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PubMed1985

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

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

Adult↗
PubMed1981

Afferent projections related to attack sites in the ventral midbrain tegmentum of the cat.

Quiet attack was elicited by electrical stimulation of the ventrolateral midbrain tegmentum of the cat. The paw was not used other than to position or hold the rat during the bite. Bites were directed toward the head and neck region and were not accompanied by autonomic responses other than pupillary dilation and sometimes slight piloerection on the back. Horseradish peroxidase was deposited at the attack sites. Cells labeled with the peroxidase reaction product were located in gyrus propreus, gyrus genualis, nucleus accumbens, bed nucleus of the stria terminalis, bed nucleus of the anterior commissure, nucleus of the diagonal band, substantia innominata, anterior amygdaloid area, ventromedial hypothalamic area, paraventricular nucleus, perifornical hypothalamic area, lateral hypothalamic area, dorsal hypothalamic area, field of Forel, midbrain reticular formation, superior colliculus, ventral central grey, lateral central gray, locus coeruleus, parabrachial nuclei, nucleus of the lateral lemniscus, oral pontine reticular nucleus, and the dorsal raphe. Other regions were less prominently labeled. Previous studies have shown most of these sites to have some involvement in attack.

Afferent Pathways↗
PubMed1985

The organization of the hypothalamic pathways mediating affective defense behavior in the cat.

The purpose of this study was to describe the hypothalamic pathways which mediate affective defense in the cat utilizing the methods of [14C]2-deoxyglucose (2-DG) and [3H]leucine radioautography in concert with the technique of electrical brain stimulation. The feline affective defense response, characterized by pupillary dilatation, piloerection, ear retraction, hissing, growling and striking with the forepaws, was elicited consistently by stimulation of sites within the ventromedial hypothalamus and anterior aspect of the medial hypothalamus. In one series of experiments, 2-DG autoradiography was employed to describe the brain regions activated following stimulation of sites in the region of the ventromedial hypothalamus from which affective defense had been elicited. Ventromedial hypothalamic stimulation produced activation primarily in forebrain regions situated rostral to the level of the stimulating electrode. These structures included principally the anteromedial hypothalamus and medial preoptic area, as well as the bed nuclei of the stria terminalis and anterior commissure, diagonal band and lateral septal area. The caudal extent of activation included only the dorsal and perifornical hypothalamus at the level of the stimulation site. In a second series of experiments, affective defense sites in the anteromedial hypothalamus were stimulated and the regional distribution of 2-DG label was identified. In contrast to the results obtained from ventromedial hypothalamic stimulation, these experiments revealed a marked descending distribution of label within the posterior hypothalamus, midbrain central gray and ventral tegmental area. Results obtained from studies in which tritiated amino acids were injected into affective defense sites in both the ventromedial nucleus and anteromedial hypothalamus confirmed the general findings observed with 2-DG autoradiography. From these observations, we have concluded that the organization of the pathway mediating affective defense behavior from the ventromedial hypothalamus to the midbrain involves an initial synapse within the region of the anteromedial hypothalamus and a second synapse in the midbrain central gray substance. The significance of the anteromedial hypothalamus for the expression of affective defense behavior was considered in the Discussion.

Aggression↗
PubMed1985

Enhanced sensitivity of cerebellar Purkinje cells to iontophoretically-applied serotonin in thiamine deficiency.

Electrophysiological aspects of thiamine depletion in the rat induced by dietary deficiency are described. Behavioral changes as well as qualitative and quantitative alterations in the sensitivity of cerebellar Purkinje cells to iontophoretically-applied 5-hydroxytryptamine (5-HT) were observed. Thiamine-deficient rats were characterized essentially by ataxia, piloerection, paresis, apparent weakness, and hypothermia after 4-6 weeks on a thiamine-free diet. Basal Purkinje cell firing frequency was unaffected by thiamine deficiency. The response of Purkinje cells to iontophoretically-applied 5-HT was solely inhibitory in deficient rats. In control rats, however, responses to 5-HT were excitatory, biphasic, or inhibitory. Neurons in the thiamine-deficient animals were more sensitive to the inhibitory effects of 5-HT, as demonstrated by a significant parallel shift to the left of the dose-response curve. Durations of 5-HT effects were similar in both groups. Dose-response relationships for GABA-induced inhibition of Purkinje cell firing from thiamine deficient and control rats did not differ from one another. These data demonstrate a relatively selective effect of thiamine depletion on cerebellar serotonergic neurotransmission assessed electrophysiologically. We believe there is up-regulation of 5-HT receptors on Purkinje cells caused by thiamine deficiency-induced impairment of indoleamine input to the cerebellum from raphe and related nuclei.

