Pineal atrophy and other neuroendocrine and circumventricular features of the naked mole-rat,heterocephalusglaber (Rüppell), a fossorial,equatorial rodent

Summary Quantitative aspects of the microanatomy of the pineal gland and other neuroendocrine and circumventricular structures were studied in a small, reproductively suppressed, female Naked Mole-rat from central Kenya, Africa. The atrophic pineal is the smallest in absolute size (0.002135 mm³) of any so far described in a species of rodent, and in size relative to body weight is second only to that of another tropical species. The subcommissural organ and posterior collicular recess are also relatively small and less well differentiated than those in most other examined rodent species. In contrast, the subfornical organ, OVLT and median eminence are large and well vascularized. It is concluded that the pineal in this species follows the previously described trend among rodents of relatively smaller size in species whose centers of distribution are in lower latitudes. Although the pineal is atrophic, the Naked Mole-rat still exhibits 24-hour and seasonally timed patterns of behavior and seasonal reproduction. However, in this species these events are probably cued by moisture, temperature and social factors rather than by photic information.     

Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. II. New synapse formation in the medial amygdaloid nucleus by fibers from the bed nucleus of the stria terminalis

The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 ± 0.1 (mean±S.E.M.) per unit area (2500 μm² in the molecular layer, and 3/0 ± 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 ± 0.6 per unit area in the molecular layer and 4.5 ± 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury.     

A transcrista galli, translamina terminalis approach for highly placed basilar bifurcation aneurysms

Summary Surgery for highly placed basilar bifurcation aneurysms is one of the most difficult operations in neurosurgery. Specific surgical techniques have been developed including the temporopolar, zygomatic, transzygomatic subtemporal, transclinoid trans-sellar transcavernous, and trans third ventricular approaches. The authors present some technical advances which have been developed for the transcristagalli translamina terminalis approach for the treatment of this aneurysm.     

Effects of androgens and estrogens on the vasopressin and oxytocin innervation of the adult rat brain

Recently we reported that castration of rats eliminates vasopressin immunoreactivity in the lateral septum and other areas that appear to receive vasopressin innervation from the bed nucleus of the stria terminalis. Testosterone treatment counteracts this effect of castration. In the present study, we investigated whether this action of testosterone depends on its androgenic or estrogenic metabolites by treating long-term castrated rats with estradiol (E) and/or 5 alpha-dihydrotestosterone (DHT) or testosterone. The brains were then processed for immunocytochemistry or radioimmunoassay. DHT did not increase vasopressin staining in the lateral septum, although it fully restored the size of the seminal vesicles. E did restore the original fiber density, but individual fibers stained more weakly than in sham-operated males. Only treatment with both E and DHT fully restored the vasopressin innervation. This pattern was also reflected in the radioimmunoassay data. The vasopressin content of the lateral septum decreased about 90% after castration but was fully restored by either testosterone or E + DHT treatment. E alone, however, was only half as effective as E + DHT. The treatments had no effect on the oxytocin content of the septum, or on the vasopressin or oxytocin content of the dorsal vagal complex. The results suggest that E mediates most of the effects of testosterone on the vasopressin innervation of the lateral septum. DHT enhances the response to E but has little effect on its own.     

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.     

Regulation of fluid intake in dogs following water deprivation

Whereas water loss in land living animals occurs continuously, water intake takes place discontinuously. At the normal operating set point of plasma osmolality, urine is more concentrated than plasma due to secretion of vasopressin. Thus animals operate around a state of mild dehydration. As water loss occurs, the severity of dehydration and thirst increase in intensity and at some point water intake occurs. Sufficient water is consumed to return plasma osmolality to the normal operating set point. Food intake and water balance are interdependent as food provides the osmoles which determine obligatory renal solute excretion. When dry food with the same osmotic content was substituted for canned food (water content 74%), dogs increased water intake from 24.2 +/- 4.3 to 62.2 +/- 8.8 ml/kg. Urine output and urine osmolality were unchanged, as under conditions of normal hydration, near maximal urine concentration is achieved. Changing water intake is the only available variable to maintain water balance. During water deprivation, the major renal mechanism appears to be natriuresis. In rehydration, satiety mechanisms ensure appropriate water intake and renal sodium conservation restores sodium balance.     

