Vagotomized Cats Research Articles

Role of glutamate receptors in the lateral parabrachial nucleus in regulation of cardiac sympathoexcitatory reflexes

Stimulation of cardiac sympathetic afferents by ischemic metabolites like bradykinin (BK) evokes sympathoexcitatory reflex responses and activates neurons in the external lateral parabrachial nucleus (elPBN). The present study tested the hypothesis that the elPBN processes these reflexes through a glutamatergic mechanism. BK (0.1–1 μg) was injected into pericardial sack of anesthetized and bilateral vagotomized cats. Hemodynamic and renal sympathetic nerve activity (RSNA) responses to repeated intrapericardial BK before and after microinjection of kynurenic acid (Kyn, 25 mM, 50 nl) into the elPBN were recorded. Intrapericardial BK application evoked significant increases in mean blood pressure (MAP, 50 ± 6 mmHg) and RSNA (59 ± 8.6 %) in six cats. Kyn in the elPBN reduced BK-evoked reflex responses including MAP (50 ± 6 vs. 29 ± 2 mmHg, before vs. after) and RSNA (59 ± 8.6 vs. 29 ± 4.7 %, before vs. after). In contrast, inadvertent microinjection into areas surrounding the elPBN did not alter the responses to intrapericardial BK (MAP, 49 ± 3 vs. 51 ± 4 mmHg; RSNA, 64 ± 4 vs. 62 ± 2%, before vs. after). These data suggest that glutamate receptors in the elPBN play an important role in processing cardiac sympathoexcitatory reflex responses (supported by NIH HL-66217).

Rostral ventrolateral medullary but not medullary lateral tegmental field neurons mediate sympatho-sympathetic reflexes in cats

This study was designed to build on past work from this laboratory by testing the hypothesis that medullary lateral tegmental field (LTF) neurons play a critical role in mediating sympathoexcitatory responses to activation of sympathetic afferent fibers. We studied the effects of microinjection of N-methyl-d-aspartate (NMDA) or non-NMDA receptor antagonists or muscimol bilaterally into the LTF on the area under the curve of the computer-averaged sympathoexcitatory potential in the right inferior cardiac nerve elicited by short trains of stimuli applied to afferent fibers in the left inferior cardiac or left splanchnic nerve (CN, SN) of baroreceptor-denervated and vagotomized cats anesthetized with a mixture of diallylbarbiturate and urethane. In contrast to our hypothesis, sympathoexcitatory responses to stimulation of CN (n = 5-7) or SN (n = 4-7) afferent fibers were not significantly affected by these procedures. We then determined whether the rostral and caudal ventrolateral medulla (RVLM, CVLM) and nucleus tractus solitarius (NTS) were involved in mediating these reflexes. Blockade of non-NMDA, but not NMDA, receptors in the RVLM significantly reduced the area under the curve of the sympathoexcitatory responses to electrical stimulation of either CN (P = 0.0110; n = 6) or SN (P = 0.0131; n = 5) afferent fibers. Neither blockade of excitatory amino acid receptors nor chemical inactivation of CVLM or NTS significantly affected the responses. These data show that activation of non-NMDA receptors in the RVLM is a critical step in mediating the sympatho-sympathetic reflex.

A Selective Inhibitory Effect of the Posterior Cerebellar Vermis on 10‐Hz Sympathetic Nerve Discharge

We compared the changes in inferior cardiac sympathetic nerve discharge (SND) and mean arterial pressure (MAP) produced by aspiration of portions of lobule IX and in some cases lobule X of the posterior cerebellar vermis with those produced by chemical inactivation (muscimol microinjection) or electrical stimulation of the same regions. The experiments were performed on 13 baroreceptor‐denervated and vagotomized cats anesthetized with urethane. Autospectral analysis was used to decompose SND into its frequency components. Special attention was paid to the question of whether the experimental procedures differentially affected the rhythmic and aperiodic components of SND. Aspiration or chemical inactivation with muscimol of lobule IX produced an approximately three‐fold increase in the 10‐Hz rhythmic component of SND (P = 0.05). In contrast, wideband SND at lower frequencies (= 6 Hz) was either slightly reduced or unaffected. Total power (0‐ to 20‐Hz band) was unchanged. Despite this, there was a statistically significant increase in MAP. High frequency (50‐Hz) electrical stimulation of depressor sites in lobule IX of the posterior vermis selectively and significantly reduced 10‐Hz power in SND. The lower frequency components of SND were unchanged. These results demonstrate for the first time a role of cerebellar cortical neurons of the posterior vermis in regulating the frequency composition of naturally occurring SND. The functional implications of these findings are discussed.(Supported by NIH HL33266.)

