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A V Ferguson

Publications and source records attributed to A V Ferguson.

98 records · Page 6Linked to original sources

Facilitatory influence of noradrenergic afferents on the excitability of rat paraventricular nucleus neurosecretory cells.

The role of the A1 and A2 noradrenergic cell groups of the caudal medulla in regulating the activity of paraventricular nucleus neurosecretory cells was examined with electrophysiological methods in anaesthetized male Sprague-Dawley rats. Antidromically identified neurosecretory cells were classified as vasopressin or oxytocin secreting on the basis of spontaneous firing patterns and responsivity to baroreceptor activation. The effect on cell firing of single pulses (25-200 microA) delivered to either the A1 or A2 cell group areas was then examined using peri-stimulus histograms. Stimulation of the A1 region enhanced the activity of 78% of putative vasopressin-secreting neurones tested (n = 18), but failed to affect the activity of the majority (73%) of putative oxytocin-secreting units (n = 15). A2 stimulation enhanced the firing rate of both putative vasopressin- (60%, total n = 14) and putative oxytocin-secreting (70%, total n = 27) neurones. Destruction of the paraventricular nucleus catecholamine terminal plexus by pre-treatment with the neurotoxin 6-hydroxydopamine abolished the facilitatory effects of both A1 and A2 stimulation. These findings suggest that noradrenergic afferents of medullary origin facilitate the activity of paraventricular nucleus neurosecretory cells. The role of the projection from the A1 cell group appears to differ from that of the A2 group, however, in that its effects are specific to putative vasopressin-secreting units.

Adrenergic Fibers↗

Subfornical organ stimulation excites paraventricular neurons projecting to dorsal medulla.

Electrical stimulation in the subfornical organ (SFO) of pentobarbital-anesthetized Sprague-Dawley rats was noted to influence the excitability of paraventricular nucleus (PVN) neurons antidromically identified as projecting to the dorsomedial medulla. Extracellular recordings indicated that 60% (n = 34) of these caudally projecting PVN neurons increased activity in response to single shock stimuli delivered to the SFO. Short-latency [30.0 +/- 2.7 (SE) ms] and long-latency (162.5 +/- 32.5 ms) responses were observed. The remaining neurons were either unaffected (38%) or inhibited (2%) by SFO stimulation. These data suggest functional connectivity between the SFO and the dorsomedial medulla. It is proposed that such a pathway may mediate pressor responses observed to follow electrical stimulation in the SFO.

Animals↗

Subfornical organ efferents influence the excitability of neurohypophyseal and tuberoinfundibular paraventricular nucleus neurons in the rat.

Electrical stimulation in the subfornical organ (SFO) alters the excitability of antidromically identified paraventricular nucleus neurons. Extracellular recordings demonstrate that the dominant effect of single stimuli delivered to the SFO on neurohypophyseal oxytocin and vasopressin containing neurons is an increase in excitability. In 35% of cells tested, this excitation showed a long latency (44.3 +/- 3.4 ms) prolonged duration (208.7 +/- 23.5 ms), while in 16% of the neurons the excitation observed may be described as short latency (24.7 +/- 1.8 ms) short duration (11.6 +/- 1.4 ms). Of the remaining cells antidromically identified as projecting to the posterior pituitary, 12% showed initial decreases in excitability following SFO stimulation while the remaining 37% were unaffected. Evidence is presented demonstrating that stimulation in the region of the SFO results in short latency (27.9 +/- 2.4 ms) short duration (7.8 +/- 0.7 ms) increases in excitability in 22% of antidromically identified PVN tuberoinfundibular neurons tested. These data provide electrophysiological evidence in support of the proposed role of the subfornical organ in the control of posterior and anterior pituitary function.

Animals↗

An investigation of the age-related deficits in the febrile response of the rabbit.

