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PubMed1993

Hypothermia induced by hyperbaric oxygen is not blocked by serotonin antagonists.

Exposure to HBO causes hypothermia, bradycardia, head weaving, resting tremor, piloerection, and straub tail in rats. These physiological and behavioral responses can also be evoked by selective activation of serotonin1A (5-HT1A) receptors. The purpose of the current study was to determine if hypothermia caused by HBO is due to increased activation of 5-HT1A receptors. The levels of brain biogenic amines were measured in brain regions of Sprague-Dawley (SD) rats exposed to HBO. Exposure to HBO caused an increase in the levels of 5-hydroxyindoleacetic acid (5-HIAA) in the striatum (92%, p < 0.05) and occipital-temporal cortex (116%, p < 0.05), but not in other brain regions. Exposure to HBO did not change the levels of tryptophan, serotonin (5-HT), other biogenic amines, or their metabolites. It is hypothesized that the Fawn Hood (FH) rat, which is reported to be resistant to hypothermia induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), has an abnormality of 5-HT1A receptor activity. Although the FH rat was more resistant to hypothermia induced by HBO than the SD rat, we were not able to confirm that this rat was resistant to hypothermia induced by 8-OH-DPAT. The 5-HT receptor antagonists, 1-(1H-Indol-4-yloxy)-3-[(1-methylethyl)amino]-2-propanol (Pindolol), 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl] piperazine hydrobromide (NAN-190), and methysergide, did not block hypothermia induced by HBO in SD rats. A series of control experiments were used to confirm that the antagonists blocked hypothermia induced by serotonin agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Hydroxytryptophan↗
PubMed1987

Increases in plasma catecholamines during naturally elicited defensive behavior in the cat.

Defensive behavior was evoked in 12 adult cats by the presentation of both interspecific (barking dog) and intraspecific (hypothalamically stimulated cat) stimuli. Each stimulus was presented 3 times. Concomitant activation of the sympatho-adrenal (SA) system was evaluated by radioenzymatic assay of plasma norepinephrine (NE) and epinephrine (E). The somatic and autonomic displays which accompanied defensive behavior were similar between stimuli, consisting of mydriasis, piloerection, growling, hissing and paw strikes. However, the sympatho-adrenal responses associated with interspecific and intraspecific defensive behaviors were different. Interspecific defensive behavior was accompanied by adrenal medullary release of both NE and E, which decreased with successive trials. Intraspecific defensive behavior was initially associated with release of E from the adrenal medulla; the pattern of catecholamine release in successive trials suggested that in later trials NE was released primarily from the sympathetic nerves. Furthermore, increases in plasma NE and E, as well as increases in heart rate and mean arterial blood pressure during the first trial were significantly greater when the behavioral stimulus was a dog. Although aspects of the feline display to threatening stimuli are stereotyped, the data suggest that the sympatho-adrenal response is more specific, and indicates preparation for fighting or escape.

Animals↗
PubMed1989

Cardiovascular and motor components of the defence reaction elicited in rats by electrical and chemical stimulation in amygdala.

In rats anesthetized with Saffan, electrical and chemical (D,L-homocysteic acid, DLH) stimulation in amygdala complex induced vasodilation in the hindlimb muscle, renal vasoconstriction and tachycardia. Chemical stimulation of cell bodies was effective only in the basolateral nucleus, while electrical stimulation produced the response from a larger area: central, basolateral and basomedial nuclei of amygdala. In non-anaesthetized rats, electrical stimulation in these nuclei elicited arching of the back, piloerection, sitting up and boxing with the forepaws or running, jumping or squealing. It is concluded that the area within the amygdala complex controlling the defence reaction is probably restricted to the basolateral nucleus, responses obtained from neighbouring nuclei might be due to activation of the afferent or efferent pathways leading to or from the basolateral nucleus.

Alfaxalone Alfadolone Mixture↗
PubMed1995

Cloning, expression and characterization of biologically active feline tumour necrosis factor-alpha.