Carotid baroreceptor control of liver and spleen volume in cats

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (–67.8%), cardiac output (–26.6%), total peripheral resistance (–49.5%), and heart rate (–15%) and significantly increased spleen volume (9.7%, corresponding to a 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Carotid baroreceptor control of liver and spleen volume in cats

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (–67.8%), cardiac output (–26.6%), total peripheral resistance (–49.5%), and heart rate (–15%) and significantly increased spleen volume (9.7%, corresponding to a 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Carotid baroreceptor control of liver and spleen volume in cats

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Carotid baroreceptor control of liver and spleen volume in cats

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (–67.8%), cardiac output (–26.6%), total peripheral resistance (–49.5%), and heart rate (–15%) and significantly increased spleen volume (9.7%, corresponding to a 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Forebrain rhythm generators influence sympathetic activity in anesthetized cats

Autospectral and coherence analyses were used to study the frequency-domain relationships between frontal-parietal cortical activity [electroencephalogram (EEG)] and the discharges of the interior cardiac and renal sympathetic nerves of baroreceptor-denervated and vagotomized cats anesthetized with either alpha-chloralose or pentobarbital sodium. Delta slow-wave activity in the EEG was correlated to sympathetic nerve discharge (SND) as shown by sharp peaks between 0.5 and 4 Hz in the coherence function. The relationship was stronger in chloralose- than in pentobarbital-anesthetized cats. Coherence of the two signals could be attributed to descending influences of forebrain delta slow-wave generators on sympathetic circuits, since midbrain transection preferentially reduced the power in SND at frequencies that cohered to the EEG before transection. In contrast, the power in the EEG was not reduced by midbrain transection. The relationship between cortical delta slow-wave activity and SND was stronger during than between cortical spindlelike events that lasted 1-3 s and recurred once every 5-10 s. These events were similar to cortical spindles observed during the early stages of sleep and under light barbiturate anesthesia. These observations raise the possibility that the influences of forebrain delta slow-wave generators on SND are gated by thalamic mechanisms normally involved in the sleep-wake cycle.

Action and specificity of ventral medullary vasopressor neurones in the cat

An investigation has been made into the mode and specificity of action of ventral medullary pressor neurones. These were activated by microinjections of excitant amino acid into the ventral brain surface of chloralose-anaesthetized. artificially ventilated cats, and a number of autonomic responses were measured. Indirect assessment of cardiac output (by CO 2 delivery to the lungs) suggested that it was either unchanged or fell during pressor responses. The inference that activating the pressor neurones caused vasconstriction was confirmed directly for hindlimb and mesenteric vascular beds, by a rise in inflow pressure when they were perfused at constant flow. Sympathetic activity also increased in cervical, splanchnic and inferior cardiac nerves. Bradycardia often (but not always) accompanied pressor responses, but this was abolished by vagotomy, although not by cutting the sinus and aortic nerves. In vagotomized cats, tachycardia could be produced during pressor responses even after either bilateral adrenalectomy or removal of the stellate ganglia, indicating both direct sympathetic drive to the heart and release of adrenal catacholamines. Plasma adrenaline levels were measured and found to increase by up to 20.2 times control values, plasma noradrenaline up to 12.6 times, and dopamine by a smaller amount. Activating ventral medullary pressor neurones appeared to have no significant action on pupils, nictatating membranes or piloerection. In three adrenalectomized, vagotomized cats, only small, inconsistent effects were measured on intestinal motility following pressor neurone excitation However, large electrodermal responses could be evoked from the ventral medulla, but from a distinct area medial to the pressor neurones. These data and those of the preceding paper have been incorporated into a new map of the functional organization of the ventral medullary surface.