Expression of Fos in rat brain in relation to sodium appetite: furosemide and cerebroventricular renin

Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. In the first experiment, rats were depleted of sodium by treatment with furosemide 24 h prior to sacrifice and without access to either food or sodium solution. Some rats had access to distilled water, and others had no fluids available during the 24 h. All of the furosemide-treated rats showed Fos-IR in both the subfornical organ (SFO) and around the organum vasculosum laminae terminalis (OVLT). Rats with access to distilled water during the depletion period showed no Fos-IR in the supraoptic (SON) or paraventricular hypothalamic nuclei (PVN) and, in parallel behavioral studies, comparably-treated rats consumed only 0.3 M NaCl solution at the end of the 24 h. In rats that had no fluids during the deprivation period, only about one half showed Fos-IR in SON and PVN and, in parallel behavioral studies, comparably treated rats consumed both water and 0.3 M NaCI solution at the end of 24 h. In a second experiment, cerebroventricular administration of renin stimulated short latency intake of 0.3 M NaCI and water. The relative intakes of water and NaCl were comparable at a low dose of renin, but intake of water exceeded that of NaCl after higher doses. Renin induced Fos-IR in SFO, MnPO, peri-OVLT region, SON and PVN. Both Fos-IR and fluid intake were antagonized by administration of losartan, an angiotensin 11 type 1 receptor antagonist. Thus, only the circumventricular organs of the lamina terminalis showed Fos-IR during each natriorexigenic regimen in these studies. These data support the view that Ang 11 of both central and peripheral origin activates the SFO and/or peri-OVLT region and contributes to sodium appetite.     

Projections of the ventral subiculum to the amygdala, septum, and hypothalamus: a PHAL anterograde tract-tracing study in the rat.

The projections of the ventral subiculum are organized differentially along the dorsoventral (or septotemporal) axis of this cortical field, with more ventral regions playing a particularly important role in hippocampal communication with the amygdala, bed nuclei of the stria terminalis (BST), and rostral hypothalamus. In the present study we re-examined the projection of the ventral subiculum to these regions with the Phaseolus vulgaris leucoagglutinin (PHAL) method in the rat. The results confirm and extend earlier conclusions based primarily on the autoradiographic method. Projections from the ventral subiculum course either obliquely through the angular bundle to innervate the amygdala and adjacent parts of the temporal lobe, or follow the alveus and fimbria to the precommissural fornix and medial corticohypothalamic tract. The major amygdalar terminal field is centered in the posterior basomedial nucleus, while other structures that appear to be innervated include the piriformamygdaloid area, the posterior basolateral, posterior cortical, posterior, central, medial, and intercalated nuclei, and the nucleus of the lateral olfactory tract. Projections from the ventral subiculum reach the BST mainly by way of the precommissural fornix, and provide rather dense inputs to the anterodorsal area as well as the transverse and interfascicular nuclei. The medial corticohypothalamic tract is the main route taken by fibers from the ventral subiculum to the hypothalamus, where they innervate the medial preoptic area, "shell" of the ventromedial nucleus, dorsomedial nucleus, ventral premammillary nucleus, and cell-poor zone around the medial mammillary nucleus. We also observed a rather dense terminal field just dorsal to the suprachiasmatic nucleus that extends dorsally and caudally to fill the subparaventricular zone along the medial border of the anterior hypothalamic nucleus and ventrolateral border of the paraventricular nucleus. The general pattern of outputs to the hypothalamus and septum is strikingly similar for the ventral subiculum and suprachiasmatic nucleus, the endogenous circadian rhythm generator.     

Amygdaloid control over interspecies and shock-induced aggression in the rat (author's transl)]

The effect of lateral amygdala or stria terminalis lesions on two different kinds of aggressive behavior have been studied in the rat. The lateral amygdala lesion does not change the non-killing rat's behavior towards mice; but it markedly reduces the shock-induced intraspecific aggression, without changing the flinch and jump thresholds to the electric shocks. A bilateral interruption of the stria terminalis elicits aggressive reactions in previously non killing rats. This initiation of mouse killing behavior is clearly facilitated through a prior food deprivation for 3 days. The interruption of the stria terminalis changes neither the shock induced aggression, nor the response thresholds. As the stria is the main efferent pathway of the cortico-medial nuclei of the amygdala, these results are in accordance with previous conclusions that tentatively localized in this part of the amygdala an essential component of a mechanism which inhibits muricide behavior in the non killing rat, probably through interactions with the olfactory input. This system is largely independent of amygdaloid structures which facilitate shock-induced intraspecific aggression.