We report the cloning, expression and characterization of biologically active feline tumour necrosis factor-alpha (fTNF-alpha). Messenger RNA was extracted from feline peritoneal macrophage cultures and used to synthesize cDNA for polymerase chain reaction (PCR) amplification. The PCR products were cloned into the plasmid vector pCRII and sequenced, showing 99.3% homology with a published fTNF-alpha gene sequence. Subcloning into the vector pGEX-2T and subsequent expression resulted in a 43 kDa fusion protein of fTNF-alpha and glutathione S-transferase (GST). Thrombin cleavage of the fusion protein yielded a 17 kDa protein. This protein cross-reacted with a monoclonal anti-human TNF-alpha antibody in Western blotting, but not with a polyclonal anti-murine TNF-alpha serum. Recombinant fTNF-alpha (rfTNF-alpha) and rfTNF-alpha-GST had a CD50 of 15 ng ml-1 and 230 ng ml-1, respectively, in the L929 cytotoxicity assay. Cats given rfTNF-alpha-GST intravenously manifested the typical biological effects of TNF-alpha, including fever, depression, and piloerection. The rfTNF-alpha-GST upregulated IL-2 receptor and MHC-II antigen expression on peripheral blood mononuclear cells stimulated in vitro, but had no effect on TNF-alpha receptor and MHC-I antigen expression.

Animals↗
PubMed1981

Immediate behavioral effects of kainic acid injections into the midbrain reticular core.

Microinjections of kainic acid into the midbrain reticular core were performed in chronically implanted, unanesthetized cats. The immediate effects of kainate excitation were studied during the first 8 h, in animals without any behavioral or EEG signs of epilepsy. Animals displayed pupillary dilatation, piloerection, accelerated respiration, a frozen attitude with a complete lack of facial expression, and no or only very slight orienting reactions. The most structural syndrome was a hallucinatory-type behavior that began in the first hour following the injection. Animals moved forward in a crouched position as if stalking a prey, vocalizing and opening their mouth in an attacking attitude, or moved back as if defending themselves against as imaginary menacer, seeming virtually terrified. The EEG desynchronization began 20-30 sec after the onset of injection and lasted for 12-14 h without any trace of alpha rhythm, spindles or slow waves. Control injections of buffer solution into the midbrain core and kainic acid in other cerebral structures were followed neither by the hallucinatory defense-attack syndrome, nor by comparably long-lasting EEG desynchronization. The hallucinatory-type behavior elicited during the waking state in the present experiments is compared to the oneiric behavior described by Jouvet and Delorme [21] during paradoxical sleep in animals with suppression of muscular atonia, and possible common mechanisms are discussed.

Amygdala↗
PubMed1987

High-dose clonidine motor syndrome: relationship to serotonin syndrome.

Reciprocal forepaw treading, hindlimb abduction, and Straub tail are some of the abnormal motor behaviors of the classical 'serotonin syndrome,' which results from activation of serotonin (5-HT) receptors. However, we also observed them in the syndrome evoked by the alpha-adrenergic agonist clonidine, at high doses (5-40 mg/kg). Other features of the clonidine syndrome (scored from videotapes) were body and head tremor, forelimb hyperextension, ataxia, vertical jumping, tactile hyperreactivity, and autonomic signs (piloerection, pupillary dilatation, salivation, proptosis). The clonidine syndrome persisted for several hours and was not lethal. Clonidine suppressed locomotor activity (photocell recording) and induced episodes of catalepsy and 5-HT-independent impairment of motor habituation. Single high doses of drugs active at several different neurotransmitter receptors significantly reduced total behavioral score through effects primarily on tremor and autonomic signs, but none prevented the clonidine syndrome. Lesions of monoaminergic neurons [intracisternal 5,7-dihydroxytryptamine (DHT) or 6-hydroxydopamine] or monoamine depletion by intraperitoneal reserpine all failed to prevent this motor syndrome. Co-administration of 5-HTP and clonidine did not exacerbate the clonidine syndrome in naive rats and did not prevent the onset of the serotonergic syndrome in rats with DHT lesions. These data suggest that neither catecholamines nor 5-HT have a major role in the serotonin-like behavioral responses to high doses of clonidine.

Adrenergic alpha-Antagonists↗
PubMed1989

A mapping study of hypothalamic defensive attack and related responses in cats.

