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P R Howe

Publications and source records attributed to P R Howe.

At least 55 records · Page 3Linked to original sources

Effects of chronic alcohol consumption and alcohol withdrawal on blood pressure in stroke-prone spontaneously hypertensive rats.

The development of blood pressure was monitored by the tail-cuff method in normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) receiving ethanol (alcohol) in drinking water from weaning (approximately 1 month of age). Alcohol administration over a 3-month period attenuated the development of hypertension in SHRSP and also caused a small reduction of the initial blood pressure rise in WKY. This was accompanied by a reduction of fluid intake and an increase of circulating antidiuretic hormone (arginine vasopressin; AVP). Circulatory volume remained constant. Direct measurement of arterial blood pressure in conscious rats before and after autonomic blockade confirmed the antihypertensive effect of alcohol in SHRSP and indicated that it is at least partly dependent on altered activity of neural mechanisms. Sudden withdrawal of alcohol caused an immediate increase of fluid intake followed by a rise of blood pressure lasting several days in both WKY and SHRSP. This withdrawal hypertension could not be attributed to changes in plasma catecholamines or AVP.

Animals↗

An increased pool of secretory hormones and peptides in adrenal medulla of stroke-prone spontaneously hypertensive rats.

Secretory components of the adrenal medulla were compared in normotensive Wistar-Kyoto (WKY) rats and in stroke-prone spontaneously hypertensive rats (SHRSP) at both 4 and 12 months of age. Noradrenaline, adrenaline, dopamine, neuropeptide Y, and chromogranins A and B were significantly higher in adrenal glands of SHRSP than those of WKY rats at 4 months. At 12 months, the levels of these components in SHRSP had increased even more (about 200% in WKY rats). There was no change in the relative composition of the adrenal "secretory cocktail." Neither the chromogranin A/chromogranin B ratio nor their apparent proteolytic processing in chromaffin granules differed between SHRSP or WKY rats. The lack of a significant change in membrane-bound cytochrome b561 and the small increase in dopamine beta-hydroxylase suggest that the higher levels of secretory components in SHRSP are not simply caused by an increase in the number of chromaffin granules, but possibly by a selective increase in the secretory content of these organelles providing a larger package for quantal release by exocytosis. This may be relevant for the elevation of blood pressure in this strain. The immunological methods described in this paper allow for the first time a determination of the secretory quantal levels in catecholamine storage. This should be useful for further studies in hypertensive models.

Adrenal Medulla↗

Antihypertensive effect of alcohol in spontaneously hypertensive rats.

The influence of ethanol (alcohol) consumption on blood pressure during and after the development of hypertension was examined by using spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP). Normotensive Wistar-Kyoto (WKY) rats were also used for comparison. Substituting alcohol (5-20%) for drinking water at 1 month of age retarded the age-dependent rise of blood pressure in all three strains so that, at 7 months, blood pressure measured by a tail-cuff method was 24 mm Hg, 26 mm Hg, and 41 mm Hg lower in the alcohol-treated WKY rats, SHR, and SHRSP, respectively, than in untreated rats. Significant differences in blood pressure were seen in each strain after only 3 months. Withdrawal of alcohol at this stage caused an acute rise of blood pressure then a return to subnormal levels, which persisted for a further 3 months. Administration of 15% alcohol to adult WKY rats and SHR for 2 months had no significant effect on blood pressure. Increasing alcohol content to 20% for a further 2 months prevented rises of blood pressure in both strains. Thus, although continuous drinking of alcohol does not lower blood pressure, it appears to counteract the development of hypertension in rats.

Aging↗

Is phenylethanolamine-N-methyltransferase (PNMT) contained in rat hypothalamic neurons?

Three polyclonal antisera raised against bovine adrenal phenylethanolamine-N-methyltransferase (PNMT) were used to stain PNMT-containing neurons in rat medulla oblongata and hypothalamus. Without colchicine pretreatment all three antisera stained nerve fibres in both the medulla and hypothalamus and nerve cell bodies in the medulla only. In colchicine pretreated rats one antiserum only stained cell bodies in the hypothalamus as well. All staining was prevented by prior absorption of the antiserum with purified bovine PNMT. Thus, if PNMT is present in the rat hypothalamic neurons then it is not identical to the form of PNMT present in rat medullary neurons.

