Chemosensitivity of neurons in the dorsal motor nucleus of the vagus that responded to portal infusion of hypertonic saline in rats

Neural responses in the dorsal motor nucleus of the vagus (DMV) to topical administrations of sodium and portal infusions of hypertonic saline were investigated electrophysiologically by using multibarrel electrodes in anesthetized rats. Of 102 neurons that showed antidromic response to electrical stimulation of the ventral gastric vagus or the accessory celiac vagus, 51 neurons increased and 13 neurons decreased their discharge rates in response to the electrophoretic administration of sodium. The other 38 neurons did not respond to this stimulation. The portal infusion of hypertonic saline elicited neural responses of some DMV neurons whose axons are involved into either the ventral gastric or the accessory celiac vagus. Further, effects of the topical administration and the portal infusion of hypertonic saline were examined on 33 neurons. Typical response was characterized by an increase in discharge rate responding to both of the portal infusion and the topical administration. In conclusion, the DMV neurons receiving the afferent inputs from hepatoportal osmoreceptors may have an enteroceptor function detecting the change in osmotic pressure of their environment.     

Calretinin is differentially localized in magnocellular oxytocin neurons of the rat hypothalamus. A double-labeling immunofluorescence study

By use of a double-labeling immunofluorescence method with a confocal laser scanning microscope, we have examined whether a calcium-binding protein, calretinin, is localized in magnocellular oxytocin and vasopressin neurons of the rat hypothalamus. In the supraoptic nucleus, all oxytocin-labeled cells were stained for calretinin. However, in the magnocellular part of the paraventricular nucleus, almost all oxytocin-stained cells were devoid of calretinin immunoreactivity. All vasopressin-positive cells of both the supraoptic nucleus and the magnocellular part of the paraventricular nucleus lacked calretinin immunoreactivity. No calretinin immunoreactivity was found in oxytocin-labeled cells of the the anterior commissural nucleus or in vasopressin-labeled cells of the suprachiasmatic nucleus. We previously showed that another calcium-binding protein, calbindin-D28k, was localized in magnocellular oxytocin neurons of the supraoptic nucleus but not in those of the paraventricular nucleus. These findings suggest that, in general, magnocellular oxytocin neurons of the supraoptic nucleus and those of the paraventricular nucleus can be chemically distinguished, that is, the former contain both calretinin and calbindin-D28k but the latter lack the two calcium-binding proteins.     

Release of vasopressin from supraoptic neurons within the median eminence in vivo. A combined microdialysis and push-pull perfusion study in the rat

The present study was designed to investigate whether or not arginine vasopressin (AVP) is released from magnocellular neurons within the median eminence (ME) in vivo. Urethane-anesthetized adult male Wistar rats were equipped with a microdialysis probe aimed at the supraoptic (SON) or paraventricular nucleus (PVN), a push-pull perfusion probe resting in the ME, and a blood microdialysis probe within the jugular vein. Dialysis of the SON (but not the PVN) with Ringer's solution containing 56 mmol l⁻¹ K⁺ resulted in an increase in AVP release within the ME (to 492 ± 192% of release during basal conditions,P < 0.05) and into blood (to 138 ± 9%,P < 0.01) whereby the release probably occurred from axonal swellings and nerve terminals of supraoptic neurons which project through the internal zone of the ME to the posterior pituitary. The calculated amount of AVP released into the extracellular fluid of the ME was high enough (approximately 1 pg/μ1) to hypothesize that the neuropeptide could enter the portal blood capillaries in physiologically relevant concentrations. Taken together, the present study indicates that activation of magnocellular neurons is accompanied by release of AVP within the median eminence. We assume that AVP released in this way might mediate a communication between the hypothalamic-neurohypophysial system and the hypothalamic-pituitary-adrenal axis in response to selected stressful stimuli.     

Neuronal changes in the basolateral complex during development of the amygdala of the rat

Neuronal changes in the amygdala basolateral complex were studied during development and maturation in fetal and postnatal rat brains using morphometrical methods. Forty brains of animals of various ages were fixed in formalin, frozen and cut into 25 μm thick sections and stained with cresyl violet or haematoxylin and eosin (H&E). In cresyl violet preparations, the complex appeared for the first time on embryonic day (E)17 and was composed of two homogeneous nuclei—lateral and basolateral. On about the seventh postnatal day, each of these nuclei was divided into two parts—the first one into the dorsolateral and ventromedial and the second one into the anterior and posterior. Morphometric investigations showed a different increase of the neuronal and nuclear size in various parts of the basolateral complex up to postnatal day (P)14; after that time these parameters did not change significantly. The neuronal density and the total number of neurons stabilized at P7 in all parts of this complex, except for the dorsolateral part of the lateral nucleus in which a 30% decrease of the total number of cells was observed. From P14, in all nuclei under study, the total number of neurons did not change significantly.     

