bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebellar contributions to the papez circuit
Authors: Snider Ray S. , Maiti A. 
Published: January 2005

AbstractCerebellar influences on the various substructures in the Papez Circuit are indicated by the following.
Anatomical studies indicate that the major midbrain areas to which this circuit projects are : (1) ventral tegmental area; (2) interpeduncular area; and (3) periaquenductal gray areas; and these same areas project back to the limbic system. There are projections to these regions from the cerebellar nuclei, as indicated by terminal degeneration studies which show that cerebellar nuclei connect, mostly by fine fibers, with a continuum of cells located on either side of the midline in the ventral tegmentum of the midbrain. Observations that the cerebellum also projects to the locus ceruleus (NA system) and VTA (DA system) indicate that cerebellar influences can also reach the limbic areas via the catecholamine fiber bundles.
Electrophysiological studies indicate that vermian and fastigial stimulation induce evoked responses in the basolateral amygdala, the hippocampus, and the septum, with laterncies to the peak of first wave ranging from 4 to 8 msec and to the second wave of 16–29 msec. Citations from the physiological literature indicate that electrical stimulation of the cerebellum, especially the vermis, can modify a wide range of responses which involve fuctional activities of either the sympathetic or parasympathetic nervous systems.
Studies on electrically induced afterdischarges in the septum, Hippocampus, and amygdala indicated that cerebellar stimulation can shorten the duration of or terminate that afterdischarges, and the site of lowest threshold is the midline cortex. Focal cooling of the vermis promotes prolongation of the afterdischarges as does preteatment of animals with 6‐OH dopamine. Chemical lesions in the catecholamine system induced by 6‐OH dopamine reduce the effectiveness of the cerebellar stimulation, as do lesions of nucleus fastigii, These data are interpreted to indicate that the cerebellum can exert a tonic suppressor (inhibitory?) influence on substructures within the Papez Cricuit.
Citations from animal behavioral studies indicate that electrical stimulation of the anterior cerebellum can induce responses such as arousal, predatory attack, and feeding which mimic those obtained by amygdaloid stimulation. Fastigial stimulation can produce drowsiness and EEG changes which resemble the sleep patterns resulting from stimulation of the ventral amygdala.
Cellular and subcellular distribution of the S‐100 protein in rabbit and rat central nervous system
Authors: Haglid K. G. , Hamberger A. , Hansson H.‐A. , Hydén H. , Persson L. , Rönnbäck L. 
Published: January 2005

AbstractThe cellular and subcellular distribution of the S‐100 protein in rabbit and rat central nervous system was studied both quantitatively and qualitatively. Microcomplement fixation estimations on bulk‐prepared neuronal and glial cells showed at least five to six times higher amounts of water‐soluble S‐100 protein. High levels of S‐100 protein were found in mitochondria and soluble protein fractions. Immunoelectron microscope investigations demonstrated S‐100 protein in neuronal structures, such as the postsynaptic membrane and part of the plasma membrane. Among glial cells the astrocytic filaments contained high levels of S‐100 protein. S‐100 was also found in most subcellular membranes of astrocytes and oligodendrocytes.
Effects of cannabis sativa on ultrastructure of the synapse in monkey brain
Authors: Harper Jon W. , Heath Robert G. , Myers William A. 
Published: January 2005

AbstractElectron microscopic study of brain tissues of monkeys chronically exposed to psychoative Cannabis showed widening of the synaptic cleft, electron opaque material in the cleft and in pre‐ and postsynaptic regions, and some “clumping”: of synaptic vesicles. In contrast, tissues of control monkeys showed no ultrastructural changes.
Pharmacology of the brachium conjunctivum: Red nucleus synaptic system in the baboon
Authors: Huffman Ronald D. , Davis Ross 
Published: January 2005