Animals↗

Distribution of monoamine-synthesizing neurons in the human medulla oblongata.

We have employed immunohistochemical and morphometric procedures to study the distribution of monoamine-synthesizing neurons in the medulla oblongata of the adult human, utilizing antibodies to tyrosine hydroxylase (TH), phenylethanolamine N-methyltransferase (PNMT), and phenylalanine hydroxylase (PH8). In the human brain, the antigen with which PH8 reacts occurs within neurons that presumably synthesize serotonin (Haan et al., '87). Neurons containing these antigens were mapped and counted in successive coronal sections with the aid of a computer-assisted procedure. The results indicate that monoamine-synthesizing neurons are distributed in the human brain in patterns broadly similar to those described for other species. TH-immunoreactive cells extended caudorostrally for approximately 32 mm commencing at the spinomedullary junction and ending 8 mm caudal to the pontomedullary junction. In coronal sections these TH-immunoreactive neurons were seen in the lateral medulla dorsal to the inferior olive extending in a continuous band to the dorsomedial medulla. Above the obex the majority of these cells apparently synthesize adrenaline since many PNMT-immunoreactive cells were also found in this region. There were few or no PNMT-immunoreactive cells caudal to the obex, indicating that the TH-immunoreactive cells in this region synthesize either noradrenaline or dopamine. Approximately 65% of these TH-immunoreactive neurons contained melanin pigment, whereas few or no PNMT-immunoreactive cells contained melanin pigment. PH8-immunoreactive cells extended throughout the rostrocaudal extent of the medulla oblongata (approximately 40 mm). In coronal sections the majority were found in the medullary raphe nuclei. However, many cells throughout the rostrocaudal extent of the medulla were found laterally intermingled with catecholamine-synthesizing neurons. Occasional neurons in the lateral medulla appeared to contain both PH8- and TH-immunoreactivity.

Aged↗

Distribution of substance P-like immunoreactive neurons in the human medulla oblongata: co-localization with monoamine-synthesizing neurons.

The raphe nuclei also contained SP-like immunoreactivity (up to 30%) while few monoamine-synthesizing neurons in the lateral and dorsomedial medulla contained SP-like immunoreactivity (approximately 5% of presumed serotonin-, noradrenaline-, and adren- the adult human. The majority of SP-like immunoreactive neurons were found in four main regions: the lateral medulla, the dorsomedial medulla, the spinal trigeminal nucleus, and the raphe nuclei. The morphology of immunoreactive cells varied according to the region in which they were found. In contrast to previous studies, we found large numbers (90,000) of SP-like immunoreactive neurons throughout the adult human medulla oblongata. The distribution of these SP-like immunoreactive neurons appears to be significantly different from those described in the rat and cat. These results were compared to the distributions of monoamine-synthesizing and neuropeptide Y (NPY)-like immunoreactive neurons in the human medulla previously reported (Halliday et al.: Neuroscience, in press, 1988a; J. Comp. Neurol., in press, 1988b). Colocalization studies revealed that many presumed serotonin-synthesizing neurons in the raphe nuclei also contained SP-like immunoreactivity (up to 30%) while few monoamine-synthesizing neurons in the lateral and dorsomedial medulla contained SP-like immunoreactivity (approximately 5% of presumed serotonin-, noradrenaline-, and adrenaline-synthesizing neurons). The distributions of SP- and NPY-like immunoreactive neurons were similar, although SP-like immunoreactive neurons were concentrated in the lateral regions of the same structures. We have found that the distributions of monoamine-synthesizing, NPY-, and SP-like immunoreactive neurons significantly overlap, particularly in the lateral medulla of the adult human. There is a large increase in the number of these cells in this region compared to other species, emphasizing the neuroanatomical differences between humans and other species.

Aged↗

The distribution of neuropeptide Y-like immunoreactive neurons in the human medulla oblongata.

