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R M McAllen

Publications and source records attributed to R M McAllen.

At least 37 records · Page 2Linked to original sources

Tonic drive to sympathetic premotor neurons of rostral ventrolateral medulla from caudal pressor area neurons.

The responses of sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) to activation or inactivation of neurons in the caudal pressor area (CPA) were studied in urethan-anesthetized rats. Extracellular recordings were made from 32 barosensitive single units in the RVLM, of which 26 were antidromically activated from the cervical cord. Unilateral microinjections of L-glutamate (0.5-5 nmol) into the CPA increased firing in 13 of 14 premotor neurons by 90 +/- 30% while raising blood pressure. Both ipsilateral and contralateral injections were effective. Unilateral or bilateral inhibition of CPA neuron activity by microinjecting glycine (5-200 nmol/side) lowered blood pressure, while it reduced firing in 9 of 10 and 16 of 17 premotor neurons, respectively, by 45 +/- 9 and 39 +/- 6%. A significant proportion of tonic activity in RVLM sympathetic premotor neurons is thus driven, directly or indirectly, by neurons in the CPA.

Animals↗

The lumbar preganglionic sympathetic supply to rat tail and hindpaw.

The segmental origins of the preganglionic sympathetic neurons which control the circulation of the rat tail were investigated and compared with those that supply the hindpaw. The left ventral roots of the first, second and sometimes the third lumbar segments were stimulated with 2-min pulse trains in 10 male Sprague-Dawley rats, which were anaesthetised with urethane (1-1.5 g/kg i.v.) and paralysed with pancuronium. Rats were warmed to increase cutaneous blood flow, and vasoconstrictor responses were detected by thermocouples as stimulus-locked falls in skin temperature. Stimulating the L2 ventral root always vasoconstricted the tail: in 50% of the rats, it also vasoconstricted the ipsilateral hindpaw, while in 50%, it did not. Stimulating the L1 ventral root always vasoconstricted both tail and hindpaw. Stimulating the L3 ventral root caused no measurable effect. Electrodermal potentials were recorded from the ipsilateral hindpaw pad in 7 rats: these accompanied hindpaw vasoconstrictor responses but were not seen otherwise. We conclude that at least in 50% of rats, the preganglionic neurons supplying hindpaw and tail skin are not clearly segregated by spinal segment. Sweat glands and blood vessels in the hindpaw are supplied by the same segments.

Animals↗

Sympathetic burst activity: characteristics and significance.

1. The activity recorded from mammalian sympathetic nerves comes in bursts, which result from large numbers of fibres firing synchronously. 2. Human sympathetic nerve activity behaves similarly to that in animals, although burst rates may be lower. 3. Vasomotor, cardiac and sudomotor nerve fibres all fire in bursts. Whether other sympathetic pathways do so is unknown. 4. Sympathetic activity is intrinsically 'bursty' but not intrinsically regular. 5. Bursting is a population phenomenon, not usually evident in the firing of individual neurons. 6. Bursts in post-ganglionic nerves are driven by synchronously firing preganglionic neurons. 7. The origin of bursts remains controversial. Preganglionic neuron properties are likely to be important in at least shaping bursts. 8. Burst amplitude, which reflects the number of fibres firing together, and burst probability are controlled independently. 9. Baroreceptors affect burst probability over a wide range, but have less effect on mean burst amplitude. How they affect burst timing within the cardiac cycle is discussed. 10. Burst probability is determined 'downstream' of the rostral ventrolateral medulla, implicating either the spinal cord or recurrent brainstem connections in burst generation. 11. Neuroeffector responses are too slow to follow individual bursts. However, bursting will promote spatial facilitation at both ganglionic and effector levels, which may increase the dynamic range of neural control.

Animals↗

Brain angiotensinergic pathways mediate renal nerve inhibition by central hypertonic NaCl in conscious sheep.

