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PubMed2005

Neuroembryotoxic effect of 5- Fluorouracil in rat: injecting in late phase of gestation.

Macro and microscopic findings in developing brain of rat fetuses were observed after intraperitoneal injection with a single dose (30mg/kg) of 5-Fluorouracil (5-FU) in late phase of gestation. 5-FU induced more than 60.0% lethality with significant reduction (p<0.001) in weight and various dimensions of the developing brain. Macroscopic findings of the developing brain revealed microcephaly, regression or absence of the olfactory lobe and obliteration of the various fissures on the dorsal surface. Microscopic examination of the olfactory lobe of treated brain showed the obliteration of the olfactory ventricle, distortion of the cellular arrangement of various layers of the olfactory cortex with clumping of degenerated neurons and glial cells. Cerebral cortex of the treated brain revealed the distortion of normal cytoarchitecture of the various cortical layers. The neurons of the treated brain revealed the degeneration, deeply stained eccentric nucleus with loss of mitotic figures and pyknotic changes. Subcortical zone of the treated cerebrum showed the degenerative changes in the fibrous structure along with paucity of the glial cells. The hippocampus of the treated brain revealed the loss of normal cytoarchitecture and shrinkage of all the layers. Neuroembyopathic effect of 5-FU is severe, when given in late phase of pregnancy, so it is advisable that the drug should be avoid during the late period of pregnancy.

Animals↗
PubMed1991

gamma-Aminobutyric acidA receptor heterogeneity in rat central nervous system: studies with clonazepam and other benzodiazepine ligands.

The properties of [3H]clonazepam, [3H]diazepam and [3H]zolpidem (N,N,6[trimethyl-2-(4-methyl-phenyl)imidazo[1,2-a]pyridine-3-acetamide hemitratrate) binding to synaptic membranes of cerebellum, cortex, olfactory bulb, striatum and spinal cord of rat were compared to the binding properties of [3H]flunitrazepam, [3H]flumazenil and [3H]midazolam. In the cerebellar, cortical and olfactory bulb membranes, the density of high-affinity binding sites of all these tritiated benzodiazepine (BZ) ligands is almost identical. In contrast, in the striatum, the density of [3H]clonazepam and [3H]zolpidem binding sites is approximately 60 and 30%, respectively, of the density of [3H]diazepam, [3H]flunitrazepam or [3H]flumazenil sites. In spinal cord membranes, the number of high-affinity binding sites of [3H]clonazepam and [3H]zolpidem is less than 20% of the number of binding sites for [3H]diazepam, [3H]flunitrazepam, [3H]flumazenil and [3H]midazolam. Moreover, the displacement of [3H]flunitrazepam from spinal cord membranes by clonazepam and zolpidem was characterized by high IC50 values and Hill slopes significantly less than 1. Because [3H]BZ ligand binding in the spinal cord is enhanced by gamma-aminobutyric acid (GABA), these data suggest that different regions of the rat central nervous system may contain different GABA-BZ receptor subtypes. The different pharmacological properties of clonazepam, diazepam and zolpidem (i.e., regarding their ability to enhance bicuculline seizure threshold, to decrease locomotor activity, to induce ataxia or to elicit anticonflict action) further support the concept that in the rat central nervous system preferential occupancy of heterogeneous GABAA receptors by these drugs can be related to their effects on behavior.

Animals↗
PubMed1986

Adenosine-containing neurons in the brain localized by immunocytochemistry.