We have described the distribution of neuropeptide Y-like immunoreactive neurons in the medulla oblongata of the adult human. The majority of neuropeptide Y-like immunoreactive cells were found in four regions of the medulla: the ventrolateral reticular formation, the dorsomedial medulla, the secondary sensory nuclei and the rostral raphe nuclei. The morphology of neuropeptide Y-like immunoreactive cells varied in each of these regions. In the ventrolateral reticular formation, the labelled neurons were round and pigmented caudal to the obex but elongated and non-pigmented rostral to the obex; in the dorsomedial medulla, they were triangular and pigmented caudal to but not rostral to the obex; in the secondary sensory nuclei, they were multipolar, non-pigmented and significantly smaller than in the other areas; in the rostral raphe nuclei, they were bipolar and non-pigmented. Colocalization studies revealed that many neuropeptide Y-like immunoreactive cells also synthesize monoamines, consistent with conclusions based on a quantitative comparison of their distributions. Neuropeptide Y-like immunoreactivity was present in about 25% of presumed noradrenaline-synthesizing cells in the caudal ventrolateral medulla (corresponding to the A1 region); about 50% of adrenaline- and 70% of presumed serotonin-synthesizing cells in the rostral ventrolateral medulla (C1 and B2-3 regions); 90-100% of presumed noradrenaline-synthesizing cells in the dorsomedial medulla at and above the obex (A2 region); about 50% of adrenaline-synthesizing cells in the rostral dorsomedial medulla (C2 region); about 5% of presumed serotonin-synthesizing cells in the rostral raphe nuclei (B2-3 region). The largest of these groups was the presumed serotonin-synthesizing cells that contained neuropeptide Y-like immunoreactivity in the rostral ventrolateral medulla. This is the first report of such a cell group in the medulla of any mammal, and emphasizes the neuroanatomical differences between humans and other species.

Aged↗

Pressor responsiveness of the sub-retrofacial nucleus and the midbrain reticular formation in the rat after 6-hydroxydopamine-induced lesions of ascending and descending catecholamine pathways.

We have recently shown that intracerebroventricular (icvt) administration of 6-hydroxydopamine (6-OHDA) inhibits centrally-evoked pressor activity. To see whether this effect is attributable to the disruption of descending bulbospinal or, alternatively, ascending suprabulbar catecholamine (CA) pathways, spontaneously hypertensive rats (SHR) were given localized intracerebral injections of 6-OHDA. One month later, pressor responses evoked by electrical or chemical stimulation in the rostral ventrolateral medulla or midbrain were examined under urethane anaesthesia. Injections of 6-OHDA into the medial forebrain bundle, which depleted noradrenaline and adrenaline in the hypothalamus, lowered basal blood pressure but potentiated the pressor responses to stimulation. In contrast, intraspinal injection of 6-OHDA raised basal blood pressure and attenuated pressor responses. This was accompanied by a partial depletion of adrenaline and the almost complete disappearance of noradrenaline in the spinal cord. Thus, the attenuation of pressor responses observed previously following icvt 6-OHDA can be attributed to an effect on spinal CA pathways. The effects on basal blood pressure suggest that, in SHR, ascending CA pathways are tonically pressor, while spinal CA pathways are depressor. Whilst it is unlikely, therefore, that spinal CAs mediate vasomotor outflow, the altered responses to stimulation after 6-OHDA suggest that central CA pathways can modulate the sensitivity of vasomotor neurones.

Animals↗

Ontogeny of catecholamine-synthesizing enzymes and enkephalins in the sheep adrenal medulla: an immunocytochemical study.

An immunocytochemical staining technique was used to investigate the development of the sheep adrenal medullary cells containing enkephalins and the catecholamine synthetic enzymes dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyl transferase (PNMT). No staining was observed in the adrenocortical cells with any of the antisera used in this study. Positive staining with anti-DBH was observed throughout the medulla in both adult and fetal adrenal glands from 80 days of gestation. Positive staining with anti-PNMT was observed in all glands from as early as 80 days of gestation, and staining with this antiserum was mainly confined to the peripheral medullary cells, which were adjacent to, and interdigitated between, the cells of the adrenal cortex. In the fetus between 80 and 120 days of gestation, staining for the enkephalins was observed in both the peripheral columnar and the central polygonal adrenal medullary cells. After 125 days of gestation and in the adult ewe, the peripheral columnar cells were uniformly stained with anti-enkephalin whereas many unstained cells were present in the central medullary region. Therefore, enkephalin-containing peptides are present in the catecholamine cells of the fetal and adult sheep adrenal and there appears to be a changing pattern in the distribution of the enkephalins in the fetal adrenal in late gestation.

Adrenal Medulla↗

Organization of galanin-immunoreactive inputs to the paraventricular nucleus with special reference to their relationship to catecholaminergic afferents.