AbstractAcetylcholine, biogenic amines, and certain amino acids were applied by microintophoresis to parvicellular and magnocellular red nucleus (RN) neurons of baboon while recording brachium conjunctivum (BC)‐evoked and amino acid‐evoked unit discharge from these neurons. Glycine, γ‐aminobutyric acid, and β‐alanine were potent depressants of BC‐RN synaptic transmission, amino acid‐evoked firing, and spontaneous activity of all RN neurons studied. Glycine was clearly more potent than the other 2 depressant amino acids. L‐Glutamic and DL‐homocysteic acid were strong excitants of all RN neurons tested. Dopamine, noradrenaline, and 5‐hydroxytryptamine depressed the excitability of both parvicellular and magnocellular RN neurons; no excitatory effects were observed with these biogenic amines on RN neurons. Acetylcholine increased the rate of firing of spontaneously discharging parvicellular RN neurons and facilitated the amino acid‐induced firing of these same neurons. Acetylcholine did not facilitate BC‐RN synaptic transmission nor could this transmission be blocked by cholinergic antagonists. Unlike parvicellular RN neurons, the responsiveness of magnocellular neurons was either unaltered by acetylcholine or slightly decereased. These experiments demonstrate a difference in the pharmacologic responsiveness of parvicellular and magnocellular RN neurons to acetylcholine but do not provide evidence for a cholinergic input to RN via the brachium conjunctivum.
The effect of chronic administration of d‐amphetamine on regional changes in catecholamines in the rat brain
Authors: Lynch Marina , Kenny Marie , Leonard B. E. 
Published: January 2005

AbstractChanges in the dopamine, noradrenaline and dihydroxyphenylacetic acid (DOPAC) concentrations were determined in 6 regions of the rat brain following chronic amphetamine administration for 2 weeks and at intervals of up to 7 days after drug withdrawal. Chronic amphetamine administration caused pronounced stereotypy; following withdrawal the animals were behaviourally depressed for at least 7 days. The noradrenaline concentration of all brain areas investigated was decreased throughout most of the experimental period; only in the midbrain and the olfactory lobes did the noradrenaline concentration return to control values 7 days after drug withdrawal. In contrast, the dopamine concentration was raised in the midbrain, hippocampus, and olfactory lobes following drug administration but reduced in the striatum, brain stem, and amygdaloid cortex. Following amphetamine withdrawal, most of the brain areas showed a decrease in the dopamine concentration apart from the olfactory lobes which showed an increase and the midbrain and hippocampus which were largely unchanged. The concentrations of the intraneuronal metabolite DOPAC were decreased in most brain areas throughout the duration of the experiment, suggesting that the turnover of dopamine was decreased. These results are discussed with reference to the possible decreased activity in tyrosine hydroxylase both during drug treatment and after withdrawal.
Ethanol tolerance: Evidence of “protective” effects on brains of adult rats
Authors: Klemm W. R. 
Published: January 2005

AbstractPrevious research with two biochemical markers of acute ethanol damage (sialic acid and 2‐deoxyribose) raised the possibility that tolerance developed by chronic ingestion of ethanol. However, this hypothesis required demonstration that chronic consumption was not damaging. This issue was investigated histologically in adult rats that voluntarily consumed massive doses of ethanol daily (range of 11 to 18 gm/kg/rat/day) for 28 days. By all indices (thickness measures of neocortex, hippocampus, and cerebellar molecular layer; and specific cell counts of neocortex and cerebellum), none of the ethanol‐exposed rats, even those with intentional nutritional deficiencies, revealed any physical sign of damage compared to control rats.
An interaction between the pineal gland and olfactory deprivation in potentiating the effects of melatonin on gonads, accessory sex organs, and prolactin in male rats
Authors: Blask David E. , Nodelman Jacqueline L. 
Published: January 2005

AbstractMale rats (25–26 days of age) housed with 14 hours of light per day (lights on 0600–2000 hours) were either olfactory bulbectomized (rendering them anosmic), bulbectomized plus pinealectomized (Pinx), or left intact. On the day following the operations, intact, anosmic, and anosmic‐Pinx animals began receiving single, daily afternoon (1700–1800 hours) subcutaneous injections of 50 μg of melatonin (MEL) for six weeks, while an additional group of intact controls received injections of diluent. At the end of this period, body, anterior pituitary, testicular, and seminal vesicle weights were significantly reduced in intact‐MEL‐treated animals. Anosmic animals that had been treated with MEL experienced a further, highly significant, 65%, 90%, and 85% depression in testicular, seminal vesicle, and ventral prostate weights, respectively, as compared with intact control and MEL‐treated rats. Additionally, both body and anterior pituitary weights were significantly decreased in MEL‐treated, anosmic rats. Anosmic‐Pinx rats treated with MEL had organ and body weights that were intermediate between those of intact‐MEL and anosmic‐MEL‐treated animals. Pituitary and serum levels of prolactin (Prl) were significantly lower in anosmic‐MEL‐treated rats than in intact or intact‐MEL‐treated groups. Similarly, Prl levels were depressed in the anosmic‐Pinx rats treated with MEL; however, serum Prl was not statistically lower than in intact or intact‐MEL‐treated animals. These results indicate that anosmic male rats have an increased sensitivity to antigonadotrophic and Prl‐inhibitory effects of MEL. Furthermore, the data suggest that the presence of the pineal gland in anosmic rats is important in permitting anosmia maximally to sensitize the neuroendocrine‐reproductive axis to the antigonadotrophic effects of exogenously administered MEL.
Isolation of ribosome containing synaptosome subpopulation with active in vitro protein synthesis
Authors: Verity M. Anthony , Brown W. Jann , Cheung M. 
Published: January 2005