Animals↗
PubMed1986

Effects of pontine tegmental lesions that induce paradoxical sleep without atonia on thermoregulation in cats during wakefulness.

The characteristics of thermoregulation during wakefulness of cats with pontine tegmental lesions that induced paradoxical sleep (PS) without atonia have been studied. Thresholds for shivering and for panting, brain temperature and body posture at different ambient temperatures were noted and compared with those in intact animals. Intact cats began to shiver, piloerect and curl their bodies at ambient temperatures (Ta) of 8-10 degrees C, whereas after the lesions these responses began at Ta of 15-17 degrees C. Body temperature (Tb) did not change. Cats with lesions panted and extended their bodies much earlier at high Ta than did normal cats, and Tb began rising at a lower Ta and reached a higher value. Therefore, the cats with lesions were more susceptible to thermal loads; the thresholds for shivering (heat-gain) and panting (heat-loss) were both lowered. These results obtained in wakefulness suggest that the absence of shivering previously shown in cats during PS without atonia cannot simply be the result of an overall increased threshold for heat-gain responses but, rather, are in keeping with the observation that thermoregulation is suppressed in PS.

Animals↗
PubMed1987

The pathways mediating affective defense and quiet biting attack behavior from the midbrain central gray of the cat: an autoradiographic study.

The purpose of this study was to describe the pathways which mediate feline affective defense and quiet biting attack behavior elicited from the midbrain central gray. In these experiments, methods of [3H]leucine and 2-deoxy-[14C]glucose (2-DG) radioautography were utilized in concert with the technique of electrical and chemical brain stimulation. Affective defense behavior elicited from the midbrain central gray is characterized by marked vocalization such as hissing and growling, pupillary dilatation, urination and piloerection. In contrast, quiet biting attack elicited from the midbrain central gray lacks overt autonomic signs observed with affective defense response as well as the stalking component which is typically associated with stimulation of the lateral hypothalamus. Nevertheless, central gray-elicited attack resulted in a directed bite of the neck of an anesthetized rat in a manner similar to that observed from the hypothalamus. Affective defense was elicited from the dorsal half of the midbrain central gray, while quiet biting attack was obtained following stimulation of the ventral half of the midbrain central gray, thus indicating a functional differentiation of the central gray with respect to these two forms of aggression. In a separate series of experiments, affective defense or quiet biting attack response was identified by electrical stimulation through a cannula electrode situated in the midbrain central gray. The affective defense responses were subsequently elicited following microinjections of D,L-homocysteic acid through the same cannula electrode in order to demonstrate that these responses were the result of direct stimulation of cell bodies within the central gray. Then, one of the following autoradiographic tracing procedures was utilized: (1) [3H]leucine was injected through a cannula electrode and the animal was sacrificed after a 4- to 14-day survival period; or (2) a 2-DG solution was systemically injected and electrical stimulation was applied through the cannula electrode in order to metabolically activate the pathways associated with each of these responses. In general, the pattern of labelled target regions as indicated by 3H-amino acid radioautography was similar to that obtained from the 2-DG autoradiographic analysis. The principal ascending pathway associated with affective defense was traced to the anteromedial hypothalamus and medial thalamus. Concerning descending projections, label was traced into the central tegmental fields of the midbrain and pons, locus coeruleus and motor and main sensory nuclei of the trigeminal complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1988

Integrated defence reaction elicited by excitatory amino acid microinjection in the midbrain periaqueductal grey region of the unrestrained cat.