Immunohistochemical and axonal transport techniques were used to characterize the origin and distribution of galanin-immunoreactive inputs to the paraventricular (PVH) and supraoptic (SO) nuclei of the hypothalamus in the rat. In the parvicellular division of the PVH, the most prominent inputs were confined to the anterior and periventricular parts of the nucleus rostrally and the dorsal and ventral medial subdivisions caudally; the galaninergic inputs to the magnocellular division of PVH and SO were very sparse and were preferentially distributed to regions containing predominantly oxytocinergic neurons. A combined retrograde transport-immunohistochemical method was employed to identify sources of these projections. Galanin immunoreactivity was found to coexist with dopamine-beta-hydroxylase (DBH) immunoreactivity in subsets of retrogradely labeled neurons of the A1 and A6 (locus coeruleus) catecholamine cell groups; no evidence was adduced for the presence of galanin in adrenergic (i.e., phenylethanolamine-N-methyltransferase-positive) neurons that project to the PVH. Apart from minor contributions from the mesencephalic raphe nuclei, no other brainstem cell groups contributed to the galaninergic innervation of the PVH. In the forebrain, the most prominent grouping of doubly labeled cells was centered in the rostral part of the dorsomedial nucleus of the hypothalamus (DMH), though significant numbers were also found in the lateral hypothalamic area, the arcuate nucleus, and the medial preoptic area. In experiments designed to define the subnuclear specificity of some galanin-containing inputs to the PVH, iontophoretic deposits of the anterogradely transported plant lectin, Phaseolus vulgaris-leucoagglutinin (PHA-L), were placed in the A1 and A6 cell groups and in the DMH. Sections through the PVH were prepared so as to allow colocalization of anterogradely transported PHA-L and galanin immunoreactivity in individual fibers and varicosities. Consistent with the retrograde transport data, the greatest degree of galanin-PHA-L correspondence was seen after lectin deposits in the DMH, and over 80% of the doubly labeled varicosities were confined to the anterior, periventricular, and medial parvicellular subdivisions of the nucleus. The galanin-containing projection from the locus coeruleus was most circumscribed, with the vast majority of doubly labeled varicosities confined to the periventricular and adjoining aspects of the anterior and medial parvicellular subdivisions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Effects of 6-hydroxydopamine and the PNMT inhibitor LY134046 on pressor responses to stimulation of the subretrofacial nucleus in anaesthetized stroke-prone spontaneously hypertensive rats.

The subretrofacial nucleus of the rostral ventrolateral medulla is an important site for the control of sympathetic vasomotor tone and is the location of the C1 PNMT-containing cell bodies. In the present study the involvement of central monoaminergic neurons in the pressor responses evoked by chemical or electrical stimulation of this nucleus was examined in urethane-anaesthetized stroke-prone spontaneously hypertensive rats (SHRSP). Vehicle-treated rats were compared to animals treated with the PNMT inhibitor LY134046, the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) or a combination of 6-OHDA and the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). LY134046 caused a 43% depletion of adrenaline content in the hypothalamus and medulla but not in the spinal cord but had no effect on the pressor responses to stimulation of the subretrofacial nucleus. However, intraventricular administration of 6-OHDA reduced the pressor responses to subretrofacial nucleus stimulation by 50%. 6-OHDA caused profound depletion of noradrenaline in the brain and spinal cord, and adrenaline in the hypothalamus. Combined treatment with 6-OHDA and 5,7-DHT caused the additional depletion of serotonin to 34% and 13% in the hypothalamus and spinal cord, respectively, but caused no further reduction of pressor responses than with 6-OHDA alone. These results suggest that the pressor responses elicited by subretrofacial nucleus stimulation involve a 6-OHDA-sensitive pathway (presumably catecholaminergic) other than the bulbospinal adrenaline pathway but that serotonergic mechanisms do not contribute.

Anesthesia↗

Distribution of tyrosine hydroxylase and neuropeptide Y-like immunoreactive neurons in rabbit medulla oblongata, with attention to colocalization studies, presumptive adrenaline-synthesizing perikarya, and vagal preganglionic cells.

