Central temperature regulation in the conscious rabbit after monoamine oxidase inhibition

1. Measured thermal loads were applied to conscious rabbits by intravenous infusions of hot or cold saline. The responses of the central temperature regulating mechanism were assessed by measuring hypothalamic temperature change. The relationship between thermal load and temperature response was established in normal animals.

2. Intramuscular injection of tranylcypromine (20 mg/kg. day for 6-8 days) had no effect upon resting temperature or the temperature response to thermal loads, though the diencephalic concentrations of noradrenaline and 5-hydroxytryptamine (5-HT) were increased.

3. Either hypothalamic monoamines are not concerned in the regulation of normal temperature or there is a monoamine `pool' in the hypothalamus which is concerned with temperature regulation but which is unaffected by monoamine oxidase inhibition.

     

Central regulation of ejaculation

Ejaculation is a reflex mediated by a spinal control center, referred to as a spinal ejaculation generator. This spinal ejaculation generator coordinates sympathetic, parasympathetic and motor outflow to induce the two phases of ejaculation, i.e., emission and expulsion. In addition, the spinal ejaculation generator integrates this outflow with inputs that are related to the summation of sexual activity prior to ejaculation that are required to trigger ejaculation. Recently, a group of spinothalamic neurons in the lumbar spinal cord (LSt cells) were demonstrated to comprise an integral part of the spinal ejaculation generator. Specifically, lesions of LSt cells completely ablate ejaculatory function. Moreover, LSt cells are activated following ejaculation, but not following other components of sexual behavior. Furthermore, based on their relationship with autonomic nuclei, motoneurons and genital sensory inputs, LSt cells are also in the ideal anatomical position to integrate sensory inputs and autonomic and motor outflow. Additionally, the spinal ejaculation generator is under inhibitory and excitatory influence of supraspinal sites, including the nucleus paragigantocellularis (nPGi), the paraventricular nucleus of the hypothalamus (PVN) and the medial preoptic area (MPOA). Finally, sensory information related to ejaculation is processed in the spinal cord and brain, possibly contributing to the rewarding properties of ejaculation. One candidate pathway for relay of ejaculation-related cues consists of LSt cells and their projections to the parvocellular subparafascicular thalamic nucleus. Moreover, neural activation specifically related to ejaculation is observed in the brain and may reflect of processing of ejaculation-related sensory cues.     

Central regulation of sodium appetite

Sodium appetite, the behavioural drive to ingest salt, is stimulated by prolonged physiological sodium deficiency in many animal species. The same neural mechanisms that are responsible for sodium appetite in laboratory animals may influence human behaviour as well, with particular relevance to the dietary salt intake of patients with diseases such as heart failure, renal failure, liver failure and salt-sensitive hypertension. Since the original experimental work of Curt Richter in the 1930s, much has been learned about the regulation of salt-ingestive behaviour. Here, we review data from physiology, pharmacology, neuroanatomy and neurobehavioural investigations into the stimulatory and inhibitory signals that regulate sodium appetite. A rudimentary framework is proposed for the brain circuits that integrate peripheral information representing the need for sodium with neural signals for the gustatory detection of salt in order to drive a motivated ingestive response. Based on this model, areas of remaining uncertainty are highlighted where future information would allow a more detailed understanding of the neural circuitry responsible for sodium appetite.     

抑癌基因PTEN调控机制研究进展

PTEN/PI3K/Akt通路是细胞整合外界刺激的主要信号转导通路之一，PTEN是PI3K/Akt通路的主要负调控因子，PTEN功能的缺失在人类肿瘤中广泛存在。除了基因或染色体本身的改变影响其功能活性或表达水平外，还有许多影响PTEN功能的因素，包括与脂膜的结合、亚细胞定位、基因转录、翻译及翻译后水平的调节等。     

The mechanisms of vasomotor regulation

Summary The reflexes on the arterial pressure and on the blood vessels of the posterior extremity elicited by electric stimulation of the afferent fibers of different somatic nerves were studied on anesthetized cats. The reflexes on the blood vessels of the extremity were studied by the method of resistography (perfusion under constant flow). Weak reflex stimulations cause a depressor reflex and dilatation of vessels of the extremity. More intense stimulations cause a vasoconstriction in the extremity with subsequent rise of the arterial pressure, which shows the difference in the thresholds of the regional vasoconstriction for the vessels of different organs. Further increase in the strength of the stimulation is associated with the transition of the regional vasoconstriction into the secondary reflex vasodilatation. The similarity of the latter phenomenon with the reversal of the spinal motor reflexes is emphasized.Presented by Active Member of the AMN SSSR V. N. Chernigovskii     