Effective stimulation sites for the hypothalamic defensive attach and its related responses were mapped in 65 tame adult cats (107 sites). The hypothalamic defensive attack was classified into two types according to its locomotion component: one with only directed attack and the other with retreat. The retreat appeared accompanied by back arching and intermingled with the directed attack. Otherwise, the directed attack and the retreat were accompanied by the same kinds of threat responses, including piloerection, ear retraction, growling and hissing. Stimulation sites for the directed attack with thresholds under 100 microA were located at the dorsal half of the ventromedial hypothalamic nucleus (VM) and areas just rostral to it. Directed attack with thresholds above 100 microA was elicited by stimulation of the marginal portion of the VM and adjacent areas, especially those rostral to it. Stimulation sites for the directed attack, which was replaced by stereotyped circling at higher intensities, were located at the part of the above-mentioned areas most distant from the VM. The retreat was elicited from the ventral half of the VM. Stimulation sites which evoked stereotyped circling with threat responses were distributed in a wider area of the medial hypothalamic area outside the VM.

Animals↗
PubMedDate not supplied

Behavioral effects of thyrotropin releasing hormone in frontal decorticated rats.

A low dose intracerebroventricular injection of thyrotropin releasing hormone (TRH, 100 ng) changed many behavioral responses in the rat. TRH increased locomotion, scratching, body shaking, piloerection, and rearing, but decreased sniffing, and resting. Ablation of frontal neocortex further enhanced the TRH effects on locomotion and resting. A dose effect of TRH (0, 5, 10, 50, 100 ng) to increase general activity was established and the effect was further enhanced by decortication. In our test situations decortication had no effect by itself. Since the TRH effects became much more pronounced without the frontal neocortex it appears that the cortex exerts a powerful inhibitory effect to moderate the TRH effects. The TRH effect does not depend upon the frontal cortex, actually a cortical function is to dampen the TRH effects on various behavioral responses.

Animals↗
PubMed1987

Toxicity of methylenedioxymethamphetamine (MDMA) in the dog and the rat.

Methylenedioxymethamphetamine (MDMA) was administered to dogs and rats orally once a day for a 28-day period to evaluate the morphological and neuropathological effects. Major clinical signs associated with the administration of MDMA in the dog included circling, depression, dilated pupils, hyperactivity, rapid breathing, and salivation. Major clinical signs in the rat included hyperactivity, excitability, piloerection, exophthalmos, and salivation. Gross observations at necropsy in the dog possibly related to administration of the test article included reduced testicular size (one high and one medium dose) and prostatic enlargement in two high-dose animals. No gross lesions were seen in the rats at necropsy. The medium- and the high-dose groups in both sexes in both the rats and the dogs gained significantly less weight than the control and low-dose groups. Food consumption decreased the first week for the high- and medium-dose groups, but a significant reversal toward more normal consumption was noted in the following weeks in both the rats and the dogs. Hematologic, clinical chemistry, and urinalysis values did not appear to be affected by the administration of the test article in the dog. In the rat clinical pathology variables showing a trend to decrease with dose included urinary pH, blood urea nitrogen, glucose, creatinine (females), lactate dehydrogenase (LDH) (females), and chloride. Clinical pathology variables showing a trend to increase with dose included total white blood cell count and phosphorus. Microscopically, testicular atrophy was present in one medium-dose and two high-dose male dogs. Prostatic hyperplasia was present in two high-dose male dogs. No test article-related lesions were seen in the brains of either species.

3,4-Methylenedioxyamphetamine↗
PubMed1987

The developmental toxicity of triethylene glycol dimethyl ether in mice.