We studied the distribution, within the rabbit medulla oblongata, of neuronal cell bodies containing either tyrosine hydroxylase or neuropeptide Y-like immunoreactivity. Both avidin-biotin and immunofluorescence procedures were used. Because the two primary antibodies were raised in different species it was possible to perform simultaneous colocalization studies with the immunofluorescence procedure. Tyrosine hydroxylase-containing neurons in the rostral medulla were demonstrated to contain a catecholamine by the colchicine-enhanced FAGLU (formaldehyde-glutaraldehyde) fluorescence histochemical procedure. These neurons are presumably adrenergic, corresponding to the C1 and C2 groups described in the rat. No C3 group was found in the rabbit. The distribution of tyrosine hydroxylase-containing neurons in the caudal medulla was in accordance with previous descriptions of the A1 and A2 groups based on the unenhanced FAGLU procedure. Neuropeptide Y-like immunoreactivity was observed in cell groups corresponding to those already described in the rat, but additional groups were discovered in the rabbit. Some neurons containing neuropeptide Y-like immunoreactivity were observed in nucleus raphe pallidus and these also contained serotonin (5-HT). In the nearby nucleus reticularis gigantocellularis there were occasional neurons that contained neuropeptide Y-like immunoreactivity without any colocalized 5-HT. Neuropeptide Y-like immunoreactivity was also observed in the dorsal motor nucleus of the vagus, rostral to the obex, and these neurons were demonstrated to be true vagal preganglionic cells by colocalization of neuropeptide Y-like immunoreactivity and Fast Blue retrogradely transported from the cervical vagus. We found that neuropeptide Y-like immunoreactivity was colocalized in approximately 75% of the tyrosine hydroxylase-containing neurons in the rostral medulla (C1 and C2 cells). A smaller proportion of the A1 cells also contained this peptide but it was absent from both the most caudal A1 cells and from the A2 cells. Some tyrosine hydroxylase-containing neurons occur in direct apposition to vagal preganglionic cells in both the dorsal motor nucleus of the vagus and the nucleus ambiguous. However, colocalization studies revealed that none of these neurons contained Fast Blue when this dye was retrogradely transported from the cervical vagus. Medullary catecholamine-synthesizing neurons apparently do not contribute axons to the vagus nerve. This finding is consistent with our own studies in the rat but is in contrast to studies in this species published by other workers.

Animals↗

The effect of a high-fat diet and sucrose drinking option on the development of obesity in spontaneously hypertensive rats.

1. Energy intakes, body-weights, body fat index, total body fat and interscapular brown adipose tissue (IBAT) were examined in adult male, spontaneously hypertensive, stroke-prone (SHR-SP) rats and normotensive Wistar/Kyoto (WKY) controls given one of four diets for 33 d: (a) a starch diet, (b) a starch diet and a sucrose solution drinking option, (c) an 80% energy from fat (F80) diet, (d) the F80 diet and a sucrose drinking option. 2. The SHR-SP rats showed a complete resistance to obesity on all four diets. For the high-fat diet the WKY animals became markedly obese with approximately two-fold increases in body-weight gain and body fat index when compared with the SHR-SP rats. The gain in total body fat was also significantly greater. IBAT as a percentage of total body-weight did not differ between the WKY and SHR-SP groups. 3. Compared with the WKY animals, the SHR-SP rats showed a reduced food intake but had the same potential to gain weight from the high-fat diet. 4. It is concluded that the resistance to obesity by the hypertensive animals is the result of a diminished energy intake.

Animals↗

Effects of short-term modification of dietary sodium intake on plasma catecholamines and blood pressure in prehypertensive children.

The influence of dietary sodium intake on plasma catecholamines was examined as part of a dietary intervention study in 21 prehypertensive school children. Diastolic blood pressure was significantly elevated in girls after 3 weeks on a high sodium diet compared with a low sodium diet. Plasma adrenaline levels were raised slightly by the high sodium intake but plasma noradrenaline was significantly reduced. Increases of plasma catecholamines in response to standing or cold stress were unaffected by changes in sodium intake. The results indicate that the pressor effect of dietary sodium in children is not attributable to increased sympathetic nerve activity.

Adolescent↗

Colocalization of neuropeptide Y immunoreactivity in brainstem catecholaminergic neurons that project to the paraventricular nucleus of the hypothalamus.