Unilateral microinjections (0.20 microliter) of the excitatory amino acids (EAA), L-aspartate (ASP), D,L-homocysteate (DLH) or kainate (KA) were made into the midbrain of freely moving cats. Injections of DLH (20 nmol) or ASP (200 nmol) made within the midbrain periaqueductal grey matter (PAG) consistently elicited a threat display characteristic of defensive behaviour (i.e., pupillary dilatation, piloerection, retraction of the ears, sideways backing, arching of the back, hissing, howling, growling), whereas injections of DLH or ASP made in the tegmentum bordering the PAG did not elicit such behaviour. Injections of KA (940 pmol) made within the PAG, but not the tegmentum, elicited not only a threat display but also directed attack (striking with unsheathed claws and biting). As injections of EAA depolarize cell bodies, but not axons, the results suggest that a population of neurones whose excitation elicits all of the behavioural signs of defence, including directed attack, is found within the PAG. Histology indicated that the region of the PAG from which the defence reaction was elicited was not confined to any PAG subnucleus. Rather, the 'defence region' of the PAG formed a cylindrical column lateral to the midbrain aqueduct, approximately 1.5 mm in diameter and 5.0 mm in length, the rostral end of which lay dorsal to the caudal end. Further, it was found that EAA microinjections made in different portions of the defence region of the PAG elicited defence reactions characterised by different patterns of vocalization and differing intensities of display. It was also observed following unilateral injection of KA into the PAG that defence reactions, including attack, were elicited by approach in the visual hemifield or touch of the body contralateral, but not ipsilateral, to the injection site. The asymmetry of the defence reaction was not due to any obvious ipsilateral motor impairment and thus suggests that the PAG mediation of the defence reaction, in addition to controlling the outflow to the somatic and autonomic motor systems, also affects sensory processing.

Animals↗
PubMed1990

Activity of cat locus coeruleus noradrenergic neurons during the defense reaction.

The single-unit activity of locus coeruleus noradrenergic (LC-NE) neurons was recorded in freely moving cats during naturally induced defense reactions. Defense reactions, consisting of arched back, piloerection, flattened ears and mydriasis, were elicited by exposing the cat either to a dog, or to a cat displaying aggressive behavior induced by electrical stimulation of the hypothalamus. LC-NE neurons were identified using previously established criteria, including suppression of firing during rapid eye movement (REM) sleep and in response to clonidine administration. Exposure to a dog evoked defense reactions and increased the tonic firing rate of LC-NE neurons (n = 8) from a baseline of approximately 0.9 spikes/s to approximately 2.5 spikes/s. Exposure to an aggressive cat evoked defense reactions that were qualitatively very similar to those produced by dog exposure, and elevated the tonic firing rate of LC-NE neurons (n = 8) from a baseline of approximately 1.0 spikes/s to approximately 2.5 spikes/s. In addition to these tonic elevations of activity, LC-NE neurons discharged in phasic bursts (as high as 10 spikes in a 500 ms period) in close association with specific threatening acts made by the dog or hypothalamically stimulated cat. The mere presence of a dog was sufficient to evoke tonic activation of LC-NE neurons, even in the absence of threatening advances by the dog, whereas exposure to a hypothalamically stimulated cat produced LC-NE neuronal activation only when the stimulated cat showed aggressive behavior. These results extend our previous work, which examined the response of LC-NE neurons to environmental and physiological stressors, into a more ethologically relevant domain, and suggest that LC-NE neuronal activation may play a role in the response to threatening or challenging situations.

Aggression↗
PubMed1981

Thyrotropin-releasing hormone and amphetamine produce different patterns of behavioral excitation in rats.

We compared the arousal and hyperactivity produced by intraperitoneal (i.p.) injections of thyrotropin-releasing hormone (TRH, pGlu-His-Pri-NH2; 10, 20, 30 and 60 mg/kg) and 0.3 and 2 mg/kg d-amphetamine (low and moderate amph., respectively) by measuring the occurrence of discrete behavioral items with a behavioral sampling and scoring method. To minimize extraneous variables affecting activity, rats were caged singly inside isolated observation chambers and tested in the daytime after a 2.5 h period of habituation. Under these conditions, vehicle (0.9% NaCl)-treated rats were inactive and either rested or slept through 80% of all time samples taken in the hour after injection. Both TRH and amph. produced significant arousal from sleeping, but TRH, at all doses tested, produced less arousal than moderate amph. and a pattern of behavioral responses which differed from both low and moderate amph. Moderate amph. produced marked increase in forward locomotion and rearing, but low amph. and TRH did not. Both TRH and low amph. increased grooming (perhaps simply by increasing wakefulness), but TRH failed to increase sniffing, a cardinal feature of ampha.-induced excitement. Unlike amph., TRH produced wet-dog shakes, piloerection, tail elevation and teeth chattering. Both mod. amph. and TRH significantly produced increased activity when compared to controls as assessed with photocell counts, though the amph. effect was more robust. The lack of arousal after i.p. injections of thyroid-stimulating hormone (10 I.U./kg) or melanocyte-stimulating hormone release-inhibiting factor (Pro-Leu-Gly-NH2; 60 mg/kg) is evidence that TRH-induced arousal is neither mediated by activation of the pituitary-thyroid axis nor by a non-specific effect of tripeptides generally.