Two mechanisms underlying inhibition of return

Inhibition of return (IOR) refers to slower reaction times to targets presented at previously stimulated or inspected locations. Taylor and Klein (J Exp Psychol Hum Percept Perform 26(5):1639–1656, 2000) showed that IOR can affect either attentional/perceptual or motor processes, depending on whether the oculomotor system is in a quiescent or in an activated state, respectively. If the motoric flavour of IOR is truly non-perceptual and non-attentional, no IOR should be observed when the responses to targets are not based on spatial information. In the present experiments, we demonstrated that when the eyes moved to the peripheral cue and back to centre before the target appeared (to generate the motoric flavour), IOR was observed in detection tasks, for which the spatial location is an integral feature of the onset that is reported, but not in colour discrimination tasks, for which the outcome of a non-spatial perceptual discrimination is reported. When eye movements were prevented, both tasks showed robust IOR. We, therefore, conclude that the motoric flavour of IOR, elicited by oculomotor activation, does not affect attention or perceptual processing.     

General mechanisms of coagulation and their physiological inhibition. II. The regulation of coagulation by physiological inhibitors

Inopportune coagulation of blood in vessels is prevented by defense mechanisms, in which plasma inhibitors play an important role. The inhibitors are glycoproteins and belong to two different groups, according to their mechanism of action. The first group consists of the inhibitors of serine proteases, which form inactive complexes with various coagulation enzymes; it includes antithrombin III, heparin cofactor II, alpha 2-macroglobulin, alpha 1-antitrypsin and C1S-inhibitor. The second group includes protein C and its cofactor, protein S. Protein C, activated by thrombin complexed with a protein cofactor present on the endothelial cell surface (thrombomodulin), is responsible for the proteolytic degradation of two coagulation cofactors (Va and VIII: Ca). The clinical importance of both antithrombin III, protein C and protein S is attested by the strong association between recurrent venous thromboembolic manifestations and inherited deficiencies of one or the other of these proteins.     

Pharmacological regulation of opioidergic antinociceptive mechanisms

Laboratory of Pharmacology of Analgesia, Institute of Pharmacology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 8, pp. 151–155, August, 1991.     

Memory inhibition and energy regulation

At a simple behavioral level, food intake and body weight regulation depend on one's ability to balance the tendency to seek out and consume food with the ability to suppress or inhibit those responses. Accordingly, any factor that augments the tendency to engage in food seeking and eating or that interferes with the suppression of these behaviors could produce (a) caloric intake in excess of caloric need; (b) increases in body weight leading to obesity. This paper starts with the idea that excess body weight and obesity stem from a failure or degradation of mechanisms that normally function to inhibit eating behavior. Unlike previous approaches, we focus not on failures of traditional physiological (e.g., neural, hormonal) regulatory control mechanisms, but on disruptions of inhibitory learning and memory processes that may help to regulate energy intake. This view of energy dysregulation as a type of "learning disorder" leads us to the hippocampus, a brain structure that has long been regarded as an important substrate for learning and memory and which we think may be critically involved with a specific type of memory inhibition function that could contribute to the suppression of food intake. With this focus, the search for environmental origins of the current obesity epidemic in Western populations is directed toward factors that alter hippocampal functioning. We conclude by offering a preliminary account of how consumption of foods high in saturated fats might lead to impaired hippocampal function, reduced ability to inhibit caloric intake and, ultimately, to increased body weight.     

Central κ1 receptors and mechanisms of arrhythmogenesisreceptors and mechanisms of arrhythmogenesis

Agonists of κ₁-opiate receptors injected in brain ventricle potentiate arrhythmogenic effect of adrenaline. Antagonist of κ₁-opiate receptors norbinaltorphimine or ganglioblocker hexamethonium completely abolish proarrythmic effects of κ₁-agonists. Norbinaltorphimine possesses intrinsic antiarrhythmic activity. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 6, pp. 656–658, June, 1997