东莨菪碱对大鼠下丘脑室旁核精氨酸升压素的影响

目的 观察东莨菪碱对大鼠下丘脑室核精氨酸升压素的影响。方法 以不同浓度Ｓｃｏｐ推挽灌流大鼠下丘脑室旁核 结果 扣留出液中精氨酸升压素含量随推挽时间延长而增多。结论Ｓｃｏｐ可促进ＰＶＮ释放内源性ＡＶＰ，这对了解Ｓｃｏｐ抗休克的机理有重大的意义。     

增殖细胞核抗原在口腔鳞状细胞癌中的表达

采用鼠抗ＰＣＮＡ单克隆抗体，ＡＢＣ法，对１１例正常口腔粘膜及２９例口腔鳞癌进行了染色。结果表明：正常粘膜仅在基底层中有少量的ＰＣＮＡ阳性细胞，其阳性分级为１级。而鳞癌阳性分级主要是３～４级，随着组织学分级的升高，ＰＣＮＡ阳性表达率也相应增高。经统计学分析，正常组织与鳞癌之间及鳞癌各级均有非常显著差异（Ｐ＜００１）。提示：ＰＣＮＡ的表达与口腔鳞癌组织学分级有关。     

Down-Regulation of Estrogen Receptor Immunoreactivity by 17β-estradiol in the Guinea Pig Forebrain

Low amplitude pulses of estradiol-17β (E₂-17β) are more effective than large single bolus injections or constant exposure to E₂-17β in inducing progesterone-facilitated sex behavior in female rats and guinea pigs. The present study examined whether the increased responsiveness to E₂-17β is due to an increase in the number of estrogen receptors in the estrogen receptor rich areas of the hypothalamus and amygdala. Initial studies examined the rapid effects (20 min) of a high dose of E₂-17β (50 μg) on estrogen receptor immunostaining using either the H222 antibody or the ER 21 antiserum. ER 21 immunostaining was not affected by the E₂-17β treatment suggesting that it binds to both occupied and unoccupied estrogen receptors. Therefore the ER 21 antiserum was used to characterize the regulation of estrogen receptor immunoreactivity (ER-IR) by E₂-17β. ER-IR was examined for 48 h and serum E₂-17β for 24 h following a 2 μg s.c. injection of E₂-17β (a dose similar to that used in multiple pulse paradigms). Serum E₂-17β peaked 15 to 30 min following the injection and returned to baseline values by 1 h. In all but one area maximal suppression of ER-IR occurred at 12 h. In summary, 1) decreases in estrogen receptor immunoreactivity following E₂-17β are consistent with studies in which estrogen receptors were assayed by binding assays and estrogen receptor mRNA was determined by in situ hybridization; 2) the ER 21 antiserum is able to detect both occupied and unoccupied estrogen receptors and 3) H222 immunoreactivity is influenced by the presence of E₂-17β, so that the level of H222-IR is a reflection of ligand/receptor binding dynamics. The data suggest that up-regulation of estrogen receptors does not account for the increase in behavioral sensitivity which is observed following multiple pulses of E₂-17β.     

Inhibitory action of a conditioning procedure on visual responsive neurons of the nucleus reticularis thalami in rats

Summary In urethane anesthetized rats neuronal responses of the visual part of nucleus reticularis thalami (vTR) to light were compared with those during pairing light as a conditioned stimulus (CS) with the electrical stimulation of the rat's tail (US). The intensity of the US was adjusted to the minimum required to evoke a slight freezing behavior in the awake rat. The firing rate of most vTR neurons decreased in the period between light and US application (P < 0.01). Significant response modulations to light were observed in 39% of the units, in most of them they persisted over an extinction period of 15 min. In addition, neurons which were predominantly inhibited by conditioning sometimes changed from regular spiking to a burst pattern. The results support the hypothesis that conditioning related facilitation of geniculate neurons observed in previous experiments can be explained at least partly by disinhibition of geniculate units from vTR.