Immunohistochemical methods were used in the rat to plot the distribution of neuropeptide Y (NPY) immunoreactivity in the paraventricular (PVH) and supraoptic (SO) nuclei of the hypothalamus, and a combined retrograde transport-double immunohistochemical labeling technique was used to determine the extent to which NPY immunoreactivity is coexpressed in brainstem cell groups that stain with antisera to phenylethanolamine-N-methyltransferase (PNMT; a marker for adrenergic neurons) or dopamine-beta-hydroxylase (DBH; a marker for adrenergic and noradrenergic neurons) and also project to the PVH. The results confirm the existence of a major NPY-immunoreactive pathway that is in a position to influence each major class of output neurons in the PVH. Thus, most parts of the parvicellular division receive a dense input that is similar to, though somewhat more extensive than, the one stained by DBH antisera. However, in the magnocellular division catecholaminergic inputs are preferentially associated with vasopressinergic neurons, while NPY-stained fibers tend to be more evenly distributed in regions containing both oxytocinergic and vasopressingergic neurons, and their density appear to be lower than that of DBH-stained fibers. In the SO, only a moderate NPY-stained input was apparent, while, as described previously, DBH-immunoreactive fibers are rather dense and are preferentially distributed in vasopressinergic regions of the nucleus. The results of combined retrograde transport-double immunohistochemical labeling experiments may be summarized as follows: the vast majority of cells in the medulla that were retrogradely labeled after discrete implants of the fluorescent tracer true blue into the PVH, and were PNMT-immunoreactive, also stained for NPY. However, less extensive co-localization was detected in noradrenergic cell groups of the caudal medulla. About 60% of the retrogradely labeled-DBH positive cells in the A1 cell group were also NPY-positive, while those in the caudal part of the nucleus of the solitary tract (the A2 cell group) usually failed to stain with anti-NPY. Similarly, in the locus coeruleus (the A6 cell group) where virtually all retrogradely labeled neurons were DBH-positive, only rarely were triply labeled cells detected. These results suggest that NPY immunoreactivity is extensively co-contained within adrenergic neurons of the C1, C2, and C3 groups that project to the PVH, while the correspondence in noradrenergic cell groups is less complete, and generally limited to a subset of neurons in the A1 cell group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗

Influence of dietary sodium on blood pressure in baroreceptor-denervated rats.

One possible explanation for the salt sensitivity of blood pressure (BP) in certain hypertensive individuals is that neural mechanisms which normally counteract the pressor effect of a high dietary sodium intake are defective. We have tested this possibility in normotensive Wistar-Kyoto rats (WKY) by surgically ablating the arterial baroreflex mechanism. This manoeuvre, by itself, conferred substantial salt-sensitivity on the WKY rats whose BP is normally relatively insensitive to dietary sodium intake. The treated rats responded to a high sodium diet with a significant rise in systolic BP which was reversed by substituting a low sodium diet. Thus, impaired baroreflex function which has been observed in essential hypertension and in hypertensive animals, may be responsible for the hypertensive effect of sodium.

Animals↗

Visualisation of catecholamine-fluorescent nerve cell bodies in the rat brain after colchicine treatment.

Central administration of colchicine causes accumulation of catecholamines in nerve cell bodies and enhances their visualisation in the rat brain by the formaldehyde-glutaraldehyde (FAGLU) histofluorescence method. The detection of catecholamine-containing nerve cells by the FAGLU method was considerably improved in rats pretreated with colchicine, and adrenaline-synthesising nerve cells, which are not normally detected by the FAGLU method, could be readily localized after colchicine. The identity of the FAGLU-fluorescent nerve cells was confirmed by simultaneous immunofluorescent detection of catecholamine-synthesising enzymes in sections of the medulla oblongata. The FAGLU method applied to colchicine-treated animals could provide a simple means of detecting central adrenaline nerve cells in other species.

Animals↗

Evidence that adrenaline neurons in the rostral ventrolateral medulla have a vasopressor function.

Focal electrical or chemical stimulation in the rostral ventrolateral medulla of the rat and rabbit evoked large increases in arterial pressure when the stimulus sites were in the region containing a high density of adrenaline synthesizing neurons, but much smaller or no responses when the sites were outside this region. The adrenaline neurons were identified in the rat by an immunohistochemical procedure, and in the rabbit by a modification of the FAGLU catecholamine fluorescence method. By combining the fluorescence procedure with the method of retrograde transport of horseradish peroxidase, many of the adrenaline synthesizing neurons in the rabbit were shown to project to the spinal cord.

Animals↗