Akathisia, Drug-Induced↗
PubMed1982

An antagonist-induced benzodiazepine abstinence syndrome.

Cats were treated for 35 days with flurazepam, 5 mg/kg per day. The drug was administered through a gastric fistula. Ro15-1788, a benzodiazepine antagonist, caused an abstinence syndrome when administered through the gastric fistula 24 h after the last dose of chronic treatment. Abstinence signs included increased muscle tone, tremor, piloerection, pupillary dilation, panting, and excessive salivation. Neither convulsions nor delirium was seen. Severity of abstinence was similar after Ro15-1788 doses of 2-100 mg/kg, but lasted longer (8-10 h) after the higher dose. Readministering Ro15-1788 a week after the end of chronic treatment precipitated an attenuated abstinence syndrome, but was inactive after 2 weeks.

Animals↗
PubMed1984

Acute administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reduces dopamine and serotonin but accelerates norepinephrine metabolism in the rat brain. Effect of chronic pretreatment with MPTP.

Acute administration of MPTP (a synthetic heroin substitute) at 10-30 mg/kg (s.c.) produced 'Straub tail' phenomena, piloerection and reduced pelvis elevation in rats. The same dose decreased the concentrations of dopamine metabolites and reduced the rate of dopamine synthesis in the striatum. MPTP also reduced the metabolism of serotonin but accelerated that of norepinephrine in their corresponding terminal areas. The effects on central monoamines probably were not due to an agonistic action of MPTP on dopaminergic and serotonergic receptors, since MPTP only exhibited micromolar affinity to the corresponding binding sites. Furthermore, MPTP failed to induce rotational behavior in animals with unilateral nigrostriatal lesions. Chronic treatment of rats with MPTP (10 mg/kg s.c., daily for 3 weeks) did not result in massive degenerative changes in the nigrostriatal system. Histochemical analysis showed intact dopaminergic neurons. Striatal dopamine levels only were reduced by 10%. Dopaminergic neurons in rats chronically treated with MPTP responded normally to a pharmacological stimulus increasing their transmitter synthesis. Chronic treatment did not affect their response to an acute injection of MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1984

Neurochemical and behavioral effects of systemic and intranigral administration of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the rat.

At doses of 5-10 mg kg-1, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (NMPTP) produces in rats acute immobility, retropulsion, straub tail, piloerection, exophthalmos, salivation and clonic movements of the forepaws. It does not produce analgesia as measured by the tail test, nor does it produce permanent motor impairment after chronic or intranigral administration. The acute retropulsion and immobilizing effects can be blocked by methysergide. Administered acutely, NMPTP doubles levels of serotonin in the raphe nucleus and substantia nigra. At the same time, levels of dopamine increase in the caudate nucleus and decrease in the substantia nigra. The NMPTP-induced decrease in dopamine content of the substantia nigra persists in chronically treated rats, but there is no significant decrease in striatal dopamine. After chronic administration of NMPTP, striatal levels of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were decreased by about 50%. Intranigral administrations of NMPTP (10 micrograms daily for 5 days) failed to produce a 6-hydroxydopamine-like lesion in the nigrostriatal system. These results indicate that NMPTP in the rat does not cause selective destruction of dopaminergic neurons, but it does produce acute tryptamine-like effects.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Precipitated diazepam withdrawal elevates noradrenergic metabolism in primate brain.