Specific sensitive rabbit antisera directed against the adenosine derivative laevulinic acid (O2',3'-adenosine acetal), which are capable of detecting as little as 1 pmol of adenosine by radioimmunoassay and which require more than 1000- to 40,000-fold greater concentrations of adenine nucleotides to displace adenosine binding to antisera, have been developed. These antisera were employed to localize adenosine immunoreactivity throughout the rat CNS using the peroxidase-antiperoxidase (PAP) complex and avidin-biotin-peroxidase complex (ABC) immunocytochemical techniques. Intense staining for adenosine immunoreactivity was localized to the cytoplasm of perikarya and fibers in neuronal cell groups of discrete rat brain regions. Areas containing highest levels of immunoreactivity included the pyramidal cells of the hippocampus, the granule cells of the dentate gyrus, subnuclei of the thalamus, amygdala, and hypothalamus, the primary olfactory cortex, and many motor and sensory nuclei of the brain stem and spinal cord. High levels also occurred in certain layers of the cerebral cortex, the caudate-putamen, the septal nuclei, and the Purkinje cell layer of the cerebellum. Varying the extent of tissue hypoxia altered only the levels of endogenous immunoreactive adenosine without changing the pattern of distribution of the immunoreactivity. Staining was abolished by immunoabsorption and by pretreatment of tissue sections with adenosine deaminase. The localization of adenosine to discrete neuronal groups in the brain supports the possibility of a neurotransmitter or neuromodulatory role for adenosine.

Adenosine↗
PubMed1989

Regional changes in brain 2-14C-deoxyglucose uptake induced by convulsant and non-convulsant doses of lindane.

Lindane-induced dose- and time-related changes in regional 2-14C-deoxyglucose (2-DG) uptake were examined in 59 discrete rat brain structures using the 2-DG autoradiographic technique. At different times (0.5-144 hr) after administration of a seizure-inducing single dose of lindane (60 mg/kg), 2-DG uptake was significantly increased in 18 cortical and subcortical regions mainly related to the limbic system (e.g., Ammon's horn, dentate gyrus, septal nuclei, nucleus accumbens, olfactory cortex) and extrapyramidal and sensory-motor areas (e.g., cerebellar cortex, red nucleus, medial vestibular nucleus). There was also a significant increase in superior colliculus layer II. In addition, significant decreases occurred in a group of 6 regions (e.g., auditory and motor cortices). Non-convulsing animals treated with the same dose of lindane showed a regional pattern of 2-DG uptake less modified than the convulsant group. A non-convulsant single dose of lindane (30 mg/kg) also modified significantly the 2-DG uptake (0.5-24 hr) in some brain areas. Although the various single doses of lindane tested produced different altered patterns of brain 2-DG uptake, some structures showed a similar trend in their modification (e.g., superior colliculi and accumbens, raphe and red nuclei). Repeated non-convulsant doses of lindane produced defined and long-lasting significant elevations of 2-DG uptake in some subcortical structures (e.g., dorsal cochlear nucleus, dentate gyrus). Considering the treated groups all together, 2-DG uptake increased significantly in 26 of the 59 regions examined but only decreased significantly in 9 of them during the course of lindane effects. This fact can be related to the stimulant action described for this neurotoxic agent. The observed pattern provides a descriptive approach to the functional alterations occurring in vivo during the course of lindane intoxication. These results may be linked to the proposed mechanism of lindane neurotoxicity postulating an initial action on the GABAA receptor-chloride channel sites.

Animals↗
PubMed1989

Widespread expression of amyloid beta-protein precursor gene in rat brain.

The neuritic plaque is a characteristic finding in Alzheimer's disease. A major component of the plaque core is a 4.2 kd polypeptide, amyloid beta-protein (ABP), which is derived from the C-terminus of a larger precursor protein (ABPP). The authors have studied the transcription of ABPP mRNA in the adult rat brain by Northern analysis and in situ hybridization, and report that the ABPP gene gives rise to essentially the same multitranscript family of mRNAs as in the human, and that differential transcription patterns exist between brain and kidney. Morphologically, ABPP mRNA is expressed ubiquitously in neurons of the fore and hindbrain. ABPP transcripts also are present less frequently in occasional glial cells and at moderate to low frequency in nonneural cell types, namely, the choroid plexus epithelium, ependymal cells, and leptomeningeal membranes. Neuronal transcripts are most abundant in cerebral cortical layers II and V, the pyramidal cell layer of the hippocampus, the olfactory cortex, nucleus basis pontis, cranial nerve nuclei, and, significantly, in Purkinje cells and cerebellar granule cells. Because the cerebellum is relatively uninvolved in Alzheimer's disease, these findings suggest that high intraneuronal expression of ABPP may be a necessary but not sufficient requirement for plaque formation.