The febrile response of the New Zealand White rabbit in animals less than 1 yr old was compared with that in 3-yr-old animals. A reduced febrile response to both endotoxin and live bacteria injected intravenously was observed in the older group of animals. Peripheral vasoconstriction was observed, suggesting the drive to increase body temperature remained. Plasma catecholamines increased significantly in both groups of animals during fever. However, significantly greater increases in plasma epinephrine were observed in the older animals. A significant deficit in catecholamine-induced thermogenesis was observed in the older group of rabbits. This deficit alone does not explain the reduced febrile response, as beta-adrenergic blockade does not suppress the febrile response of young animals. Thus it is suggested that the primary deficit resulting in a reduced febrile response in the 3-yr-old rabbits is due to other age-related changes in the thermoregulatory system.

Aging↗

Evidence of environmental influence on the development of thermoregulation in the rat.

Sprague-Dawley rats were raised in an environmentally controlled room at 33 degrees C. Thermoregulatory responses of animals reared in this way were compared with those of control and warm-acclimated rats. Warm-reared animals demonstrated a significantly greater fall in colonic temperature during cold exposure when compared with both warm-acclimated (p less than 0.01) and control (p less than 0.001) animals. Warm-reared animals also show a modified response to central infusion of noradrenaline; they produce a hyperthermia in contrast with the hypothermia observed in control and warm-acclimated rats. These results suggest that the early thermal environment may modify the development of temperature regulation in the Sprague-Dawley rat in a way different from the normal acclimation process.

Acclimatization↗

Age-related differences in the febrile response of the New Zealand White rabbit to endotoxin.

The effect of age on the febrile response of New Zealand White rabbits was investigated by administering bacterial endotoxin intravenously to animals from two different age groups. Rabbits greater than 2.0 years of age developed significantly smaller fevers than did animals that were less than 1.0 year old (p less than 0.001). The deficit in the febrile response of older animals was specifically related to an absence of the second peak of fever.

Aging↗

Modification of thermoregulatory responses in rabbits reared at elevated environmental temperatures.

1. Pregnant New Zealand white rabbits were kept from 14 days pre-partum at an environmental temperature of 33 degrees C, and their offspring were reared at this temperature. 2. In response to a 4 hr cold exposure, animals (aged 90-180 days) raised in this way showed significant drops in colonic temperature (-2.7 +/- 0.5 degrees C) while control animals reared at 20 degrees C did not (+0.05 +/- 0.1 degrees C). 3. A reduced, monophasic endotoxin fever was observed in animals reared at 33 degrees C, while a normal biphasic fever was seen in rabbits originally reared at 20 degrees C and subsequently acclimated to 33 degrees C. 4. A greatly reduced temperature response to intravenous infusion of noradrenaline was also found in animals raised at 33 degrees C. 5. It is proposed that thermal afferent input during early life may play an important role in the development of the thermoregulatory system.

Acclimatization↗

Role of gastric acid secretion and blood flow in the development of vagal stimulation induced gastric mucosal damage.

Vagal stimulation has been shown to result in the development of gastric mucosal erosions in the rat, although the mechanisms underlying the development of such erosions are not known. The effects of vagal stimulation on gastric acid secretion and mucosal blood flow were examined in urethane-anesthetized male Sprague-Dawley rats to determine whether changes in these factors correlate with the mucosal damage in response to vagal stimulation. Electrical stimulation (5 Hz, 5 V, 1 ms for 60 min) of afferent or efferent components of the vagi was not found to induce any significant increase in the mean acid secretory rate compared with control animals (p > 0.05). In contrast, stimulation of intact vagus nerves induced a significant increase in the mean acid secretory rate compared with control and efferent- and afferent-stimulated groups (p < 0.01). Measurement of gastric blood flow with laser-Doppler flowmetry demonstrated intact vagal stimulation to have no significant effect on gastric blood flow. These data suggest that such vagal stimulation induced increases in acid secretion in urethane-anesthetized animals may represent a part of the integrated physiological response to such stimulation which leads to the development of gastric mucosal erosions within 60 min. Pretreatment with antisecretory agents such as cimetidine and interleukin-1 beta significantly reduce the gastric mucosal injury compared with untreated animals (p < 0.05), emphasizing the important role of acid secretion in the development of vagal-induced gastric damage.

Animals↗