Triethylene glycol dimethyl ether (triEGdiME) is structurally related to several compounds which produce reproductive and developmental toxicity, including teratogenicity in laboratory animals. In the present study, triEGdiME (0, 250, 500, or 1000 mg/kg/day) was administered by gavage to timed-pregnant CD-1 mice during major organogenesis (Gestational Days (gd) 6-15). Maternal clinical status was monitored daily during treatment. At sacrifice (gd 17), confirmed-pregnant females (26-28 per group) were evaluated for clinical status and gestational outcome; each live fetus was examined for external, visceral, and skeletal malformations. No maternal death or morbidity was observed. Clinical signs of toxicity including piloerection were minor. Maternal weight gain during treatment, gestation, and maternal weight gain during gestation corrected for gravid uterine weight were not affected. Gravid uterine weight decreased in a dose-related manner, indicating compromised pregnancy status. Relative maternal liver weight (% body wt) was significantly increased over controls at doses greater than or equal to 500 and 1000 mg/kg/day. Average fetal body weight per litter was significantly reduced at doses greater than or equal to 500 mg/kg/day. The percentage malformed live fetuses per litter (0.3, 0, 0.8, and 11.1%) was significantly increased at 1000 mg/kg/day. Major malformations affected primarily the development of the neural tube, craniofacial structures, and the axial skeleton. In summary, oral administration of triEGdiME during major organogenesis produced only marginal signs of altered maternal status, as evidenced by an increase in maternal liver weight, and caused selective adverse effects upon fetal growth and morphological development at doses greater than or equal to 500 mg/kg/day.

Abnormalities, Drug-Induced↗
PubMed1988

The acute toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) in the male Fischer rat.

Polychlorinated dibenzofurans are ubiquitous environmental pollutants which have great potential for human exposure. To characterize the toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), male F344 rats were administered a single oral dose of 0, 100, 250, 500, 1000, or 2000 micrograms 4PeCDF/kg. A progressive and dose-dependent loss of body weight was evident by 3 days after treatment. Signs of toxicity included piloerection, hair loss, hypoactivity, morbidity, and death. Death occurred as soon as 14 days after treatment and continued throughout the 35-day observation period. The LD50/35 was estimated to be 916 micrograms/kg with a 95% confidence interval of 565-1484 micrograms/kg. Dose-dependent increases were observed in serum cholesterol, triglyceride, and bile acid concentrations and in sorbitol dehydrogenase and aspartate aminotransferase activities. The hematocrit, hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin concentrations were depressed in a dose-dependent fashion. Hepatic ethoxyresorufin-O-deethylase (EROD) activity was increased in all treatment groups approximately 25 times above that of control animals. Lymphoid depletion in the thymus and spleen was observed in the three highest doses and thymic atrophy was present at all dose levels. Absolute liver weight and the liver:body weight ratio were significantly increased above controls. Hepatotoxicity was dose-dependent and was characterized by lipid accumulation resulting in hepatocytomegaly. Epithelial hyperplasia and focal ulcerations of the forestomach was observed in animals administered 500 micrograms 4PeCDF/kg. Spontaneous cardiomyopathy was exacerbated by treatment with 2000 micrograms/kg. Since 4PeCDF and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produce a similar spectrum of toxic effects, the biochemical mechanism(s) of toxicity for these chemicals may be similar.

Animals↗
PubMed1990

Toxicologic studies on a novel antineoplastic bis-Mannich base, derived from a conjugated styryl ketone.

A new bis-Mannich base (NC758) derived from a conjugated styryl ketone has demonstrated activities against human and animal tumors, both in vitro and as xenografts in athymic mice. The present study examined the toxicity of this candidate anticancer drug, when administered intraperitoneally by undertaking LD50, acute dose-response and time-response toxicity studies using CD-1 mice following OECD guidelines. An LD50 of 46.9 +/- 1.4 mg/kg (males) and 65.2 +/- 1.5 mg/kg (females) was calculated using the moving averages method. Signs of toxicity included diarrhea, piloerection, and coma. Gross pathologic findings consisted of an acute fibrinous peritonitis in animals surviving 24 hr or more before death. The acute dose-response study revealed anorexia in mice 24 hr after receiving 25 mg/kg NC758 or more, lasting up to 72 hr in the 50 mg/kg treated group. Neutrophils were significantly elevated in the 25 and 50 mg/kg groups in conjunction with the observed acute peritonitis. Treatment (p = 0.0001), sex (p = 0.0008), and treatment/sex interaction (p = 0.0001) effects were seen in the myeloid-erythroid ratio (MER) of bone marrow. Pathologic changes included thymic necrosis (in all treated mice) and intestinal villous atrophy (in mice treated with 25 and 50 mg/kg). In time-response studies, pathological changes disappeared after 14 days, except for the MER which remained abnormal in males. It was concluded that NC758 was corrosive; hence future studies should utilize the intravenous route, or be given intraperitoneally as divided doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Amines↗
PubMed1994

Effect of grapefruit juice on drug metabolism in rats.