Alzheimer Disease↗
PubMed1986

Convulsant action of naloxone in the rat amygdala.

Increasing doses of naloxone hydrochloride (100-1000 nmol) were micro-injected unilaterally into the rat amygdala and the behavioral, neuropathological and electrographic responses were studied. Microinjections of low doses of naloxone (100-250 nmol) produced staring, gustatory automatisms and wet shakes whereas higher doses additionally resulted in motor limbic seizures and status epilepticus. The electroencephalogram showed a sequence of alterations characterised by high voltage fast activity, spiking, bursts of polyspiking, electrographic seizures and postictal depression which first appeared in the amygdala and rapidly spread to hippocampal and cortical areas. The neuropathological analysis of frontal forebrain sections by means of light microscopy revealed seizure-related brain damage in amygdala, olfactory cortex, thalamus, hippocampal formation, substantia nigra and neocortex. Diazepam, 10 mg/kg i.p., when given prior to the microinjection of naloxone into the amygdala, abolished the epileptogenic and neurotoxic effects of the drug. The results suggest that naloxone, when microinjected into rat amygdala elicits electrographic and motor limbic seizures followed by seizure-related brain damage.

Amygdala↗
PubMed1986

The threshold for limbic seizures in rats is decreased by intranigral morphine.

Microinjection of morphine hydrochloride into the substantia nigra pars reticulata, bilaterally, converts non-convulsant dose of pilocarpine hydrochloride, 100 mg/kg, into a convulsant one. The ED50 of morphine for the generation of seizures after pilocarpine, 100 mg/kg, is 3.8 nmol (2.5-5.8). Electrographic and behavioral monitoring both show a pattern of convulsant activity similar to those produced by pilocarpine in doses exceeding 350 mg/kg. Morphological analysis of frontal forebrain sections reveals epilepsy-related damage to the hippocampus, thalamus, olfactory cortex, substantia nigra, neocortex and amygdala. The proconvulsant action of morphine in the substantia nigra is reversed by co-administration of naloxone hydrochloride. The results show that the threshold for limbic seizures may be modulated by opiates in the substantia nigra.

Animals↗
PubMed1988

Physostigmine enhances blood flow-metabolism ratio in neocortex.

Inhibition of central nervous system cholinesterase with a single pulse of physostigmine induces a pronounced increase of blood flow in the neocortex, cingulate gyrus, claustrum, and amygdala. This phenomenon is not accompanied by an increase in energy metabolism and may help explain the effect of this drug on memory in normal humans and patients with Alzheimer's disease, as well as other conditions. In contrast, a parallel increase of blood flow and metabolism was observed in the superior colliculus, a component of the visual pathways. Prolonged administration of physostigmine lead to persistent vasodilatation in the neocortex, a lessening of this effect in cingulate gyrus, claustrum and amygdala, and an increase in primary olfactory cortex and hippocampus when compared with single pulse administration. Effects of physostigmine on glucose utilization remained essentially the same as with pulse administration.

Animals↗
PubMed1988

[Development of short-term habituation in surviving brain slices].

Effects of repeated stimulation with different frequencies (1, 5, 10, 100/sec) of the lateral olfactory tract on the field potentials (FPs) were investigated in the rat olfactory cortex slices. An increase in the frequency of stimulation produced a decline of the FPs. Spontaneous recovery of the FP amplitudes occurred within 5-10 sec following the termination of the stimulation. Polysynaptic FPs revealed a more obvious habituation than monosynaptic potentials. Depression of the inhibitory processes (the population IPSP) was also rapid and profound. The data obtained suggest the habituation phenomenon and are discussed in terms of learning processes.