The renal sympathetic responses to infusion of hypertonic solutions into the lateral cerebral ventricles were investigated in conscious sheep. Intracerebroventricular infusion of artificial cerebrospinal fluid (CSF) containing 0.6 M NaCl, at 1 ml/h for 20 min, reduced renal sympathetic nerve activity (RSNA) by 81 +/- 5% (n = 6, P < 0.001). Plasma renin concentration also fell (P < 0.05), whereas arterial pressure increased by 6.4 +/- 0.7 mmHg (P < 0.01). Intracerebroventricular hypertonic sorbitol (0.9 M in CSF at 1 ml/h) had no effect. The AT1 receptor antagonist losartan (1 mg/h) abolished the plasma renin and arterial pressure responses to intracerebroventricular hypertonic saline and significantly reduced the fall in RSNA to 17 +/- 10% (P < 0.001). During intracerebroventricular hypertonic saline, the baroreflex relation of RSNA to diastolic pressure was shifted to the left and that to central venous pressure was abolished compared with control relations obtained by manipulating pressure with intravenous phenylephrine. These findings indicate that 1) RSNA is inhibited by a central mechanism that senses high sodium (or perhaps chloride) concentration rather than hypertonicity; 2) this inhibition occurs independently of reflexes from high- and low-pressure baroreceptors, although these may enhance the inhibition; and 3) inhibition of RSNA by hypertonic saline involves a central angiotensinergic pathway.

Angiotensin II↗

Cardiac sympathetic premotor neurons.

To locate premotor neurons controlling the cardiac sympathetic supply and to determine their relation to brain stem vasomotor pathways, the rostral ventrolateral medulla (RVLM) was mapped in seven chloralose-anesthetized cats, with the use of microinjections of sodium glutamate (5-10 nl, 0.1 M) to excite neuronal cell bodies. Cardiac sympathetic responses were recorded from the ipsilateral inferior cardiac nerve, while recordings were made simultaneously from postganglionic vasoconstrictor fibers to skeletal muscle (ipsilateral peroneal nerve). Baroreceptors were denervated to eliminate the reflex effects of blood pressure changes. Most of the 115 injected RVLM sites excited both sympathetic nerves. Inferior cardiac nerve activity increased by up to 395% (mean 105 +/- 86%, SD), and muscle vasoconstrictor activity increased by up to 487% (110 +/- 107%). Their relative response varied with injection site, however. For 16 of the most rostromedial injections, the inferior cardiac nerve-to-muscle vasoconstrictor response ratio exceeded that expected by two- to sevenfold; for 9 very caudolateral injections that ratio was strongly reversed, favoring muscle vasoconstrictors by two to fivefold. Intervening sites gave more equal responses. Overall, the response ratio varied systematically with injection site. These findings demonstrate that neurons with preferential or selective actions on the cardiac sympathetic outflow are present in the RVLM and are organized topographically. The simplest interpretation is that a population of selective cardiac sympathetic premotor neurons occupies a territory substantially overlapping, but centered rostromedially to, the population controlling vasoconstriction in muscle.

Animals↗

Baroreceptor-independent renal nerve inhibition by intracerebroventricular angiotensin II in conscious sheep.

The effect of central administration of angiotensin II (ANG II) on efferent renal sympathetic nerve activity (RSNA) was studied in conscious sheep. ANG II (1 nmol/h), infused for 30 min into the lateral cerebral ventricles in five sheep, did not alter mean arterial pressure (MAP) but reduced RSNA to 38 +/- 5% of control. Intracerebroventricular infusion of higher doses of ANG II (3 and 10 nmol/h), which increased MAP by 12 +/- 2 and 14 +/- 3 mmHg, respectively, reduced RSNA to 9 +/- 5 and 11 +/- 7% of control. MAP and RSNA gradually returned to control over a period of 2 h after the infusions. Intracerebroventricular losartan (1 mg/h for 1 h before, and then during, angiotensin infusion) blocked all the effects of angiotensin (3 nmol/h). Baroreflex relationships constructed from the beat-to-beat relationship of RSNA to diastolic pressure showed a significant leftward shift during intracerebroventricular ANG II compared with the control relationship. The beat-to-beat relationship between central venous pressure and RSNA was abolished during intracerebroventricular infusion of ANG II. These findings demonstrate that intracerebroventricular ANG II has a direct central inhibitory action on RSNA that is independent of both arterial and low-pressure baroreceptors. This effect of angiotensin is mediated by central angiotensin AT-1 receptors.

Angiotensin II↗

Distinct preganglionic neurons innervate noradrenaline and adrenaline cells in the cat adrenal medulla.

