coronary occlusion in the vagotomized and Low-CSP groups was delayed significantly despite a significant fall in arterial blood pressure. These results show that vagal afferents from the heart may play a role of inhibiting the sympathetic augmentation mediated by arterial baroreceptors during cardiogenic hypotension. An excessive activation of cardiac receptors with sympathetic afferents may be induced by the profound fall in blood pressure, resulting in further impairment of cardiac function due to progressive myocardial ischemia under the condition of high sympathetic tone activated by baroreceptor reflex.

High threshold aortic baroreceptor afferents in the sympathetic nerve.

In anaesthetized cats, 40 sympathetic sensory units in the bracheocephalic artery (30 units) and the descending aorta (10 units) were recorded by means of single-unit preparation. Direct evidence is available for the mechanosensitive nature of the receptors in the sympathetic afferents at the level of T3 and T4. Two distinct types of receptors were found (Type I and Type II). Type I receptors, which were fast adapting, gave a spike discharge at each systolic height of pressure (70-110 mmHg). However, they sometimes failed to appear even at such systolic pressure. When the systemic pressure was increased by occluding the descending aorta or by infusing adrenaline solution intravenously, the frequency of discharge of Type I receptors increased and they behaved much the same as the typical sinoaortic baroreceptors. Type II receptors were activated by mechanical probing and at high systemic pressure, though they did not fire always synchronously with heart beat. On the basis of the study it may be suggested that Type I receptors are high threshold baroreceptors and like other systemic baroreceptors, play a role in homeostatic control presumably in a state of high blood pressure, but on the other hand Type II receptors do not play such a role.

Cardiac receptors: Their function in health and disease

Cardiac receptors include both mechanically and chemically sensitive receptors located in atria and in ventricles. Atrial receptors innervated by myelinated vagal afferent fibers reflexly regulate heart rate and intravascular volume. On the other hand, stimulation of ventricular receptors can cause either reflex bradycardia and hypotension or, alternatively, excitation of the cardiovascular system. The former response is mediated by vagal afferents, whereas the latter is mediated by sympathetic (spinal) afferents. Under normal circumstances, cardiac receptors sense changes in wall motion or diastolic pressure and perhaps provide a fine tuning of the cardiovascular system. However, under certain pathological conditions such as coronary ischemia, which cause release of substances such as bradykinin and prostaglandins, there is an exaggerated response of the ventricular receptors. Because these receptors cause a reflex depression of the cardiovascular system and, in particular, induce renal vasodilation, they may protect the heart and kidney by lessening myocardial oxygen requirements and by increasing renal blood flow. In the situation of heart failure both atrial and ventricular receptors are reset and therefore provide for an exaggerated neurohumoral discharge. Finally, patients with aortic stenosis may demonstrate a paradoxical vasodilation and syncope during exercise when there likely is excessive stimulation of left ventricular receptors by the high transmural pressure.

Phenol topically applied to canine left ventricular epicardium interrupts sympathetic but not vagal afferents.

The intracardiac pathways carrying the cardiovascular reflex responses mediated by cardiac sympathetic and vagal afferent fibers were examined in this study. We investigated the response to epicardial applications of bradykinin (5 micrograms) and nicotine (50 micrograms) before and after regional epicardial applications of 85% phenol in chloralose anesthetized open-chest dogs. Bradykinin stimulated sympathetic afferents, while nicotine stimulated vagal afferents. Topical applications of phenol were used to interrupt these pathways. Before phenol encircling, bradykinin significantly increased--whereas nicotine significantly decreased--mean arterial blood pressure when applied at the same sites. After phenol, nicotine applied to all sites within and outside the phenol circle continued to decrease mean arterial pressure, whereas bradykinin applied to sites within the circle no longer increased mean arterial pressure. Removal of aortic and carotid baroreceptors did not significantly affect these responses. Painting horizontal stripes of phenol on the anterior and posterior left ventricular free wall basal to the site of bradykinin application eliminated the elevation in mean arterial pressure produced by bradykinin. Reapplication of bradykinin basal to the stripe restored its response. Phenol stripes eliminated the nicotine vasodepressor response only when the stripe was painted in the atrioventricular groove. When bradykinin and nicotine were injected via a nonocclusive intracoronary catheter, both drugs elicited an early depressor response (interrupted by vagotomy) and, in some animals a late pressor response (interrupted by stellectomy). Epicardial phenol encircling the flow distribution of the cannulated coronary artery interrupted most or all of the sympathetic afferents mediating pressor responses to bradykinin or nicotine, while leaving the depressor responses intact. The depressor responses were eliminated by applying phenol to the atrioventricular groove or by transecting the cervical vagi. These data suggest that sympathetic afferent fibers travel in the superficial subepicardium in an apex-to-base direction. Vagal afferent fibers travel deeper in the myocardium until they approach the atrioventricular groove, where they ascend to the superficial subepicardium.