Vagal cardioinhibitory area in and around the caudal inferior olivary nucleus of cats. I. Localization and connection

Bradycardia was produced by electrical stimulation and injection of glutamate (200 nl, 1 M) to the regions in and around the extremely caudal parts of the inferior olivary nucleus (ION) in chloralose-urethane anesthetized cats. Either medullary transection at 4 mm rostral to the obex, spinal transection at C2–3 or both transections together did not abolish the ION-induced bradycardia. Bradycardia induced by stimulating one ION was slightly reduced and completely abolished by unilateral and bilateral vagotomies, respectively. The ION-evoked bradycardia was also slightly reduced by a raphe lesion. This lesion together with unilateral vagotomy abolisted only the bradycardia induced from the ION on the vagotomized side. In 28 left vagotomized cats, the left ION-induced bradycardia was subjected to the effects of destroying the right ION, dorsal motor/solitary nucleus (DM/SN) and ambiguus nucleus (AN). The bradycardia was completely abolished by ION lesion (7/7), greatly reduced (7/13) or completely abolished (6/13) by DM/SN lesion, and slightly increased (5/8) or decreased (3/8) by AN lesion. We concluded that cells and/or fibers in and around the ION may project fibers to the ipsilateral DM/SN and through the raphe nucleus to the contralateral ION which may send fibers to the other DM/SN.

Clonidine inhibits nicotinic effects in ganglia of the cholinergic-sympathetic system

The electrodermal potential (EDP) recorded with surface electrodes between the palm and the shaven back of the forepaws of anaesthetized cats was taken as a measure of sudomotor activity in response to submaximal activation of cholinergic-sympathetic efferents with the nicotinic ganglionic stimulant DMPP. The intravenous injection of 30 μg/kg clonidine inhibited EDPs in despinalized cats and in vagotomized cats with chronic denervation of the stellate ganglion. In vagotomized cats clonidine (30 μg/kg i.v.) shifted the dose-response curve of DMPP (4–256 μg/kg i.v.) to the right. An inhibitory effect was also observed in despinalized cats upon topical application of 0.1 and 1 μg clonidine to the stellate ganglion. In all preparations the inhibitory effect of clonidine could be antagonized by intravenous injection of 200 μg/kg yohimbine. As all substances used were also active when injected during arrest of blood flow to the foreleg by means of a tourniquet, actions at the level of the sweat gland could be excluded. The results lead to the conclusion that the activation of postsynaptic somadendritic α 2-adrenoceptors in sudomotor ganglia of the cholinergic-sympathetic nervous system inhibits the effects of nicotinic ganglionic stimulation. It is assumed that this action is due to the known ganglionic hyperpolarization induced by α 2-adrenoceptor stimulants.

Cardiac sympathetic afferent influences on renal nerve activity.

Afferent neurons contained within cardiac sympathetic nerves can have excitatory influences on central sympathetic outflow. The normal or pathological circumstances during which such excitatory reflexes occur are not well understood. The purpose of this research was to investigate the possibility that cardiac sympathetic afferent neurons make a significant contribution to cardiovascular control during myocardial ischemia. Afferent influences on renal nerve activity were characterized during occlusion of coronary arteries and in response to chemical stimulation of cardiac receptors by bradykinin. Reflexes were investigated in chloralose-anesthetized cats in which arterial baroreceptors had been denervated. In vagotomized cats afferent stimulation by coronary occlusion or by bradykinin caused significant increases in renal nerve activity. When vagi remained intact, coronary occlusion or epicardially applied bradykinin caused increases, decreases biphasic responses or no significant change in renal nerve activity. Thus, excitatory reflexes could be initiated by the sympathetic afferent neurons in some cats despite simultaneous vagal afferent stimulation. The responses to chemical stimulation followed the same pattern as those to coronary occlusion suggesting that a component of the afferent stimulus during ischemia may be chemical in nature. Finally, the central pathways mediating these excitatory reflexes were investigated by comparing responses to epicardially applied bradykinin in vagotomized cats prior to and following high cervical spinal cord transection or midcollicular decerebration. Excitation of renal nerve activity by this chemical afferent stimulation was reduced but still present in spinalized cats and unchanged in decerebrate cats. Thus spinal pathways may mediate at least a component of these excitatory reflexes but forebrain regions are not essential to their initiation. In summary, these findings are consistent with the contentions that: (1) cardiac sympathetic afferent neurons may initiate significant excitatory reflexes during myocardial ischemia; (2) such reflexes may be due, in part, to chemical stimulation of cardiac receptors; and (3) these reflexes can be mediated partially by spinal pathways.

