Unit activity from neurons of hypothalamic feeding and satiety mechanisms, and from adjacent hypothalamic regions was recorded in anesthetized dogs with surgically exposed hypothalamus, and in Flaxedil-immobilized cats in which a stereotaxic approach was made. Intravenous glucose or insulin, or combinations of both, were given and the changes in spike activity observed. Glucose estimations were done on blood samples taken from femoral artery and vein. In starved animals the unit activity in satiety center neurons was slower than that obtained from feeding center neurons. Frequency of spikes recorded from satiety center neurons increased and that of feeding center neurons decreased significantly after glucose was given intravenously, while spike activity from these centers showed a reverse pattern of response after intravenous insulin. No significant changes were observed from other hypothalamic and cortical neurons. Activity of neurons of the satiety center did not show a significant correlation with blood glucose level per se, but a better correlation was found between unit activity and the A-V glucose difference. It is suggested that the satiety center is activated by increased glucose utilization in the body.

Severed axons in adult mammals do not regenerate appreciably after central nervous system (CNS) injury due to developmentally determined reductions in neuron-intrinsic growth capacity and extracellular environment for axon elongation. Chondroitin sulfate proteoglycans (CSPGs), which are generated by reactive scar tissues, are particularly potent contributors to the growth-limiting environment in mature CNS. Thus, surmounting the strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. As of now, the main in vivo approach to overcoming inhibition by CSPGs is enzymatic digestion with locally applied chondroitinase ABC (ChABC), but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of the molecular mechanisms underlying CSPG action is needed in order to develop more effective therapies to overcome CSPG-mediated inhibition of axon regeneration and/or sprouting. Because of their large size and dense negative charges, CSPGs were thought to act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions. Although this may be true, recent studies indicate that two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase σ (PTPσ) and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibitory effects. CSPGs also may act by binding to two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3 (NgR1 and NgR3). If confirmed, it would suggest that CSPGs have multiple mechanisms by which they inhibit axon growth, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries, including spinal cord injury (SCI).

No abstract

In this paper we would like to discuss the role of sensory and metabolic signals in the control of food intake. The problem can be defined by perusing FIGURE 1, which presents a simplified version of a previously published schema outlining the control of intake in flow chart form (Jacobs, 1962). The initial conditions assume an animal already eating food. We shall not be concerned with the particular causes initiating the meal. Starting with the top of the FIGURE 1, then, we may ask classical question of physiologists analyzing intake regulation: What does the diet contain that can act as a signal to monitor subsequent intake? This signal can increase intake in a short-term positive feedback loop, as seen in the lower right side of the Figure, or decrease it in a negative feedback loop. The latter case we have called satiety.The two classes of physicochemical stimuli which interest us are labeled calories and taste. Both sets of signals are initiated in specialized receptor systems and relayed to the central nervous system (CNS) by nervous and/or humoral paths.It should be pointed out that our choice of the terms, taste and calories, is an oversimplification of the actual situation, which is at least hinted at in FIGURE 2.This diagram shows the same system, with the physicochemical stimuli expanded. What we have called calories are in fact only one of a large number of potential metabolic signals, and taste, only one of a number of potential seniory signals. The metabolic class includes all of the classical factors that physiologists have implicated in food intake. When a single factor is singled out and perhaps overemphasized, we have a "theory" of intake, as in the classical glucostatic and thermostatic hypotheses. Some would also consider a lipostatic or perhaps an "aminostatic" theory as well. Most people working in this area now accept Edward Adolph's dictum that food intake is under multiple factor control, and that some combination of all of the metabolic signals is involved. The sensory category summarizes the classes of stimuli contained in food which have been of interest to the sensory psychologist, but which, for the most part, have been ignored by the regulatory physiologist.FIGURE 2 suggests many interesting problems, e.g. which receptor system responds to which classes of stimuli? Where are the latter located? Are they independent? For the purpose of this discussion, we can ignore these complexities. Returning to the simpler case (FIGURE 1 ) , we can now point out that the terms,

While acute blood pressure elevations are commonly seen in the ED, not all require emergency treatment. True hypertensive emergencies are characterized by a rapid elevation in blood pressure to a level above 180/120 mmHg and are associated with acute target organ damage, which requires immediate hospitalization for close hemodynamic monitoring and IV pharmacotherapy. Recognizing the clinical signs and symptoms of hypertensive emergency, which may vary widely depending on the target organ involved, is critical. High blood pressure levels that produce no signs or symptoms of target organ damage may be treated without hospitalization through an increase in or reestablishment of previously prescribed oral antihypertensive medication. However, all patients presenting with blood pressure this high should undergo evaluation to confirm or rule out impending target organ damage, which differentiates hypertensive emergency from other hypertensive crises and is vital in facilitating appropriate emergency treatment. Drug therapy for hypertensive emergency is influenced by end-organ involvement, pharmacokinetics, potential adverse drug effects, and patient comorbidities. Frequent nursing intervention and close monitoring are crucial to recuperation. Here, the authors define the spectrum of uncontrolled hypertension; discuss the importance of distinguishing hypertensive emergencies from hypertensive urgencies; and describe the pathophysiology, clinical manifestations, and management of hypertensive emergencies.