Evidence for a spinal afferent innervation of the guinea pig lower respiratory tract as studied by the horseradish peroxidase technique

The afferent innervation of the guinea pig lower respiratory tract was studied using a retrograde axonal transport technique with application of horseradish peroxidase (HRP) onto the lining respiratory epithelium. HRP-labeled cells were observed not only in the nodose ganglia but also in the jugular and upper thoracic dorsal root ganglia (mainly at the T2&T3 levels). Thus, both vagal parasympathetic and spinal sympathetic afferents seem to have peripheral branches close to or within the respiratory epithelium suggesting a dual sensory control of the airways.

Global versus regional myocardial ischaemia: differences in cardiovascular and sympathetic responses in cats.

The cardiovascular and sympathetic responses to occlusions of the left main ("global" ischaemia) or distal left anterior descending ("regional" ischaemia) coronary artery were studied in 19 anaesthetised cats with chronic sinoaortic baroreceptor denervation. "Global" ischaemia, before vagotomy, resulted in a significant reduction of mean arterial pressure (MAP), left ventricular pressure (LVP), and LVdP/dtmax while sympathetic efferent impulse activity was significantly augmented during the initial 15 +/- 2 s of occlusion (early phase) and, vice versa inhibited during the subsequent 20 +/- 2 s of occlusion (late phase). Vagotomy did not modify the haemodynamic responses, however, a significant increase in sympathetic discharge was detectable during the whole occlusion period (early and late phases). "Regional" ischaemia, before vagotomy, resulted in a significant increase in sympathetic neural discharge and MAP, with no changes in left ventricular function. After vagotomy the occlusion elicited a significant increase in MAP, LVP, LVdP/dtmax and efferent sympathetic neural activity. These excitatory responses were abolished after the interruption of a large part of the cardiac sympathetic afferents. Thus coronary artery occlusion induced haemodynamic and sympathetic reflex responses that were dependent upon the interaction of opposite influences mediated by the simultaneous activation of cardiac vagal and sympathetic afferents. The extent of "ischaemic myocardium" represented a determinant factor for the prevailing type of neural response.

Vagal afferent inhibition of spinothalamic cell responses to sympathetic afferents and bradykinin in the monkey.

Effects of stimulating the left thoracic vagus nerve on the responses of spinothalamic neurons to electrical stimulation of cardiopulmonary sympathetic afferent fibers and to intracardiac injections of bradykinin were determined. Experiments were performed on 39 monkeys (Macaca fascicularis) tranquilized with ketamine and anesthetized with alpha-chloralose. The 30 spinothalamic cells studied had the following characteristics. They were excited by manipulation of their somatic receptive fields, were excited by electrical stimulation of cardiopulmonary sympathetic afferent fibers, and exhibited viscerosomatic convergence. Responses of 15 of 19 cells to sympathetic afferent test stimuli were inhibited by conditioning stimuli applied to left thoracic vagus nerve. A conditioning-test interval of 40-50 msec resulted in maximal inhibition of responses to both A delta and C fiber sympathetic afferents. A long time course of inhibition was present to at least a conditioning-test interval of 200 msec. Left thoracic vagus nerve stimulation inhibited 14 of 14 cells responding to intracardiac injection of bradykinin. Entrainment of activity of five cells to the cardiac cycle occurred in response to bradykinin. In each case, left thoracic vagus nerve stimulation, in addition to reducing frequency of cell discharge, disrupted the cardiac related pattern of cell activity. Bilateral cervical vagotomy abolished all inhibitory effects of left thoracic vagus nerve stimulation. These results demonstrate that vagal afferents may participate in processing of information related to cardiac pain.

Renal nerve responses to cardiac receptor stimulation with bradykinin in monkeys

Previous data from our laboratory demonstrated a species difference between the cat and dog in the arterial blood pressure (ABP) and renal nerve activity (RNA) responses to epicardial bradykinin (BK) applications. The present study was carried out to determine the ABP and renal nerve responses to chemical activation of cardiac afferents by BK in the intact and sinoaortic-denervated and vagotomized (SAD + VX) nonhuman primate. Seven Macaque monkeys (fascicularis and nemestrina) anesthetized with pentobarbital or chloralose were used in this study. The heart was exposed and suspended in a pericardial cradle. A left atrial (LA) catheter was inserted through the appendage. Changes in ABP and RNA (percent change from control) were determined when 1 and 10 micrograms/ml BK (in 1-ml volume) were applied to the anterior surface of the left ventricle or injected into the LA (0.3 and 3.0 micrograms/kg BK) in the intact and SAD + VX state. In both the intact and SAD + VX monkeys, ABP and RNA were significantly reduced with epicardial BK. In the intact state, LA injections of BK produced a significant decrease in the % delta of RNA and a depressor response. In the SAD + VX monkey, significant hypotensive responses were also observed with LA injections of BK concomitant with significant reductions in RNA. These results show the existence of a depressor response and inhibition of renal sympathetic nerve activity in the nonhuman primate mediated by the action of bradykinin on cardiac sympathetic afferents.

