Decreased hyperthermic effect of MK-801 in selectively bred hypercholinergic rats

The Flinders Sensitive Line (FSL) of rats has been selectively bred to have increased sensitivity to cholinergic agonists. However, these rats exhibit altered responsiveness to a number of noncholinergic agents, such as apomorphine, buspirone and ethanol. This study compared the FSL and control Flinders Resistant Line (FRL) rats in terms of their hyperthermic response to the phencyclidine (PCP) receptor agonist, MK-801 (0.2 mg/kg SC) and their MK-801 binding characteristics. We have found that FSL rats react with a delayed hyperthermia, having a significantly lower hyperthermia for the first 120 min of observation. Thereafter the response does not differ in FSL and FRL rats. Both groups had similar affinities and numbers of [3H]MK-801 binding sites in the hippocampus/cerebral cortex. Pretreatment with scopolamine (1 mg/kg SC) failed to affect MK-801-induced hyperthermia in either line of rats. These findings suggest that selective breeding of FSL rats attenuated the secondary mechanisms involved in the PCP receptor-mediated hyperthermic response. However, by itself cholinergic supersensitivity does not appear to be a major factor in the blunted responsiveness of FSL rats to MK-801.     

Lactation Patterns in Women with Hypertensive Disorders of Pregnancy: An Analysis of Illinois 2012–2015 Pregnancy Risk Assessment Monitoring System (PRAMS) Data

Maternal and Child Health Journal - Hypertensive disorders of pregnancy have lifelong implications on maternal cardiovascular health. Breastfeeding has a variety of maternal benefits, including...     

Binding of psychotropic drugs to isolated alpha-acid glycoprotein

Alpha1-acid glycoprotein (alpha1-AG) was purified from human sera, and its binding properties with respect to psychotropic drugs were examined by equilibrium dialysis methods in order to clarify the specificity of binding. Radioactive imipramine, a tricyclic antidepressant, was used as the primary ligand. Other drugs, representative of different classes, were tested as potential inhibitors of the alpha1-AG-imipramine binding. The K(a) for imipramine was 2.8 x 10(5) (+/- 0.8) M(-10 (mean +/- S.D.). Chlorpromazine, fluphenazine, thioridazine, loxapine and thiothixene, which are antipsychotic drugs, were competitive inhibitors of imipramine binding, and their K(a) values were in the same range. Propranolol, haloperidol and diazepam were also competitive inhibitors but their affinities were lower. Molindone, an indolic antipsychotic, when tested at the same concentrations as the other drugs, did not affect imipramine binding. Trihexyphenidyl, an anti-Parkinson drug, was a potent but noncompetitive inhibitor. These data identify the antidepressant and major tranquilizer drugs that exhibit high affinity for alpha1-AG and indicate that alpha1-AG may account for 40 per cent of total imipramine bound in serum. Since in psychiatric clinical practice two drugs are frequently administered together, possible competitive effects are discussed as well as the potential role of alpha1-AG in psychiatric illness.     

Enhanced affective aggression in genetically bred hypercholinergic rats

Affective aggression was studied in pairs of Flinders Sensitive Line hypercholinergic rats (FSL) and Flinders Resistant Line (FRL) rats in shock-induced and apomorphine-induced fighting tests. FSL rats were significantly more aggressive in both tests. They had higher pain threshold, assessed by the jump-flinch method, than FRL rats. It is concluded that genetically developed cholinergic system supersensitivity has resulted in enhanced responsiveness to stimuli eliciting affective aggression.     

Alkali metal cations: effects on aggression and adrenal enzymes

Alkali metal cations (lithium, sodium, potassium, rubidium and cesium) were given to rats on a chronic large dose schedule. Lithium depressed shock induced fighting, while potassium and rubidium facilitated this aggression. After chronic high doses of the alkali cations, all groups except the sodium treated group showed an elevation of the adrenal enzymes, tyrosine hydroxylase and phenylethanolamine-N-methyl transferase (PNMT).     

Taming effects of p-chlorophenylalanine on the aggressive behavior of septal rats.

Septal irritability and shock-induced aggression were suppressed by the administration of p-chlorophenylalanine (PCPA) to septal rats. The levels of septal irritability and shock-induced fighting were significantly lower in septal, PCPC-treated rats than in nontreated septal rats. Since both parameters of septal aggression were reduced by PCPA, and while PCPA has no effect on shock-induced fighting of unlesioned rats under similar parameters, it appears that both forms of aggression may function through a common neural mechanism.     

Facilitation of shock-induced fighting following intraventricular 5,7-dihydroxytryptamine and 6-hydroxydopa

Immobilization of albino rats for 2 h showed ambient temperature-dependent changes in rectal temperature, hypothermia at temperatures below 30° C, and hyperthermia at 35° C and above. Adrenalectomized (Adre) rats showed more hypothermia compared to sham operated controls at 25±2° C. The increased hypothermia in adrenalectomized rats was reversed by 10 mg/kg IP or 100 g/rat ICV of hydrocortisone. Groups of rats pretreated with desmethylimipramine (DMI, 25 mg/kg IP) and 6-hydroxydopamine (6-HD, 100 g/rat ICV) or methyl ester of parachlorophenylalanine (ME-PCPA, 100 g/rat ICV for 3 days) or 5,6-dihydroxytryptamine (DHT, 75 g/rat ICV) showed significantly less hypothermia at the end of 2 h of immobilization. Applying analysis of variance test, the hypothermia in Adre, ME-PCPA and DHT groups, was found to be not significantly different from their respective control groups between 0 to 45 min of immobilization but was significantly different between 45 to 120 min of immobilization. DMI-6-HD group however, showed significant difference between 0–45 min only and not between 45–120 min of immobilization. The results suggest that the early phase of immobilization induced hypothermia between 0–45 min is dopamine and the late phase of hypothermia between 45–120 min is 5-hydroxytryptamine mediated.     

Aberrant reinnervation following hypoglossal nerve damage

Hypoglossal nerve damage is a known complication of carotid endarterectomy, occurring in approximately 5% of endarterectomies. The vast majority of these patients recover without functional disability from this injury even if the tongue remains hemiplegic. We report 2 patients who suffered hypoglossal nerve section during neck surgery. Although they were initially mildly symptomatic, they developed increasingly severe dysarthria and dysphagia beginning 4 months after surgery. EMG revealed abnormal coactivation of the genioglossus and styloglossus muscles on the affected side, suggesting aberrant reinnervation. Aberrant reinnervation is a well-known complication of facial nerve injury, but has not been previously recognized in hypoglossal nerve injury. Like the face, the tongue is composed of many muscles that must perform complex movements. Normally, injury to one hypoglossal nerve causes little or no disability, but when aberrant reinnervation occurs, the tongue no longer moves in a coordinated manner, and significant dysarthria ensues.