Mechanism of reflex control of cardiac contractility by carotid sinus baroreceptors.

Effects of the carotid sinus baroreflex (CSR) on left ventricular dP/dt, mean arterial pressure (MAP), and heart rate (HR) were examined by changing the pressure in the vascularly isolated carotid sinus in anesthetized cats. When the carotid sinus pressure (CSP) was lowered, a significant increase was observed in dP/dt and MAP. These reflex changes were significantly increased after vagotomy. In vagotomized cats, cardiac sympathectomy attenuated but did not abolish the dP/dt and HR responses to CSR. The MAP response was little affected. The remaining response of dP/dt and HR were virtually abolished by subsequent adrenalectomy or beta-adrenergic blockade. Adrenalectomy reduced the MAP response by 39%. The effect of cardiac sympathectomy or adrenalectomy on the dP/dt response was greater when either procedure was performed in combination with the other. These results indicate that 1) the vagi interact with CSR and 2) both cardiac sympathetic nerves and adrenal secretion of catecholamines contribute to the reflex control of cardiac contractility by CSR in anesthetized cats. However, the relative contribution of either reflex system appears to vary depending on whether the other system in intact.

Reflex hemodynamic responses initiated from the thoracic aorta.

In anesthetized vagotomized cats with both carotid arteries occluded, stretch of the walls of the thoracic aorta performed without obstructing aortic blood flow induced reflex increases in arterial blood pressure (systolic: 136 ± 4 [SE] to 170 ± 7 mm Hg), heart rate (230 ± 10 to 236 ± 11 beats/min), and maximum rate of rise of left ventricular pressure (dP/dt max) (2,337 ± 256 to 3,155 ± 302 mm Hg/sec). In cats with spinal transection (C1), similar increases were observed. These responses were abolished by infiltrating the walls of the thoracic aorta with xylocaine. In adrenalectomized cats with intact central nervous systems, reflex responses were reduced but were still statistically significant. Phenoxybenzamine abolished the pressor response but not the increases in heart rate and dP/dt max. Propranolol drastically reduced the increases in heart rate and dP/dt max but not the pressor response. It is concluded that stretch of the thoracic aorta induced an increase in sympathetic activity affecting the h...

Stereoconfiguration requirement for central activity of isoproterenol

The effect of intracerebroventricular (i.c.v.) administration of d and dl-isoproterenol on heart rate and blood pressure was studied in chloralose anesthetized vagotomized cats. Both the racemic and dextrorotatory forms produced an immediate dose-dependent fall in diastolic blood pressure and an increase in heart rate. These changes were abolished by pretreatment with a ganglionic blocking agent administered peripherally. The cardiovascular response exhibited a marked degree of stereospecificity; the isomeric activity ratios (equipotent dose of d/dl isoproterenol) for the heart rate and blood pressure responses were 32 and 28. Systemic administration of d and dl-isoproterenol yielded isomeric activity ratios on the order of two log units. These data favor the existence of central stereospecific beta -adrenergic receptors that modify cardiovascular function.

Reflex sympathetic changes in aortic diastolic pressure-diameter relationship.