Calretinin immunoreactivity was present in a subset of preganglionic neurons retrogradely labelled from the cat adrenal gland. Overall, one-third of adrenal preganglionic neurons showed calretinin immunoreactivity, and their proportion increased in the more caudal spinal cord segments. Calretinin-immunoreactive nerve terminals were prominent within the adrenal gland, but were found only in areas of noradrenergic chromaffin cells (approximately one-third of the area of the adrenal medulla). Synaptophysin immunoreactivity was used to label terminals with and without calretinin immunoreactivity. Nerve terminals lacking calretinin immunoreactivity were present among the adrenergic chromaffin-cells and also comprised 20% of the nerve terminals innervating noradrenergic chromaffin cells. Calretinin immunoreactivity thus labels a subpopulation of cat adrenal preganglionic neurons that innervate the noradrenergic chromaffin cells.

Adrenal Medulla↗

Brainstem neurones and postganglionic sympathetic nerves: does correlation mean connection?

Short-term correlations in activity have been widely used as evidence to connect brainstem units with postganglionic sympathetic nerves. These may be detected by spike-triggered averaging, cross correlation or coherence analysis. The specificity of this type of evidence has been investigated by cross-correlating the activity of identified cutaneous vasoconstrictor postganglionic fibres with that of medullary premotor neurones of like and of unlike functional type, as determined by physiological testing (preoptic warming), in anaesthetised cats. Single medullary premotor neurones of both types were recorded from the subretrofacial nucleus: they were identified by their barosensitivity and, in most cases, their spinally projecting axons. By the test criteria chosen, the correlation method gave both false-positive and false-negative results as commonly as it gave correct ones. We conclude that it is not a reliable way to determine brainstem-postganglionic connectivity.

Animals↗

Physiological actions of angiotensin II mediated by AT1 and AT2 receptors in the brain.

1. Autoradiographic binding studies have shown that the AT1 receptor is the predominant angiotensin II (AngII) receptor subtype in the central nervous system (CNS). Major sites of AT1 receptors are the lamina terminalis, hypothalamic paraventricular nucleus, the lateral parabrachial nucleus, rostral and caudal ventrolateral medulla, nucleus of the solitary tract and the intermediolateral cell column of the thoraco-lumbar spinal cord. 2. While there are differences between species, AT2 receptors are found mainly in the cerebellum, inferior olive and locus coeruleus of the rat. 3. Circulating AngII acts on AT1 receptors in the subfornical organ and organum vasculosum of the lamina terminalis (OVLT) to stimulate neurons that may have a role in initiating water drinking. 4. Centrally administered AngII may act on AT1 receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. 5. Recent evidence shows that centrally administered AT1 antagonists inhibit dipsogenic, natriuretic, pressor and vasopressin secretory responses to intracerebroventricular infusion of hypertonic saline. This suggests that n angiotensinergic neural pathway has a role in osmoregulatory responses. 6. Central angiotensinergic pathways which include neural inputs to the rostral ventrolateral medulla may use AT1 receptors and play a role in the function of sympathetic pathways maintaining arterial pressure.

Angiotensin II↗

Nitric oxide synthase and chemical coding in cat sympathetic postganglionic neurons.

Nitric oxide synthase-like immunoreactivity was found in a subpopulation of sympathetic postganglionic neurons in the cat stellate and lower lumbar ganglia. In the ganglia of other segments such cells were rare. Double staining for tyrosine hydroxylase-like immunoreactivity and nitric oxide synthase-like immunoreactivity or the reduced nicotinamide adenine dinucleotide phosphate diaphorase reaction indicated that nitric oxide synthase-like immunoreactivity and reduced nicotinamide adenine dinucleotide phosphate diaphorase reactivity was always co-localized and was confined to tyrosine hydroxylase-negative (presumably cholinergic) ganglion cells, and was present in most of them. The occurrence of nitric oxide synthase in two subpopulations of cholinergic postganglionic neurons was investigated in triple staining experiments. Presumptive sudomotor neurons have been previously defined as scattered cells containing calcitonin gene-related peptide-like immunoreactivity, usually accompanied by vasoactive intestinal peptide-like immunoreactivity: 99% of these contained nitric oxide synthase. Presumptive muscle vasodilator neurons have been previously identified as clumped cells with strong vasoactive intestinal peptide-like immunoreactivity but no calcitonin gene-related peptide-like immunoreactivity: 70% of these contained nitric oxide synthase. Sweat glands were found in the paw pad skin surrounded by varicose fibres showing calcitonin gene-related peptide-like immunoreactivity and vasoactive intestinal peptide-like immunoreactivity, confirming previous work. Such fibres also stained for nitric oxide synthase-like immunoreactivity and reduced nicotinamide adenine dinucleotide phosphate diaphorase reactivity, although their staining was relatively weaker than in the corresponding cell bodies. Varicose fibres with the same chemical coding were also found around all large and most medium and small arteries in the paw skin as well as around arteriovenous anastomoses. Fibres with the muscle vasodilator coding (vasoactive intestinal peptide-like immunoreactivity without calcitonin gene-related peptide-like immunoreactivity) were not seen in paw skin. These results suggest that nitric oxide may act as a co-transmitter (with acetylcholine, substance P, vasoactive intestinal peptide and calcitonin gene-related peptide) in sudomotor neurons and (with acetylcholine and vasoactive intestinal peptide) in vasodilator neurons. Collateral branches of sudomotor neurons may innervate skin vessels, and release vasodilator transmitters including nitric oxide to cause the vasodilatation which provides the fluid supply for sweat formation. Alternatively, separate vasodilator neurons to skin may share the same chemical code as sudomotor neurons.