AbstractSubpopulations of synaptosomes harvested from neonatal rat brain cortices revealed a differential ability to synthesize protein in vitro. Incubation of synaptosomes with radiolbeled leucine, followed by continuous sucrose gradient centrifugation produced an asymmetric shift in the radioactivity toward the higher density sucrose fractions. The bulk of the mitochondrial cytochrome c‐oxidase activity was also found in these fractions, however, subfractionation studies of osmotically‐lysed synaptosomes suggested that the newly‐synthesized proteins reside in an osmotically sensitive, non‐mitochondrial compartment.The ability of each subpopulation of synaptosomes to synthesize protein in vitro was assessed after their isolation from linear continuous sucrose gradients. There was an enrichment of highly active protein synthesizing particles in the “heavy” subpopulations of neonatal synaptosomes. The inhibitory effects of chloramphenicol and cycloheximide on the protein synthesis in these particles were similar to those of the original synaptosome fraction. Electron microscopic analysis revealed an increase in the numbers of ribosome‐containing structures resembling dendritic dendritic and axonal growth cones.
The uptake of 3‐deoxy‐3‐fluoro‐D‐Glucose by synaptosomes from rat brain cortex
Authors: Halton D. M. , Taylor N. F. , Lopes D. P. 
Published: January 2005

AbstractD‐[3‐3H]‐3‐deoxy‐3‐fluoroglucose was synthesized chemically and shown to be transported into rat brain synaptosomes by a saturable process with a Km 6.2 × 10−4 M and a Vmax 2.8 nmole · mg protein−1. After an initial, rapid period of transport, further uptake of the fluorosugar is restricted by the rate of its phosphorylation. Both D‐glucose and cytochalasin B are competitive inhibitors of 3‐deoxy‐3‐fluoro‐D‐glucose transport with Ki values of 93 μm and 6.0 × 10−7 M, respectively. Phloretin, N‐ethylmaleimide and p‐chloromercuribenzoate also inhibit the fluorosugar uptake, whereas ouabain and changes in K+, Na+, Mg2+ and Ca2+ ions have only a small effect. The recorded 3‐deoxy‐3‐fluoro‐D‐glucose influx is slightly reduced by potassium cyanide, antimycin A, 2,4‐dinitrophenol, and rotenone. The uptake reduction caused by these four reagents is relieved by the addition of exogenous ATP. The possible influence of hexokinase activity on the uptake process is discussed.
Role of nerve growth factor in ethylnitrosourea‐induced neural carcinogenesis
Authors: Vinores Stanley A. , Perez‐Polo J. Regino 
Published: January 2005

AbstractThe sensitivity of the rat nervous system to malignant transformation by ethylnitrosourea (ENU) is a function of age at treatment. From late gestation, nervous structures decrease in sensitivity with age as non‐neural structures increase in susceptibility. There is a decrease in the proportion of neural tumors induced by ENU and an increase in survival time when nerve growth factor (NGF) levels are elevated in the fetal or neonatal stage. If antibodies directed against mouse beta‐NGF (anti‐NGF) are administered prior to neonatal ENU treatment, neural tumors appear earlier, although in the same proportion as with treatment by ENU alone. This effect is not observed if the ENU is administered first. This phenomenon seems to be attributed to an increased number of trigeminal nerve neurinomas, which have a shorter latent period than other nervous system tumors. The induced neurological tumors in rats treated neonatally with anti‐NGF prior to ENU seem to be almost exclusively neurinomas in the peripheral nervous system. Fetal anti‐NGF treatment leads to an increased number of intracerebral gliomas and a longer survival time, which corresponds to the longer latent period of these tumors. The role of NGF in the sensitivity of the rat nervous system to carcinogenesis by ENU and its possible implications in the development of the nervous system are discussed.
Respiration in rat cerebral astrocytes from primary culture
Authors: Olson James E. , Holtzman David 
Published: January 2005

