Electrical stimulation of the proximal stump of the transected sciatic nerve produces a frequency-dependent activation of glucose utilization, measured with the autoradiographic deoxy[14C]glucose method, in the dorsal horn of the spinal cord but produces no change in glucose utilization in the dorsal root ganglion cells. These results suggest that axon terminals and not the cell bodies are the sites of enhanced metabolic activity during increased functional activity of this pathway.Applications of the quantitative autoradiographic deoxyglucose method have demonstrated a close relationship between local functional activity and rates of glucose utilization in nervous tissue (1, 2), and the method has been extensively used to map functional neural pathways on the basis of evoked metabolic responses. The rate of local glucose utilization is, at least in part, regulated by spike frequency (3). It has not been clearly established, however, in which cellular elements (e.g., cell body, initial segment, axon terminals, or dendrites) the increase in glucose utilization occurs during increased impulse activity. In vivo studies in vertebrates have indicated that areas rich in neuropil have the most intense metabolic activity as compared to areas rich in cell bodies. For example, in the striate cortex of the monkey layer IV, the locus of termination of the geniculocalcarine pathway, has higher rates of glucose utilization than the cell-rich layers II and III (4). Bilateral visual occlusion lowers the rates of glucose consumption in the striate cortex as a whole, but the greatest reduction occurs in layer IV (4). It has also been found in rats that functional stimulation of the hypothalamoneurohypophysial system by salt loading enhances glucose utilization in the terminals of this pathway in the pituitary neural lobe but not in the cell bodies of origin of the tract in the paraventricular and supraoptic nuclei (5,6 Animals. Adult male Sprague-Dawley rats were purchased from Taconic Farms (Germantown, NY). The experiments were carried out on animals weighing 300-400 g. Prior to the experiment, the animals were allowed water and Purina Laboratory Chow ad libitum and were kept in a controlled environment with alternate 12-hr light and dark cycles.Preparation of the Animals. On the day of the experiment the animals were anesthetized by an intraperitoneal injection of 45 mg of sodium pentobarbital per kg of body weight, and polyethylene catheters were inserted into one femoral artery and vein. The sciatic nerves on both sides were exposed, tied, and transected bilaterally at the level of the gluteus muscles. A wire loop was inserted around the skin incision on each side and drawn to make pools in which paraffin oil, used to prevent desiccation of the nerves, could be retained. Anesthesia was subsequently maintained by intravenous administration of sodium pentobarbital as needed.Electrical Stimulation. The proximal portion of one transected sciatic nerve was placed on bipolar platinum electrodes and stimulated via a stimulu...
The quantitative autoradiographic deoxyglucose method was used to study the effects of acute adrenalectomy on local cerebral glucose utilization in conscious albino rats. Five hours following removal of the adrenal glands, glucose utilization was increased (4–55%) throughout the brain, particularly in the locus ceruleus, hypothalamic paraventricular nucleus, hippocampus, median eminence and anterior lobe of the pituitary gland. These structures are involved in the regulation of corticotropin-releasing factor, vasopressin, and adrenocorticotropic hormone. Treatment with dexametha-sone (0.25 mg/kg i.m.) substantially reduced or prevented the stimulatory effects of adrenalectomy on cerebral glucose metabolism. These results demonstrate: (1) the existence of a negative feedback loop between the brain and adrenal glands in which corticosteroids exert an inhibitory action on glucose utilization of brain regions participating in adrenotropic regulation, and (2) a general inhibitory action of glucocorticoids on cerebral metabolism.
Nitric oxide (NO), a free radical gas produced endogenously from the amino acid L-arginine by NO synthase (NOS), has important functions in modulating vasopressin and oxytocin secretion from the hypothalamo-neurohypophyseal system. NO production is stimulated during increased functional activity of magnocellular neurons, in parallel with plastic changes of the supraoptic nucleus (SON) and paraventricular nucleus. Electrophysiological data recorded from the SON of hypothalamic slices indicate that NO inhibits firing of phasic and non-phasic neurons, while L-NAME, an NOS inhibitor, increases their activity. Results from measurement of neurohypophyseal hormones are more variable. Overall, however, it appears that NO, tonically produced in the forebrain, inhibits vasopressin and oxytocin secretion during normovolemic, isosmotic conditions. During osmotic stimulation, dehydration, hypovolemia and hemorrhage, as well as high plasma levels of angiotensin II, NO inhibition of vasopressin neurons is removed, while that of oxytocin neurons is enhanced. This produces a preferential release of vasopressin over oxytocin important for correction of fluid imbalance. During late pregnancy and throughout lactation, fluid homeostasis is altered and expression of NOS in the SON is down-and up-regulated, respectively, in parallel with plastic changes of the magnocellular system. NO inhibition of magnocellular neurons involves GABA and prostaglandin synthesis and the signal-transduction mechanism is independent of the cGMP-pathway. Plasma hormone levels are unaffected by icv 1H-[1, 2, 4]oxadiazolo-[4,3-a]quinoxalin-1-one (a soluble guanylyl cyclase inhibitor) or 8-Br-cGMP administered to conscious rats. Moreover, cGMP does not increase in homogenates of the neural lobe and in microdialysates of the SON when NO synthesis is enhanced during osmotic stimulation. Among alternative signal-transduction pathways, nitrosylation of target proteins affecting activity of ion channels is considered.
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