Cardiovascular reflexes mediated by sympathetic afferent fibers

In this paper the experimental evidence supporting the hypothesis that excitatory sympathetic reflexes may participate in the tonic control of the cardiovascular system is discussed. Positive feedback pressor sympathetic reflexes can be obtained with physiological distensions of the descending thoracic aorta in conscious dogs with all nerves intact in absence of any pain reaction. These excitatory reflexes interact with supraspinal regulatory mechanisms, inhibitory in nature. A massive excitation of cardiac sympathetic afferents, produced by intracoronary injections of bradykinin, also elicits a pressor reflex, without pain reactions. In the absence of anesthesia and recent surgery, the cardiovascular excitatory reflexes, subserved by sympathetic afferent fibers, can easily prevail. We suggest that negative and positive feedback mechanisms interact continuously to achieve the most adequate neural cardiovascular control.

The role of cardiopulmonary sympathetic afferents in blood volume homoeostasis in the non-human primate.

1. Four Macaca fascicularis monkeys were bilaterally sympathectomized by removing the thoracic sympathetic chain from the middle cervical ganglion to the T-6 sympathetic ganglion. This was done chronically, allowing adequate recovery time. While under light pentobarbital anaesthesia, the animals were then subjected to blood volume expansions with isotonic, isooncotic dextran or to head-out immersions. Seven immersions and seven volume expansions were carried out. 2. With immersion, there were significant increases in blood pressure, central venous pressure, urine flow, sodium excretion, potassium excretion, glomerular filtration rate, percentage of filtered sodium excreted and free water clearance. Although blood pressure and central venous pressure initially increased during the first immersion period, heart rate continued to increase with the immersion, while blood pressure and central venous pressure remained constant. Volume expansion caused an increase in central venous pressure, urine flow, sodium and potassium excretion, osmolar clearance, free water clearance, percentage of filtered sodium excreted and glomerular filtration rate. 3. Since these results with both the immersions and volume expansions were not qualitatively different from those observed in control animals, it is concluded that cardiopulmonary sympathetic afferents are not necessary for the renal response to head-out immersion or blood volume expansion in the non-human primate.

The role of the sympathetic nervous system in congestive heart failure.

Congestive heart failure is usually accompanied by cardiovascular signs of an increased sympathetic and a decreased parasympathetic efferent activity. A current hypothesis for these autonomic changes holds the baroreceptor mechanisms mainly responsible for this complex neural reflex pattern together with a decreased responsiveness of cardiac vagal afferent ffibers. An alternative hypothesis is proposed here. Afferent sympathetic fibers with sensory endings in the atria and in the pulmonary veins are progressively excited by volume load. In cats with a chronic spinal section at C8, breathing spontaneously, an infusion of saline induces a reflex tachycardia through a sympatho-sympathetic neural circuit. In chronic dogs with intact cardiovascular innervation, the stimulation of aortic or cardiac sympathetic afferent fibers elicits an excitatory sympathetic reflex leading to hypertension and tachycardia; in addition, the sensitivity of baroreflexes is markedly reduced. Therefore, in congestive heart failure, especially in the absence of hypotension, the reflex excitation of the sympathetic outflow and the inhibition of the vagal efferent activity directed to the heart could be due to reflex mechanisms mediated by sympathetic cardiovascular afferents.

Antagonism of the excitatory effects of 5-hydroxytryptamine on sympathetic preganglionic neurones and neurones activated by visceral afferents

The responses of electrophysiologically identified sympathetic preganglionic neurones (SPGN) and interneurones activated by sympathetic visceral afferents (VA), to iontophoretic application of 5-hydroxytryptamine (serotonin) and serotonin receptor antagonists: methysergide and cinanserin, were tested in the T3 segment of the spinal cord of the cat. Serotonin had a definite and dose-dependent excitatory action on sympathetic preganglionic neurones and neurones activated by visceral afferents. This excitatory response to serotonin was characterized by the rapid development of tachyphylaxis. Methysergide antagonized the effects of serotonin in preganglionic neurones and neurones activated by visceral afferents. Cinanserin was less effective than methysergide. Preliminary data on the effect of inhibitors of serotonin uptake: chloroimipramine and fluoxetine are also reported. These findings support the idea that sympathetic output and the activity of neurones activated by sympathetic visceroafferents is modulated by an excitatory serotoninergic supraspinal input.

Competitive reinnervation of the rat superior cervical ganglion by foreign nerves

The efficacy of foreign nerves to form synapses was studied morphologically and physiologically in the superior cervical ganglion of the rat. The denervated ganglion was anastomosed to the central stump of either the vagus, the hypoglossal or both nerves together. The degree of reinnervation was assessed two to ten months later. We measured the strength of contraction of the nictitating membrane after each type of operation and compared this to the number, type and distribution of synapses in the same ganglion. Both the vagus and hypoglossal nerves preferentially reinnervated a population of neurones that are situated in the cranial pole of the superior cervical ganglion and supply the nictitating membrane. When both nerves were connected to the ganglion only the vagus nerve could be shown to reinnervate it, and no reinnervation by the hypoglossal nerve was detected. However, in this experiment neither foreign nerve did as well in competition as each did alone and the overall result was reduced functional efficiency. We conclude that not all sympathetic neurones are equivalent and that, just like sympathetic afferents, the foreign nerves are capable of selectively reinnervating preferred target cells.