The effect of grapefruit juice on in vivo drug metabolism was investigated in rats. The juice (4 ml or 8 ml/kg) was given orally once daily for 2 consecutive days and its effect on theophylline metabolism, pentobarbitone sleeping time and the tremorgenic action of tremorine was studied. The effect of grapefruit juice on some of these parameters was compared with that of the known drug metabolism inhibitor cimetidine given ip. Grapefruit juice at 4 ml and 8 ml/kg produced significant increases in pentobarbitone sleeping time that reached 46 and 79%, respectively, compared with 107% produced by cimetidine (50 mg/kg, ip). The juice at 4 ml/kg also significantly increased plasma theophylline concentration when measured 15, 30, 60 and 90 min after ip theophylline administration (10 mg/kg). Thereafter, no significant differences were detected in plasma drug concentrations between juice- and saline-treated animals. Administration of tremorine (25 mg/kg, ip) to saline-treated controls produced, within 2 or 3 min, tremors, piloerection, profuse salivation, defaecation, urination and chromodacryorrhesis (red tears). The onset of appearance of these signs was delayed to about 7 min in rats pretreated 1 hr earlier with either grapefruit juice (4 ml/kg, orally) or cimetidine (50 mg/kg, ip). The severity of the above signs was markedly reduced to a similar extent in both the juice- and cimetidine-treated rats. These results suggest that grapefruit juice may act as an inhibitor of drug metabolism in rats, and that its consumption may alter the disposition of certain concomitantly administered drugs.

Animals↗
PubMed1990

Relations between tickling and humorous laughter: preliminary support for the Darwin-Hecker hypothesis.

Following hypotheses by Darwin and Hecker on the connection between tickling and humorous laughter, questionnaire data were collected from 100 college students regarding their reported ticklishness and tendencies to laugh and show responses ancillary to laughter. Ticklishness was related to propensities to: (a) giggle, (b) laugh, (c) smile, (d) piloerect, (e) blush, and (f) cry. These findings lend preliminary support for the Darwin-Hecker conjecture that reflexes underlying ticklishness mediate humor. We speculate on possible relations among tickling and humor, and reasons why people laugh and smile when they find things funny.

Adolescent↗
PubMed1986

The effects of intracerebroventricular administration of compound 48/80 on behaviour and regional brain amine concentrations in the rat.

The intracerebroventricular injection of the mast cell degranulator, compound 48/80 (C48/80, 10 micrograms/kg), produced a marked behavioural syndrome in rats which included head and body shakes, paw tremor, excessive grooming, unusual posture and gait, mild diarrhoea, piloerection, extreme agitation and irritability to touch, sedation and catatonia. Fifteen minutes after C48/80, the histamine concentrations were decreased significantly in all brain regions examined, i.e. the cortex, cerebellum, midbrain, medulla oblongata-pons (MO-P) and hypothalamus. The noradrenaline (NA) concentrations were decreased in the cerebellum, hypothalamus and MO-P, whereas the dopamine (DA) content was decreased in the MO-P only. The concentrations of serotonin were not affected. As such, the behaviours following the acute degranulation of brain mast cells by C48/80 may result predominantly from the release of histamine and possibly NA and DA.

Animals↗
PubMed1987

Midbrain periaqueductal grey region in the cat has afferent and efferent connections with solitary tract nuclei.

Wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injections were made at the same sites within the midbrain periaqueductal grey region (PAG) of the cat at which microinjections of excitatory amino acids had previously elicited the set of autonomic and somatic reactions (i.e. pupil dilatation, piloerection, retraction of the ears, arching of the back, hissing, howling and growling) known as the 'defence reaction'. The WGA-HRP injections revealed that this PAG region has an extensive set of afferent and efferent connections with solitary tract nuclei (NTS). Within the NTS the majority of labelled neurons were distributed, in approximately equal numbers, in the ipsilateral medial solitary nucleus (SM) and the ipsilateral and the contralateral ventrolateral solitary nuclei (SVL). The densest anterograde labelling was found in the ipsilateral SM, with lighter anterograde labelling in the contralateral SM and bilaterally in the commissural solitary nucleus and SVL. The described connections between the defence region of the PAG and the NTS not only provide a new anatomical basis for cardiovascular and respiratory components of the reaction, but also add to the evidence that, in addition to the hypothalamus, the PAG is an important integrating center for the autonomic and somatic elements of the defence reaction.