In anesthetized vagotomized cats with the chest opened and artificially ventilated, aortic blood pressure (AP) and external diameter (AD; ultrasound technique) were measured in the proximal third of the descending thoracic aorta. Slow sinusoidal oscillations (0.2-0.3 Hz in aortic volume were produced by a piston pump connected to a femoral artery. Diastolic pressure-diameter relationship (PDR) curves were obtained during control conditions and during stimulation of either the cut central end of the left inferior cardiac nerve (ICN) or the decentralized thoracic sympathetic chain (SC). In six cats with both carotid arteries occluded ICN stimulation reflexly shifted the PDR curves to lower diameters for any given pressure (mean deltaAD 3.2% at control AP). A smaller response to ICN stimulation was obtained in five cats with one patent carotid artery (mean deltaAD 2.3% at control AP). Stimulation of sympathetic efferents to the aorta (SC) caused similar responses in five animals (mean deltaAD 3.4% at control AP). This reflex control of the thoracic aorta may be involved in cardioaortic coupling and may influence the sensitivity of aortic mechanoreceptors.

Mechanism of the hypotensive effect of intravenous methaqualone in the cat

Methaqualone, a non-barbiturate hypnotic, has been reported to produce hypotension in animals. Experiments were undertaken to evaluate the mechanisms responsible for this effect. In chloralose-anesthetized cats, iv administration of 0.5 to 10.0 mg/kg of methaqualone produced dose-dependent decreases in blood pressure. The hypotension was associated with decreases in contractile force and heart rate at doses of 1 mg/kg or higher. Pretreatment with atropine or bilateral vagal nerve section did not influence these cardiovascular effects. In vagotomized cats: (1) spinal section markedly reduced the depressant effects of methaqualone on blood pressure, contractile force and heart rate and (2) removal of the stellate ganglia reduced the negative inotropic and chronotropic effects of the drug. Furthermore, administration of methaqualone (31.2–500 μg/kg) into a vertebral artery of vagotomized cats produced dose-dependent decreases in blood pressure, contractile force and heart rate. In the isolated cat hindquarters preparation perfused at constant blood flow, methaqualone (31.2–1000 μg) produced transient decreases in perfusion pressure which were not altered by pretreatment with phentolamine, propranolol, atropine or tripelennamine. In the rabbit perfused isolated heart, large doses of drug (0.25 to 2.0 mg) were required to depress contractile force. These results indicate that hypotension produced by iv methaqualone results primarily from a centrally mediated depression of sympathetic neural outflow to the heart and vasculature and, to a lesser extent, from direct relaxation of vascular smooth muscle and direct myocardial depression.

Pathways from medullary nuclei to spinal cardioacceleratory neurons in the cat.

1. In 15 chloralosed vagotomized cats medullary sites of origin of descending autonomic fibres projecting to spinal sympathetic neurons were identified by activating fibre terminals in the intermediolateral nucleus (ILN) at histologically and functionally identified cardioacceleratory sites on the right side of spinal segment T2 and exploring the ipsilateral medulla for antidromically evoked field potentials. The cardiovascular function of positive sites of recording was then determined by observing the effects on heart rate and arterial pressure of electrical stimulation of these sites. Finally, precise localization of spinal pathways of descending fibres from these sites was determined by observing the effects on the medullary field potentials of restricted, histologically identified surgical or electrolytic lesions in spinal segments C5–C7. 2. Evoked field potentials recorded at 10 medullary sites from which electrical stimulation elicited cardiac slowing were eliminated by selective lesion of either the ventral (8 animals) or the dorsolateral funiculus (2 animals). Evoked field potentials at five medullary sites from which stimulation elicited cardioacceleration were eliminated by lesion of the dorsolateral funiculus. 3. Transection of the right dorsolateral funiculus in eight animals caused a decrease in heart rate and in arterial pressure; transection of the right ventral funiculus in 12 animals caused no change in heart rate or arterial pressure. 4. It is concluded that: a) inhibitory fibres from medullary nuclei to ipsilateral spinal Cardioacceleratory neurons descend in the dorsolateral and ventral funiculi of the cervical spinal cord; b) excitatory fibres descend in the ipsilateral dorsolateral funiculus; c) excitatory, but not inhibitory, medullary fibres projecting to cardioacceleratory and vasoconstrictor neurons in the ILN are tonically active in the chloralosed cat.