Animals↗
PubMedDate not supplied

The seizures induced by pilocarpine: behavioral, electroencephalographic and neuropathological studies in rodents.

Seizures produced by systemic administration of pilocarpine hydrochloride, a cholinergic muscarinic agonist, in rodents are proposed as a useful animal model of epilepsy. Pilocarpine-induced seizures in rats and mice are characterized by sequential development of behavioral and electrographic signs, which are followed by widespread damage to the forebrain (hippocampus, amygdala, thalamus, olfactory cortex, neocortex and substantia nigra). Spontaneous seizures may be observed in the long-term period following the administration of convulsant doses of pilocarpine. In experiments designed to examine neuronal networks engaged in the generation and spread of pilocarpine-induced convulsions, a marked role for the basal ganglia is demonstrated. The caudate-putamen, the substantia nigra and the entopeduncular nucleus were found to govern the propagation of seizures produced by pilocarpine. The antiepileptic potential of drugs (diazepam, clonazepam, phenobarbital, valproic acid and trimethadione) against pilocarpine-induced convulsions correlates with their depressant action on the spontaneous activity of non-dopaminergic cells in the substantia nigra. Developmental studies show age-dependent differences in the convulsant response of rats to pilocarpine and status epilepticus are first noted in 2-3 week-old rats, but there is no clear-cut correlation between seizures and evolution of brain damage at this age. The adult pattern of the damage to forebrain is seen after a delay of 1-2 weeks relative to the development of seizures and status epilepticus. The research on the pilocarpine model of convulsions and other cholinergically mediated seizure syndromes may be of value for designing new therapeutic approaches to epilepsy in.

Animals↗
PubMed1988

Effect of pre- and postnatal alcohol consumption on GABA levels of various brain regions in the rat offspring.

The effect of maternal alcohol consumption during pregnancy and lactation on gamma-aminobutyric acid (GABA) levels in different rat brain regions of 3-week-old pups was investigated. There was a significant decrease in the thalamus, pons, cerebellum and hippocampus, no change in posterior colliculus, occipital cortex, temporal cortex, hypothalamus, septum or striatum and a significant increase in frontal cortex, olfactory bulbs, anterior colliculus and amygdala. These modifications could be a consequence of alterations in membrane permeability and may be related to the behavioural disorders associated with the fetal-alcohol syndrome.

Animals↗
PubMed1981

Only certain anticonvulsants protect against kainate neurotoxicity.

Kainic acid (KA), a heterocyclic structural analog of the putative excitatory neurotransmitter, glutamate (Glu), powerfully mimics many of the neuroexcitatory and neurotoxic properties of Glu. KA differs from Glu and its straight chain "excitotoxic" analogs, however, in inducing a limbic seizure-brain damage syndrome when administered subcutaneously (12 mg/kg) to adult rats. This syndrome consists of sustained seizures, resembling amygdaloid kindled seizures, and acute destruction of neural elements in limbic brain regions (amygdala, olfactory cortex, hippocampus, lateral septum and several thalamic nuclei). Early changes consist of massive edematous swelling of glia and neuronal dendrites and either swelling or dark cell changes in neuronal somata, with subsequent necrosis of many of the neurons involved. Elsewhere we demonstrated that pretreatment with morphine markedly enhances both the convulsant and brain damaging actions of KA. Here we report that pretreatment with 2 anticonvulsants (diazepam or phenobarbital) markedly reduces both athe seizure and brain damaging actions of KA, whereas, two other anticonvulsants (phenytoin or valproic acid) fail to suppress either phenomenon. Our findings suggest that a seizure mechanism underlies much of the limbic brain damage induced by systemic KA and that the toxic mechanism may have two mutually reinforcing components--a glutamergic excitatory component and a GABAergic disinhibitory component.

Animals↗
PubMed1982

Behaviour-dependent changes of visually evoked potentials and their correlation to the respiration rate in freely moving rats.