AbstractRespiration was measured polarographically in astrocytes from dissociated neonatal rat cerebra grown in primary culture. Cells grown in a modified Eagle's minimal essential medium containing 20% fetal calf serum for 14 to 21 days respired at a rate of 34.23 n at. equiv 0 mg protein−1 min−1. Cells which were grown in this medium for 14 days and then grown in serum‐free medium containing 0.25 mM dibutyrylcyclic‐AMP (dbcAMP) for three to six days, had respiratory rates 20% higher than in cells from untreated control cultures (P = 0.005). Maximal inhibition by oligomycin required 200 p mole per mg protein for dbcAMP‐treated cells and 80 pmole per mg protein for untreated cells. Oligomycin inhibited the respiration of both dbcAMP‐treated and untreated cells by about 70%. At a concentration of 175 nmole per mg protein, 2,4‐dinitrophenol (DNP) produced a maximal stimulation of respiration, which was 191% of the resting rate in dbc AMP‐treated cells and 218% of the resting rate in untreated cells. The maximal DNP‐stimulated respiratory rates were the same in dbcAMP‐treated and untreated cells.
Metabolic neural mapping in neonatal rats
Authors: DiRocco Richard J. , Hall W. G. 
Published: January 2005

AbstractFunctional neural mapping by 14C‐deoxyglucose autoradiography in adult rats has shown that increases in neural metabolic rate that are coupled to increased neurophysiological activity are more evident in axon terminals and dendrites than neuron cell bodies. Regions containing architectonically well‐defined concentrations of terminals and dendrites (neuropil) have high metabolic rates when the neuropil is physiologically active. In neonatal rats, however, we find that regions containing well‐defined groupings of neuron cell bodies have high metabolic rates in 14C‐deoxyglucose autoradiograms. The striking difference between the morphological appearance of 14C‐deoxyglucose autoradiograms obtained from neonatal and adult rats is probably related to developmental changes in morphometric features of differentiating neurons, as well as associated changes in type and locus of neural work performed.
Glucocorticoid receptor properties and glucocorticoid regulation of glutamine synthetase activity in sensitive C6 and resistant C6H glial cells
Authors: Holbrook Nikki J. , Grasso Robert J. , Hackney John F. 
Published: January 2005

AbstractThe relationship between induction of glutamine synthetase activity by dexamethasone and binding of the steroid to cytosolic glucocorticoid receptors was examined in sensitive C6 and resistant C6H glial cell cultures.Glutamine synthetase activity increased 3–4‐fold when C6 cultures were exposed to 7.6 × 10−6 M dexamethasone. This inductive response was reversible, dose‐dependent (ED50 ∼ 2 × 10−8 M), required de novo protein and RNA synthesis, and was elicited only by glucocorticoid steroids. Progesterone, but not epicortisol, antagonized the dexamethasone‐induced enzyme increase. In contrast, only a slight inductive effect was observed in dexamethasone‐treated C6H cells.Competitive binding assays demonstrated that specific binding of [3H]‐dexa‐methasone to cytosolic receptors was also dose‐dependent. The ED50 was ∼ 10−8 M for both C6 and C6H cells. Scatchard analysis revealed that each C6 cell contained ∼10,800 receptor sites and that the equilibrium dissociation constant (Kd) was 4.5 × 10−9 M. Each C6H cell possessed ∼ 12,200 sites, and the Kd was 6.7 × 10−9 M. Unlabeled dexamethasone and cortisol (but not epicortisol) competed effectively with [3H]‐dexamethasone for binding to cytosolic receptor sites and nuclear sites of both cell types.These results suggest that induction of glutamine synthetase activity in dexamethasone‐treated C6 cells is a glucocorticoid‐directed response. Since C6H cells are refractory in this regard but contain functional cytosolic receptors which interact with cell nuclei, the basis for their resistance appears to involve some step beyond these cellular processes.
Induction of neurite outgrowth in the IMR‐32 human neuroblastoma cell line by nerve growth factor
Authors: Reynolds C. P. , Perez‐Polo J. R. 
Published: January 2005

AbstractThe nerve growth factor protein (NGF) stimulates neurite outgrowth from embryonic sensory ganglia and sympathetic ganglia at all stages of development. In addition, NGF is required for the maintenance of the differentiated state in adult sympathetic ganglia. A clonal cell line, IMR‐32, derived from a human neuroblastoma was found to contain a population of cells that respond to NGF by exhibiting morphological differentiation. The effect of NGF on these cells is compared with that of other agents known to induce differentiation of IMR‐32, including glioma‐conditioned media.
Bioassay detection of mouse nerve growth factor (mNGF) in the brain of adult mice
Authors: Scott S. M. , Tarris R. , Eveleth D. , Mansfield H. , Weichsel M. E. , Fisher D. A. 
Published: January 2005

