Passive avoidance deficit following intracerebroventricular administration of cholecystokinin tetrapeptide amide in rats

The effect of cholecystokinin tetrapeptide amide (CCK-4) injected into the lateral cerebral ventricle on memory processes was examined by a one-trial passive avoidance test in the rat. CCK-4 injection 30 and 60 min before the first retention test caused a shortened latency to response, and its chronic infusion into the lateral ventricle at a rate of 2 micrograms/day shortened the latency of the response to the level of almost complete amnesia. CCK-4 also reduced arginine-vasopressin effect on memory processes when administered simultaneously 30 min before the first retention test, but its amnestic action is short-lasting and antagonized by relatively small amounts of cholecystokinin octapeptide (CCK-8). In addition, the shortened latency to response was admitted to be not always associated with the motility effect of CCK-4.     

Attenuation of radiation- and drug-induced conditioned taste aversions following area postrema lesions in the rat

The effects of lesions of the area postrema on the acquisition of radiation- and drug-induced (histamine and lithium chloride) conditioned taste aversions were investigated. The results indicated that area postrema lesions caused a significant attenuation of the aversion produced by pairing a novel sucrose solution with radiation (100 rad) or drug injection. Further, the area postrema lesions produced a similar level of attenuation of the taste aversion in all three treatment conditions. The results are discussed in terms of the implications of this finding for defining the mechanisms by which exposure to ionizing radiation can lead to the acquisition of a conditioned taste aversion.     

Elimination of vasopressin analgesia following lesions placed in the rat hypothalamic paraventricular nucleus

Pain thresholds are increased following central administration of arginine vasopressin (AVP), an effect which appears not to be mediated through opioid analgesic processes. In addition to magnocellular projections to the posterior lobe of the pituitary gland and parvocellular projections to the zona externa of the median eminence, the paraventricular nucleus (PVN) of the hypothalamus contains VP parvocellular neurons which also project to extrahypothalamic structures involved in pain inhibition. The present study examined whether AVP analgesia as measured by the tail-flick test was altered in animals with lesions placed in the PVN at either 7 or 35 days after surgery. VP levels in the pons-medulla and the lumbo-sacral spinal cord were measured by radioimmunoassay, as well as VP-like immunoreactivity in the PVN and spinal cord with immunocytochemistry. Lesions placed in the PVN eliminated AVP analgesia on the tail-flick test at both 7 and 35 days after surgery, and decreased radioimmunoassayable VP by 59% in the lumbo-sacral spinal cord and 36% in the pons-medulla. The extent of the lesions ranged from complete destruction of the PVN to partial sparing of ventro-medial PVN cells with VP-like immunoreactivity. These data indicate that the PVN is a critical structure for the integrity of AVP analgesia.     

Selective impairment of visual motion interpretation following lesions of the right occipito-parietal area in humans

A group of eighteen patients selected on the basis of the anatomical locus of the lesion, normal visual acuity and the ability to discriminate visual motion, were assessed on the perception of Julesz Random-Dot stereograms and on three tasks of visual motion interpretation: Speed Discrimination, 3D-Structure-from-Motion and 2D-Form-from-motion. The results on these experimental tasks demonstrate a double dissociation of deficits on the visual analysis of motion and stereopsis in the patients with lesions to the posterior right hemisphere. The right occipital-parietal (ROP) group failed on the Stereopsis task and showed a dramatic impairment on the Speed Comparison and on the Structure-from-Motion experiments. They performed in the normal range, however, on the 2D-Form-from-Motion task. The right occipital-temporal (ROT) group, on the other hand, were severely impaired on the identification of two dimensional forms from motion or stereopsis. In both cases, however, they were able to obtain a coarse segregation of the figure from the background. The ROT group did not present significant deficits on the Speed Discrimination and the Structure-from-Motion tasks. The results are discussed in the light of recent physiological and psychophysical findings, and it is hypothesized that, in the human brain, visual deficits ofmotion interpretation and ofstereopsis are associated with right occipital-parietal lesions.     

Aphagia in the rat following microinjection of neurotensin into the ventral tegmental area

Neurotensin was microinjected into the lateral cerebral ventricle and the ventral tegmental area of rats which had been deprived of food for 18 hours. Both routes of administration resulted in a significant reduction of food intake compared to vehicle control injections. Additionally, the dose of neurotensin required to produce aphagia following ventral tegmental injection was substantially less than the dose required by the ventricular route. The results are discussed in relation to a possible site and mode of action for this neuropeptide.     

Adrenalectomy-induced deficits in maternal retrieval in the rat

Previous studies have indicated that a functioning adrenal gland is not necessary for the expression of maternal behavior in the rat. In the present study, adrenalectomized mothers were found to take longer to initiate retrieval and to retrieve a smaller percentage of their litters on postpartum Days 1–4 than did control mothers. Possible causes of these deficits are discussed.     