The variability of visually evoked potentials (VEP) during spontaneous changes of behavioural activity was investigated in freely moving rats with electrodes in the visual and frontal cortex, olfactory bulb and other brain structures. Averaged VEP were recorded and compared during periods of characteristic behaviour types like drowsiness, relaxed wakefulness, attentiveness, grooming and exploratory behaviour. These behavioural patterns, which are clearly distinguishable by observation, were characterized by a certain degree of visually evoked afterdischarges, recorded movements, EEG-patterns and mean respiration rate. The evaluation of early components of the VEP from single recorded samples and of the correspondent momentary respiration rate (respiration intervals) revealed strongly negative correlations. In general, the increasing behavioural activity is characterized by a decrease in the amplitudes of VEP-components, inversely correlated to the log of momentary respiration rate. During drowsiness and enhanced attentiveness, certain components are increased. During strong movements and distraction of attention (e.g. intensive scratching and licking) the VEP-components were decreased stronger. The negative complex around 62 ms increased during certain forms of behavioural activation and locomotion. The VEP-component N31, the respiration rate, and the quotient N31: N61 were found suitable parameters to characterize certain types of behaviour in comparison to relaxed wakefulness.

Animals↗
PubMed1995

Effects of acute and delayed effects of prior chronic cocaine administration on regional rates of cerebral protein synthesis in rats.

Single or repeated treatments with cocaine (15 mg/kg, i.p.) in rats modify rates of local cerebral protein synthesis (ICPSleu) measured with the [1-14C]leucine method. A single dose of cocaine to naive rats reduced ICPSleu by about 10% throughout the brain; the most statistically significant reduction was in the nucleus accumbens, shell portion (P = .0003). A comparable dose of cocaine administered acutely after 1 wk of daily cocaine injections had no effects on ICPSleu. Delayed effects of prior chronic cocaine treatment were studied in experiments in which one rat of each pair received injections with saline for 8 days and the other cocaine, and on the 15th day ICPSleu was measured. In these experiments delayed effects of the chronic cocaine treatment were observed; in the cocaine-treated rats ICPSleu was significantly increased in selective brain regions, i.e., prefrontal and primary olfactory cortex (P < .006). These results suggest that acute effects of a single dose of cocaine and residual effects of chronic cocaine treatment on ICPSleu are distinctly different and occur in different regions of the brain.

Animals↗
PubMed1993

Molecular cloning and expression of a 5-hydroxytryptamine7 serotonin receptor subtype.

We have utilized the polymerase chain reaction technique to selectively amplify a G protein-coupled receptor cDNA from rat kidney proximal convoluted tubule mRNA, which exhibits high homology with previously cloned serotonin receptors. Sequencing of a full-length clone isolated from a rat hippocampal cDNA library revealed an open reading frame of 1,212 base pairs encoding a 404-residue protein with seven hydrophobic regions predicted to represent transmembrane-spanning domains. Within the transmembrane regions, this receptor was found to be 44-50% identical with various members of the 5-HT1, 5-HT5, and 5-HT6 subfamilies with lower (37-40%) homology to the 5-HT2-like receptors. Northern blots revealed a approximately 3.6-kilobase transcript localized in various brain regions with the following rank order of abundance: hypothalamus > hippocampus = mesencephalon > cerebral cortex = olfactory bulb > olfactory tubercle. Expression of this clone in COS-7 cells resulted in the appearance of high affinity, saturable binding of [3H]lysergic acid diethylamide ([3H]LSD; KD = 5 nM) and [3H]serotonin ([3H]5-HT; KD = 1 nM). Among endogenous biogenic amines, only 5-HT completely inhibited radioligand binding. The inhibition of radioligand binding by other serotonergic agents revealed a pharmacological profile that does not correlate with any previously described serotonin receptor subtype. In addition, this receptor exhibits high affinity for a number of tricyclic antipsychotic and antidepressant drugs including clozapine, loxapine, and amitriptyline. In HEK-293 cells stably transfected with this receptor, serotonin elicits a potent stimulation of adenylylcyclase activity. The distinct structural and pharmacological properties of this receptor suggests that it represents a completely novel serotonin receptor subtype, which we propose to designate 5-HT7. Based on its pharmacology and its localization to limbic and cortical regions of the brain, it is likely that this receptor may play a role in several neuropsychiatric disorders that involve serotonergic systems.