Excitatory and inhibitory inputs from medullary nuclei projecting to spinal cardioacceleratory neurons in the cat.

1. In chloralosed vagotomized cats medullary structures projecting to spinal (T2) sympathetic neurons were identified by activating fibre terminals in the intermediolateral nucleus (ILN) at functionally and histologically identified cardioacceleratory sites and exploring the ipsilateral medulla for evoked field and single unit potentials. 2. In 23 cats evoked field potentials with a mean latency of 1.5 msec were recorded at 264 sites in 216 penetrations in the right medulla and at 101 sites in 81 penetrations in the left medulla. These potentials followed stimulation at 300 Hz and persisted after asphyxia and administration of sodium pentobarbital. 3. In 7 cats single unit activity was recorded from 39 units which followed the stimulus at a constant short latency of activation (mean 1.7 msec), exhibited cancellation of antidromic with orthodromic spikes and fractionation at high frequencies, and responded to paired stimuli delivered at short intervals (mean minimum interval 1.27 msec, range 0.58–2.3 msec). 4. Stimulation of 79 sites at which evoked field potentials were recorded in the right medulla elicited cardioacceleration mainly from N. lateralis reticularis and N. parvocellularis, and cardiac slowing mainly from N. paramedium reticularis, raphe NN. and N. medullae oblongatae centralis subnucleus ventralis; stimulation of 101 sites in the left medulla changed heart rate at only 3 sites. 5. It is concluded that: a) medullary inputs to spinal sympathetic neurons arise from discrete nuclei; b) structures from which cardioacceleration and cardiac slowing were elicited provide excitatory and inhibitory inputs, respectively, to spinal cardioacceleratory neurons; c) the efferent limb of reflexes controlling heart rate appears to be localized mainly on the right side of the medulla; d) the vasomotor centre provides multiple excitatory and inhibitory inputs from specific reticular nuclei to the ILN.

Origin and course of crossed medullary pathways to spinal sympathetic neurons in the cat

1. In 12 chloralosed vagotomized cats medullary structures projecting to contralateral spinal sympathetic neurons were identified by activating fibre terminals in the intermediolateral nucleus (ILN) at functionally and histologically identified cardioacceleratory sites at the T2 level and exploring the contralateral medulla for antidromically evoked field potentials. 2. Evoked field potentials were recorded at 20 sites in 130 penetrations in the left medulla and at 14 sites in 70 penetrations in the right medulla; responses were recorded mainly from sites in the nucleus gigantocellularis, the nucleus paramedium reticularis and the nucleus lateralis reticularis. 3. In an additional 20 cats the pathways of crossed fibres from these nuclei to the ILN were identified by observing the effects on the evoked field potentials of surgical and electrolytic lesions in the medulla and spinal cord. Evoked potentials from the left nucleus gigantocellularis were abolished by a midline section in the caudal medulla, or by right medullary hemisection (5 mm caudal to the obex), or by transection of the right ventral funiculus (C6–C7). Potentials from the left nucleus paramedium reticularis were abolished by right medullary hemisection (5 mm caudal to the obex) or by transection of the right ventral funiculus (C5–C7). Potentials from the left nucleus lateralis reticularis were abolished by left spinal hemisection 2–3 mm rostral to the level of the stimulating electrode or by transection of either the left dorsolateral or the left ventral funiculus (C5–C7). 4. It is concluded that: a) spinal sympathetic neurons receive inputs from discrete nuclei in the contralateral medulla; b) autonomic fibres from the nucleus gigantocellularis and the nucleus paramedium reticularis to the contralateral ILN cross the midline in the caudal medulla and descend in the contralateral ventral funiculus; c) fibres from the nucleus lateralis reticularis descend in the ipsilateral dorsolateral and ventral funiculi and cross the midline in the spinal cord close to their level of termination.