Following treatment for seven days with diazepam (2.0 mg/kg i.m., b.i.d.), administration of the benzodiazepine receptor antagonist RO 15-1788 (5 mg/kg) induced a severe withdrawal syndrome in vervet monkeys which included tremors, vomiting, vocalizations, chewing, and piloerection. Brain concentrations of the noradrenergic metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) were significantly higher in the precipitated withdrawal group than in the diazepam plus vehicle control group. Administration of RO 15-1788 without prior diazepam treatment had no effect on brain MHPG, nor did it produce withdrawal behaviors, but did produce an increase in the frequency of scratching. These results raise the possibility that increased central noradrenergic activity serves a role in benzodiazepine withdrawal similar to the role hypothesized for noradrenergic activity in opiate withdrawal.

Animals↗
PubMed1988

Behavioural and neurochemical effects of antipamezole, a novel alpha 2-adrenoceptor antagonist.

The effects of antipamezole (MPV-1248), a novel selective and specific alpha 2-adrenoceptor antagonist, were studied on monoamine metabolism in rat brain and CSF. In addition, the ability of the drug to antagonize the behavioural and neurochemical effects of two alpha 2-adrenoceptor agonists, detomidine and medetomidine, was assessed. Atipamezole, 0.03-3.0 mg/kg, had no gross behavioral effects on the rats. Above 3 mg/kg, the rats showed increased vocalization and some hostility, rapid breathing and piloerection. The drug caused dose-dependent, rapid and relatively long-lasting increase in the central turnover of noradrenaline (NA) as reflected by increases in the levels of the major metabolites of NA in brain and CSF and an increase in the depleting effect of alpha-methyl-para-tyrosine on brain NA levels. An increase in the turnover of serotonin (5-HT) in brain was indicated by a decrease in the concentration of 5-HT and a corresponding increase in the level of its metabolite, 5-hydroxyindoleacetic acid. Atipamezole was able to antagonize the sedative, hypothermic and neurochemical effects of two potent alpha 2-agonists, detomidine and medetomidine. These results give support for the characterization of atipamezole as a potent antagonist at central alpha 2-adrenoceptors with a rapid onset of action.

Adrenergic alpha-Antagonists↗
PubMed1983

The regulation of precopulatory behavior by ovarian hormones in the female Mongolian gerbil.

The hormonal regulation of precopulatory behavior in the female Mongolian gerbil was studied using two groups (N = 6) of sexually experienced females. A novel testing procedure was used which involved females living continuously with test males for several days. The test males showed either full sexual behavior (copulating males, C) or only precopulatory behavior (noncopulating males, NC). Experiment 1 investigated changes during the estrous cycle and following ovariectomy in females. Experiment 2 studied the effects of hormonal treatment of these ovariectomized females with 6 micrograms estradiol benzoate (EB) followed by 0.4 mg progesterone (P) or by 0.04 ml arachis oil. When tested with NC males, females displayed a greater range of precopulatory behavior. The patterns could be classified into three groups according to the manner of response to ovariectomy and hormone treatment. Group I patterns (approach, leave, and olfactory investigation of the male's head) were affected by neither ovariectomy nor EB treatment relative to Day 3 levels (Day 3, day preceding estrus; Day 4, estrus), but they were increased to estrous levels by EB and P. Group II patterns (darting, foot-stomping, and the present and piloerection postures) appeared only during estrus, did not appear after ovariectomy, and reappeared only after sequential EB and P treatment. Group III patterns (investigation of the male's anogenital area, allogrooming, ventral gland marking, and sand-rolling) were reduced relative to both estrus and Day 3 levels by ovariectomy and increased above Day 3 levels by EB alone; EB and P treatment further increased Group III patterns to the level of estrus. It is suggested that female precopulatory behavior patterns differ in their responsiveness to ovarian hormones. Estrogen appears to affect those patterns associated with the earliest stages of estrus (Group III).

Animals↗
PubMed1983

Effects of anterior pituitary hormones and their releasing hormones on physiological and behavioral functions in rats.