Animals↗

Effects of preoptic warming on subretrofacial and cutaneous vasoconstrictor neurons in anaesthetized cats.

1. Sympathetic and subretrofacial neuron responses to preoptic warming were studied in chloralose- or Saffan-anaesthetized, paralysed cats. 2. Warming a thermode in the preoptic region inhibited the activity of cutaneous vasoconstrictor fibres supplying hairy skin. Muscle vasoconstrictor fibre activity recorded at the same time was either unaffected or raised. 3. Small injections of sodium glutamate (5 nl, 0.1 M) were made into the region of the subretrofacial nucleus in the ventrolateral medulla. The part of that region where glutamate injections evoked brisk increases in cutaneous vasoconstrictor fibre activity was chosen for further study. 4. Extracellular single unit recordings were made in that area from seventy-seven subretrofacial neurons, which were identified by their barosensitivity (inhibition by carotid blind sac inflation). Forty-seven of them were antidromically activated by stimulation in the spinal cord. 5. The activity of twenty subretrofacial neurons (twelve proven bulbospinal) was significantly reduced by periods of preoptic warming. Cutaneous vasoconstrictor activity recorded at the same time also fell. Forty-nine subretrofacial neurons (thirty-five proven bulbospinal) were unaffected or excited by periods of preoptic warming that inhibited cutaneous vasoconstrictor fibres. The response of eight neurons was unclear. 6. No difference in either mean firing rate or axonal conduction velocity was found between neurons inhibited by preoptic warming and other subretrofacial neurons. 7. The subretrofacial neurons inhibited by warming were found intermingled with those unaffected or excited. Marked recording sites of warm-inhibited neurons were clustered around the ventromedial border of the subretrofacial nucleus. 8. In two cats, bilateral inhibition of subretrofacial neurons by surface application of 1 M glycine reduced cutaneous vasoconstrictor fibre activity to 32 and 44% of control levels. 9. The results suggest that specific cutaneous vasoconstrictor premotor neurons exist in the subretrofacial nucleus. These apparently provide most of the background excitatory drive to cutaneous vasomotor neurons. Central warming stimuli may act, at least in part, by withdrawing that drive.

Anesthesia↗

Localization of barosensitive neurons in the caudal ventrolateral medulla which project to the rostral ventrolateral medulla.

A population of depressor neurons in the caudal ventrolateral medulla that project to the rostral ventrolateral medulla may mediate the baroreceptor reflex. The aim of the present study was to determine the anatomical distribution of the population of neurons in the caudal ventrolateral medulla that mediate the baroreceptor reflex. Injection of the retrogradely transported tracer, rhodamine-labelled latex beads, into the pressor area of the rostral ventrolateral medulla of rats was used to identify neurons in the caudal ventrolateral medulla with projections to that area. Barosensitive neurons were identified by immunohistochemical detection of the protein Fos, a marker of neuronal activation, following infusion of the pressor agent phenylephrine (10 micrograms/kg/min, i.v. for 2 h n = 5). Isotonic saline was infused into control animals (n = 4). Neurons in the caudal ventrolateral medulla with projections to the rostral ventrolateral medulla were located at all rostrocaudal levels examined between 1 mm caudal and 0.4 mm rostral of the obex. Compared to saline infused rats, phenylephrine infusion induced a significant increase in the proportion of those neurons that expressed Fos (14% vs. 1% P < 0.000.1). These barosensitive neurons were found mainly at the level of the obex, between the lateral reticular nucleus and the nucleus ambiguus. In conclusion, this study is the first to show the distribution of the population of barosensitive neurons in the caudal ventrolateral medulla that project to the pressor region of the rostroventrolateral medulla. The results suggest there is a subpopulation of depressor neurons, confined to a small region of the rostral part of the caudal ventrolateral medulla, that are likely to be the interneurons that mediate the baroreceptor-reflex response.