Molecular structure of the axolemma of developing axons following altered gliogenesis in rat optic nerve

Axonal and axolemmal development of fibers from rat optic nerves in which gliogenesis was severely delayed by systemic injection of 5-azacytidine (5-AZ) was examined by freeze-fracture electron microscopy. In neonatal (0-2 days) rat optic nerves, all fibers lack myelin, whereas in the adult, virtually all axons are myelinated. The axolemma of neonatal premyelinated fibers is relatively undifferentiated. The P-fracture face (P-face) displays a moderate (approximately 550/micron 2) density of intramembranous particles (IMPs), whereas the E-fracture face (E-face) has few IMPs (approximately 125/micron 2) present. By 14 days of age, approximately 25% of the axons within control optic nerves are ensheathed or myelinated, with the remaining axons premyelinated. The ensheathed and myelinated fibers display increased axonal diameter compared to premyelinated axons, and these larger caliber fibers exhibit marked axonal membrane differentiation. Notably, the P-face IMP density of ensheathed and myelinated fibers is substantially increased compared to premyelinated axolemma, and, at nodes of Ranvier, the density of E-face particles is moderately high (approximately 1300/micron 2), in comparison to internodal or premyelinated E-face axolemma. In optic nerves from 14-day-old 5-AZ-treated rats, few oligodendrocytes are present, and the percentage of myelinated fibers is markedly reduced. Despite delayed gliogenesis, some unensheathed axons within 5-AZ-treated optic nerves display an increased axonal diameter compared to premyelinated fibers. Most of these large caliber fibers also exhibit a substantial increase in P-face IMP density. Small (less than 0.4 micron) diameter unensheathed axons within treated optic nerves maintain a P-face IMP density similar to that of control premyelinated fibers. Regions of increased E-face particle density were not observed. The results demonstrate that some aspects of axolemma differentiation continue despite delayed gliogenesis and the absence of glial ensheathment, and suggest that axolemmal ultrastructure is, at least in part, independent of glial cell association.     

BDNF mRNA expression in the developing rat brain following kainic acid-induced seizure activity.

Brain-derived neurotrophic factor (BDNF) mRNA expression was studied in the hippocampus at various developmental stages in normal rats and following kainic acid (KA)-induced seizure activity. Systemic administration of KA strongly elevated BDNF mRNA levels in all hippocampal subregions after postnatal day 21. In contrast, even though KA induced intense behavioral seizure activity at postnatal day 8, the seizures were not associated with elevations of BDNF mRNA levels, indicating a clear dissociation between behavioral seizures and increases in BDNF mRNA levels and contradicting the view that BDNF mRNA expression is principally regulated by neuronal activity. In the dentate gyrus at postnatal day 13, intense BDNF mRNA expression was limited to a defined area at the border between granule cell and molecular layers, suggesting the possibility that segregation of BDNF mRNA into defined subcellular compartments may play a role in establishing the well-delineated patterns of innervation in the hippocampus.     

Passive avoidance in amygdalectomized rats as affected by methylphenidate and midantan

It is shown that disturbance of conditioned reaction of passive avoidance in Wistar rats, elicited after bilateral amygdalectomy, may be compensated by administration of indirect dopamine agonist--methylphenidate. Two-fold administration proved to be effective: that before learning and that before testing. Two-fold administration of another dopamine agonist--amantadine did not restore the disturbed conditioned reaction. The results are discussed in the aspect of the role of different dopamine brain systems in passive avoidance and possible specificity of the drugs action.     

Neuronal lesions and behavioral modifications in rat following cerebral ischemia and reperfusion

Neurons of the mammalian CNS differ in their vulnerability to various disease processes and other insults, particularly in their response to total anoxia/ischemia. In this study we have tested the histological and behavioral modifications induced by experimental conditions of partial cerebral ischemia in the rats. The specific morphological and histological alterations, observed in our experimental conditions of reversiblepartial cerebral ischemia, confirm the selective vulnerability of certain neuronal populations to ischemic injury and are also evidenced by behavioral modifications which may mirror the functional impairment observed in humans after a transitory ischemic attack.     

Central nervous system lesions in the Wistar rat fetus following direct fetal injections of cadmium

During embryogenesis, maternal administration of cadmium (Cd) produces teratogenic effects, including hydrocephalus (HC), whereas later in gestation (during the fetal period), such effects have not been reported. Since there is little placental transfer of Cd late in gestation, such differences in response could be due to a lower Cd concentration in the fetus compared with the embryo after maternal Cd exposure, or could be due to a decreased sensitivity of the fetal central nervous system (CNS) to Cd. To test the susceptibility of the late gestational CNS to Cd, day 19 (sperm plug = day 0) rat fetuses were directly injected i.p. with CdCl2 (165, 100, 50 nmoles/fetus in 5 microliters saline). All fetuses in one horn were treated with Cd, while fetuses in the other horn were treated with saline. Fetuses were collected on day 21, grossly examined, weighed, fixed in Bouin's fixative, and later razor sectioned. Cd did not affect fetal viability or body weight. However, Cd caused a dose-dependent increase in hydrocephalus, with the total number of fetuses showing moderate to severe HC being 0/45, 0/11, 6/10, and 18/20 for controls, low, medium, and high doses, respectively. Mild HC was noted in one control and two low Cd fetuses. Brain necrosis was correlated with hydrocephalus, being observed in 0/45, 0/11, 5/10, and 16/20 fetuses, respectively. In medium-dose fetuses without HC or brain necrosis, extravasation of erythrocytes was noted histologically within the cortical parenchyma, suggesting that hemorrhaging may lead to brain necrosis and hydrocephalus in Cd-exposed fetuses. Thus, the fetal CNS is susceptible to the toxic effects of Cd.     

Molecular forms of hippocampal acetylcholinesterase and their changes following septal lesions in the rat.

Changes of acetylcholinesterase activity and its molecular forms, extracted by Triton X-100 and separated by polyacrylamide gel electrophoresis, were studied in the rat hippocampus following septal lesions. Detection of acetylcholinesterase was made densitometrically. While the total activity of acetylcholinesterase was decreased, its molecular forms exhibited a different pattern of changes: the heavy forms were decreased, while the light ones were increased. The results support the view that different acetylcholinesterase molecular forms serve different regulatory mechanisms.