Animals↗
PubMed1986

Action and specificity of ventral medullary vasopressor neurones in the cat.

An investigation has been made into the mode and specificity of action of ventral medullary pressor neurones. These were activated by microinjections of excitant amino acid into the ventral brain surface of chloralose-anaesthetized, artificially ventilated cats, and a number of autonomic responses were measured. Indirect assessment of cardiac output (by CO2 delivery to the lungs) suggested that it was either unchanged or fell during pressor responses. The inference that activating the pressor neurones caused vasoconstriction was confirmed directly for hindlimb and mesenteric vascular beds, by a rise in inflow pressure when they were perfused at constant flow. Sympathetic activity also increased in cervical, splanchnic and inferior cardiac nerves. Bradycardia often (but not always) accompanied pressor responses, but this was abolished by vagotomy, although not by cutting the sinus and aortic nerves. In vagotomized cats, tachycardia could be produced during pressor responses even after either bilateral adrenalectomy or removal of the stellate ganglia, indicating both direct sympathetic drive to the heart and release of adrenal catecholamines. Plasma adrenaline levels were measured and found to increase by up to 20.2 times control values, plasma noradrenaline up to 12.6 times, and dopamine by a smaller amount. Activating ventral medullary pressor neurones appeared to have no significant action on pupils, nictitating membranes or piloerection. In three adrenalectomized, vagotomized cats, only small, inconsistent effects were measured on intestinal motility following pressor neurone excitation. However, large electrodermal responses could be evoked from the ventral medulla, but from a distinct area medial to the pressor neurones.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1994

Immunologically induced sympathectomy of preganglionic nerves by antibodies against acetylcholinesterase: increased levels of peptides and their messenger RNAs in rat adrenal chromaffin cells.

Systemic administration of murine monoclonal acetylcholinesterase antibodies to rats has been shown to cause selective degeneration of sympathetic preganglionic neurons. In the present study rats were subjected to a single i.v. injection of these acetylcholinesterase antibodies, or to normal IgG or saline for control. Exophthalmos, piloerection and eyelid-drooping (ptosis) were observed within 1 h after administration of the antibodies. Rats were killed at different time-points after antibody administration, and the adrenal glands were analysed by means of indirect immunohistochemistry and in situ hybridization histochemistry. As soon as 3 h after the antibody treatment, a marked increase in the number of chromaffin cells expressing mRNA encoding, respectively, enkephalin, calcitonin gene-related peptide, galanin, neurotensin and substance P was seen. At 12 h the peptide mRNA levels were still elevated and there was a concomitant increase in the number of peptide-immunoreactive cells. All peptide levels remained high for at least 48 h; however, 77 days after the antibody treatment only enkephalin-immunoreactive cells could be encountered. A disappearance of acetylcholinesterase- and enkephalin-immunoreactive cells could be encountered. A disappearance of acetylcholinesterase- and enkephalin-positive fibers was already seen 3 h after the antibody treatment, and after 24 h no fibers were encountered. In contrast, up until 48 h there was no apparent change in the number or intensity of immunofluorescent fibers expressing calcitonin gene-related peptide, galanin, neurotensin or substance P. However, 77 days after the antibody treatment the number of calcitonin gene-related peptide- and substance P-immunoreactive fibers was increased as compared to controls. In addition, reappearance of acetylcholinesterase- and enkephalin-immunoreactive fibers was seen 77 days after antibody administration, although their number was still low as compared to controls. Double-labeling immunohistochemistry revealed that the chromaffin cells expressing peptides after the antibody treatment preferentially were adrenaline storing cells (noradrenaline-negative). The majority of these cells expressed only one peptide. Both surgical transection of the splanchnic nerve as well as treatment with acetylcholine receptor antagonists mimicked the effects seen after the acetylcholinesterase-antibody treatment, although changes were less pronounced. The present results show that interruption of splanchnic transmission induces fast, marked, and selective increases in peptide expression in rat adrenal chromaffin cells.

Acetylcholinesterase↗