Angiotensin II↗

Is CRF a ganglionic transmitter or modulator in the cat sudomotor pathway?

The presence of corticotrophin releasing factor (CRF)-like immunoreactivity distinguishes a subset of cat sympathetic preganglionic neurons which supplies sweat glands. It is abundant in their terminals in the stellate ganglion. We sought first to determine whether this immunoreactivity is due to true CRF, then to test whether CRF plays any role in ganglionic transmission in the cat sudomotor pathway. CRF-immunoreactive material extracted from cat stellate ganglia and hypothalamus were eluted on HPLC at equivalent retention times, slightly less than that of standard sheep CRF. In chloralose-anaesthetised cats, sheep CRF (0.13, 1.3 and 13 micrograms/kg, i.v.) raised plasma immunoreactive ACTH levels by between 3- and 300-fold. Submaximal stimulus trains delivered to pre- or postganglionic nerves of the right stellate ganglion evoked electrodermal responses (EDR, a measure of sweat gland activity) in the right forepaw pad as well as increases in heart rate and blood pressure. Exogenous sheep CRF (dose range 130 ng/kg to 13 mg/kg) given close-arterially to the stellate ganglion in 5 chloralose-anaesthetised cats had no consistent effect on either baseline or preganglionically-evoked EDR. Given i.v. at 13 micrograms/kg to four further cats, sheep CRF caused no significant change in mean baseline or mean preganglionically-evoked EDP (P > 0.05; CUSUM test). Hexamethonium (10 or 30 mg/kg i.v.) abolished the EDR to preganglionic nerve stimulation (7/7 cats). Increasing preganglionic stimulus voltage, frequency and train duration failed to show any hexamethonium-resistant component of the EDR, although such effects were evident in the cardioaccelerator pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Monosynaptic excitation of preganglionic vasomotor neurons by subretrofacial neurons of the rostral ventrolateral medulla.

Extracellular single unit recordings were made from barosensitive neurons in the subretrofacial nucleus (SRF) of the rostral ventrolateral medulla in chloralose-anaesthetised cats. At the same time, single preganglionic neuron activity was recorded from filaments of the cervical sympathetic trunk (CST); barosensitive units were selected for study. Evidence for monosynaptic connections between the two neuron groups was sought by cross-correlation analysis of their ongoing activity. Cross-correlograms of 16/16 SRF/CST neuron pairs showed a broad peak (100-200ms wide), reflecting the synchronizing action of arterial baroreceptors on both neurons' activity. Two of the 16 cross-correlograms additionally showed a robust, statistically significant, narrow peak of a single 2 ms bin width, providing the first physiological demonstration that ventrolateral medullary neurons monosynaptically excite preganglionic sympathetic neurons. Deductions are made about the strength, convergence and divergence of the connection.

Animals↗

Differential drives from rostral ventrolateral medullary neurons to three identified sympathetic outflows.

Simultaneous recordings were made in chloralose-anesthetized cats from muscle vasoconstrictor (MVC), visceral vasoconstrictor (VVC), and renal (RSN) sympathetic fibers. Their barosensitivity was demonstrated, after which all baroreceptor nerves were cut. Multiple microinjections of sodium glutamate (5 nl, 0.1 M) were made in a grid pattern covering the rostral ventrolateral medulla (RVLM) pressor area on seven sides of four animals. Injections increased blood pressure by up to 87 +/- 22 mmHg and MVC, VVC, and RSN activities by up to 169 +/- 55, 62 +/- 23, and 67 +/- 36%, respectively. The relative responses between nerves (taken in pairs) showed significant inhomogeneity across injections into 5/7, 6/7, and 1/7 RVLMs for MVC vs. VVC, MVC vs. RSN, and VVC vs. RSN, respectively. Calculation showed that overall, less than half the response spikes due to RVLM glutamate injections could be accounted for by a hypothetical population of neurons that excited MVC, VVC, and RSN outflows in fixed proportion. Sites that exclusively drove MVC, VVC, or RSN outflows were found in 7/7, 3/7, and 5/7 RVLMs, respectively. Sites that selectively drove either nerve of a given pair were ubiquitous. The RVLM territories from which the three outflows could be activated overlapped but showed clear differences. Their shapes and sizes differed between animals and even between sides. They covered the subretrofacial (SRF) nucleus plus a variable rostromedial extension. The data support the view that the RVLM neurons driving these three sympathetic outflows are largely, perhaps entirely, separate populations.