AbstractTwo pools of seven brains each from adult Swiss‐Webster mice were homogenized, and supernatants were collected for bioassay. PC‐12 cells were placed in a bioassay plate at time zero, at a concentration of 104 cells per well, and primed for 48 hours in a medium containing 50 ng/ml of mNGF. The PC‐12 cell bioassay for neurite outgrowth was conducted after primed cells were exposed to an NGF‐free medium for 24 hours. Suitable controls for serum toxicity and cell viability were established. The sensitivity of the bioassay approximates 100 pg NGF/ml. The results showed 80–100% neurite outgrowth in wells exposed to brain pool supernatant (BPS) alone, and control level outgrowth (3–8%) in wells containing BPS and specific anti‐β‐NGF antibody. Therefore, the brains of Swiss‐Webster adult mice contain an NGF‐like substance which promotes neurite outgrowth in PC‐12 cells. The substance probably is NGF itself, since the effect is blocked by specific NGF antiserum.
Acute and chronic effects of pentobarbital in relation to postsynaptic GABA receptors: A study with muscimol
Authors: Sivam S. P. , Nabeshima T. , Ho I. K. 
Published: January 2005

AbstractMuscimol, a GABA agonist, enhanced pentobarbital sleeping time in a dose‐dependent manner. The GABA antagonists such as bicuculline and picrotoxin, and the CNS stimulant such as pentylenetetrazol, inhibited pentobarbital sleeping time; however, all except picrotoxin produced less than 35% maximum inhibition. Picrotoxin, an agent which blocks the chloride ionophore of GABA‐receptor complex, exhibited a parallel dose‐response curve with respect to muscimol. Chronic administration of pentobarbital by pellet implantation induced tolerance as evidenced by decreased sleeping time; the tolerance receded gradually upon abrupt withdrawal. Muscimol enhanced pentobarbital sleeping time both in tolerant and withdrawal mice. Na+‐independent GABA‐receptor binding, using [3H]muscimol as a ligand, was increased after acute and chronic pentobarbital administration; withdrawal of the pentobarbital reversed the increase in receptor population. None of the treatments altered the affinity of [3H]muscimol binding. These results support the contention that pentobarbital (a) directly acts on the postsynaptic chloride ionophore and (b) augments GABA‐mediated postsynaptic effects. The functional significance of the increase in GABA receptor population after pentobarbital treatment is unclear.
A proposed method for the determination of cerebral regional intermediary glucose metabolism in humans in vivo using specifically labeled 11C‐glucose and positron emission transverse tomography (PETT). I. An animal model with 14C‐glucose and rat brain autoradiography
Authors: Sacks William , Sacks Shirley , Badalmenti Anthony , Fleischer Arthur 
Published: January 2005

AbstractBased upon data obtained with our arterio‐venous technique for the determination of cerebral metabolism in humans in vivo we have proposed a method for the determination of cerebral regional intermediary glucose metabolism in humans in vivo using specifically labeled 11C‐glucose and positron emission transverse tomography (PETT). In it we would give the subject successive intravenous injections of [3,4‐11C] glucose, [2,5‐11C] glucose and [1‐11C] glucose. There would be a 30 min period of continuous PETT measurements following each injection and a 2 hr interval after the first and second injections. The data would be used with suitable equations and algorithms to estimate for each specific region of the subject's brain the dynamics of the Embden‐Meyerhof‐Parnas (EMP) and the tricarboxylic acid cycle (TCA) metabolic pathways and the incorporation of glucose carbons into lactate, and the extent of dilution of glucose carbons in traversing the TCA with their subsequent incorporation into other carbon pools of the brain (ie, glutamate, glutamine, GABA, alanine). Using 14C as a model for 11C and autoradiographs made with rat brain slices, we have produced an animal model to demonstrate the feasibility of our proposed method. The resulting autoradiographs have provided evidence of the validity of the predictions made from our arterio‐venous data. The model was employed to show the selective reductions in the rates of incorporation of specific carbon atoms of glucose into regions of the rat brain and evidence of altered metabolic pathways following a single electroconvulsive shock (ECS) and after a series of nine ECS.