The effects of direct administration of TRH, TSH, LHRH, LH, ACTH, GH, FSH and prolactin into cerebral ventricle system on metabolic, respiratory, cardiovascular and behavioral responses were assessed in unanesthetized rats, Intraventricular administration of TRH, TSH, LHRH or LH caused hypothermia, decreased metabolism and/or cutaneous vasodilation at room temperature (22 degrees C). Intraventricular administration of FSH, ACTH or prolactin caused hyperthermia, increased metabolism and/or cutaneous vasoconstriction. Intraventricular administration of GH caused an insignificant change in thermoregulatory responses. There was no change in respiratory evaporative heat loss in response to either of the drugs tested. In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia. In contrast, intraventricular administration of prolactin caused bradycardia, hypotension and an enhancement in the epinephrine-induced reflex bradycardia in conscious rats. There was no change in cardiovascular function in response to intraventricular administration of TSH, FSH, ACTH or GH. Furthermore, following intraventricular administration of TRH, but not TSH, LHRH, LH, FSH, GH, ACTH or prolactin three main categories of behavior were provoked: activity of normal type--forward locomotion stimulation, head and body rearing; stereotype activity--increased grooming and head swaying; and abnormal type behavior--tail elevation and piloerection in rats. The data indicate that most of the anterior pituitary hormones and their releasing hormones act through a central mechanism to influence physiological and/or behavioral functions.

Animals↗
PubMed1982

Assessment of alpha 2 adrenergic autoreceptor function in humans: effects of oral yohimbine.

Administration of three oral doses of yohimbine (10 mg, 15 mg, 20 mg) to eight healthy subjects resulted in significant increases in plasma free 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG). The 15 mg and 20 mg yohimbine doses induced modest increases in systolic blood pressure and autonomic symptoms such as piloerection and rhinorrhea. Marked behavioral effects such as anxiety were not observed. These results indicate that determination of the plasma MHPG response to yohimbine may be of value in assessing alpha 2 adrenergic autoreceptor function in humans.

Adult↗
PubMed1989

Cytophotometric assessment of T-2 toxin induced alterations in azure B-RNA and Coomassie-protein in supraoptic-magnocellular neurons of rat hypothalami.

Quantitative cytophotometry was used to monitor T-2 toxin-induced alterations in azure B-RNA and Coomassie-total cell protein in supraoptic-magnocellular neurons of rat hypothalami. Thirty male Sprague-Dawley rats (200-220g) were given a single i.p. injection of T-2 toxin (0.5, 0.75, 1.00 and 1.50 x LD50), a trichothecene mycotoxin; rats were decapitated 8 hours post-dosing. After stoichiometric azure B-RNA and Coomassie-protein staining of brain sections, scanning-integrating microdensitometry was used to quantify toxin-induced alterations in these well established indices of neuronal toxicity. Within the magnocellular neurons of the supraoptic nuclei, significant reductions in azure B-RNA reactivity were observed in the 0.75, 1.00 and 1.50 x LD50 groups (i.e. 11%, 13% and 8%, respectively); no differences in RNA levels were observed between controls and the 0.50 x LD50 group. In addition, a decrease in Coomassie-total cell protein was seen in animals receiving 0.50, 0.75 and 1.50 x LD50 T-2 toxin (i.e. 33%, 21% and 12%, respectively); however, toxin administration did not alter protein levels in the 1.00 x LD50 group. Furthermore, a dose-dependent decrease in systolic blood pressure was observed at 8 hr. post-injections (i.e., approximately -39%, -52%, -66% and -64% for the 0.50, 0.75, 1.00 and 1.50 x LD50 groups, respectively). Additional observations include pronounced polydipsia, ascites, abdominal and subdural hemorrhage, and horripilation (piloerection) in experimental groups. It is postulated that the T-2 toxin-induced reductions in azure B-RNA and Coomassie-protein represent an early indication of impaired metabolic activity. Since these neurons are important sites of vasopressin (antidiuretic hormone) synthesis, these data suggest an impaired osmoregulatory ability. The pronounced polydipsia which occurred shortly after intoxication is further evidence of this impairment. Although these findings do not provide insight relating to the mechanism of osmoregulatory disruption, it is advanced that the supraoptic-magnocellular compartment represents an important site in T-2 toxin mycotoxicosis. Moreover, these findings support previous claims that T-2 toxin intoxication may critically impair the vasopressinergic response to toxin-induced cardiovascular collapse.

Animals↗