Animals↗

A comparison of hypotensive and non-hypotensive hemorrhage on Fos expression in spinally projecting neurons of the paraventricular nucleus and rostral ventrolateral medulla.

The protein, Fos, detected immunohistochemically, was used to identify neurons in the brain that were activated after hemorrhage in the conscious rat. Spinally projecting neurons in the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) were identified by the presence of rhodamine-labeled latex beads which had been previously injected into the upper thoracic spinal cord. On the experimental day, conscious rats underwent either (1) withdrawal of 4 ml of blood from a carotid cannula (n = 8) which reduced mean arterial pressure from 96.6 +/- 2.7 to 42.7 +/- 7.1 mmHg, (2) withdrawal of 2 ml of blood (n = 4) which did not affect mean arterial pressure. Animals that were not hemorrhaged were used as controls (n = 6). After the 4 ml hemorrhage, dense concentrations of Fos-positive cell nuclei were found in the lamina terminalis, supraoptic nuclei (SON), PVN and in the medulla. In contrast, the density of Fos-positive cells in 2 ml-hemorrhaged rats was not different from controls except in the SON and in the medial PVN in 2 of 4 rats. After the 4 ml hemorrhage 14.4 +/- 1.2% of the spinally projecting neurons in the PVN and 22.7 +/- 6.1% in the RVLM expressed Fos (P < 0.001 compared to control). After the 2 ml hemorrhage the proportion was 12.2 +/- 3.1% in the PVN (P < 0.001 compared control) but only 5.4 +/- 2.2% in the RVLM (P > 0.05 compared to control). The results suggest that spinally projecting neurons in the PVN and RVLM participate in the reflex responses to hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

CRF-like immunoreactivity selectively labels preganglionic sudomotor neurons in cat.

Immunohistochemical and neuronal tracing methods were used in cats to determine which type of postganglionic sympathetic neuron is innervated by preganglionic neurons which contain corticotrophin releasing factor-like immunoreactivity (CRF-LI). Preganglionic neurons with CRF-LI have their cell bodies at two restricted levels of the spinal cord and terminate in the stellate and lower lumbar ganglia. CRF-LI terminal baskets in stellate and lumbar ganglia surrounded cell bodies, 96-99% of which showed no tyrosine hydroxylase (TH)-LI (presumptive cholinergic neurons). Calcitonin gene-related peptide (CGRP)-LI was used to label the cholinergic ganglion cells which innervate sweat glands: 96-99% of those were confirmed as lacking TH-LI, while the remainder showed weak staining. Every one of over 6000 CRF-LI terminal baskets counted in 4 stellate and 6 lumbar ganglia was found to surround a cell body with CGRP-LI; conversely, 81-86% of the cell bodies showing CGRP-LI were surrounded by CRF-LI terminal baskets. In 3 cats, the retrograde tracer fluorogold was used to label postganglionic neurons projecting to the paw pads (a population which includes both cholinergic sudomotor neurons and noradrenergic vasoconstrictor neurons). Between 26 and 38% of the retrogradely labelled ganglion cells were surrounded by CRF-LI terminal baskets. We conclude that in cats, preganglionic sympathetic neurons with CRF-LI are sudomotor in function.

Acetylcholine↗

Distribution of hypothalamic, medullary and lamina terminalis neurons expressing Fos after hemorrhage in conscious rats.

The immunohistochemical detection of the protein, Fos, has been used as an anatomical marker of activated neurons. Three conscious rats were hemorrhaged (4 ml, 20-25% of blood volume) and the distribution of Fos-stained neurons was compared to that in 4 rats which did not have blood removed. In hemorrhaged rats, a higher concentration of Fos-stained neurons was present in the lamina terminalis, particularly the subfornical organ and organum vasculosum of the lamina terminalis, and in the supraoptic and paraventricular nuclei of the hypothalamus. In the medulla, Fos-stained neurons were restricted to the nucleus of the tractus solitarius, area postrema and the ventrolateral medulla. We hypothesize that those neurons are involved in mediating the physiological responses to hemorrhage.

Animals↗