Amino Acid Sequence↗
PubMed1995

Enhanced expression of peripheral benzodiazepine receptors in trimethyltin-exposed rat brain: a biomarker of neurotoxicity.

We have used the binding of the selective, high affinity, isoquinoline carboxamide, [3H]-PK11195, to measure the levels of Peripheral Benzodiazpine Receptors (PBR) in the brain of rats exposed to the well characterized neurotoxicant trimethyltin (TMT). The results demonstrate that autoradiograms of saggital sections of rats injected with a 8 mg/kg TMT dose, express a high level of [3H]-PK11195 binding in brain regions known to be damaged by TMT. The highest level of [3H]-PK11195 binding in the TMT-exposed rats occurred in the CA3/CA4 subfield of the hippocampus, followed by the primary olfactory cortex, the posteriomedial cortical amygdaloid nucleus, subiculum, and entorhinal cortex. These findings are consistent with the neuropathology of TMT in rats. The increase in [3H]-PK11195 binding in the brain of TMT-exposed rats was significant at 7 days after injection and remained elevated up to 42 days after exposure, the last time point measured in the study. This pattern is very similar to that observed for levels of the astrocyte intermediate filament protein, GFAP. The enhanced binding of [3H]-PK11195 in TMT-exposed rats was the result of a significant increase (p < 0.005) in the number of PBR with no change in affinity. The Bmax for [3H]-PK11195 binding in hippocampi from TMT-treated rats at 4 weeks post-injection was 606 +/- 25 (n = 4) fmoles/mg protein and 329 +/- 41 (n = 4) fmoles/mg protein for control. These findings suggest that the quantitative assessment of [3H]-PK11195 binding to PBR in the brain could represent a potential biomarker for assessing chemical-induced neurotoxicity. Since this ligand has been labeled with single photon (123I) or positron emitting (11C, 18F) radioisotopes, it can potentially be used with non-invasive imaging techniques such as Single Photon Emission Tomography (SPECT) or Positron Emission Tomography (PET) for human studies.

Animals↗
PubMed1996

Amino acid distribution in immature rat brain.

We compared the levels of amino acids in the free pool in 6 regions (cerebral cortex, olfactory bulb, substantia nigra, globus pallidus, caudate nucleus, and spinal cord) in the newborn rat brain. The amino acid distribution was heterogeneous, with the area of highest concentration containing 2-3 fold as much as the lowest area. These differences were considerably less than those previously found for adult brain. Although some areas often contained high levels of amino acids, and others mostly low levels, the distribution of the various amino acids was highly variable. This heterogeneity of distribution in the newborn brain was different from that in the adult brain. We conclude that there is significant heterogeneity of amino acid distribution, that it is different for each amino acid, and that it undergoes major changes during development.

Aging↗
PubMed1998

The "neostriatum" develops as part of the lateral pallium in birds.

Telencephalic organization in birds is so unusual that many homologies between avian and mammalian telencephalic areas remain controversial. Particularly contested is the avian "neostriatum," which has historically been homologized to either mammalian striatum, lateral neocortex, or endopiriform claustrum. Because homologies between these adult structures have been so difficult to resolve, we have begun to examine how telencephalic development diverges between birds and other vertebrates. To this end, biotinylated dextran was injected into the lateral telencephalon of chick embryos at 3 d of incubation, and the distribution of labeled cells was examined up to 14 d later. The data show that a definite boundary to cellular migration develops just ventral to the neostriatum between 5 and 8 d of incubation. Labeled polyclones within the neostriatum stretch from the ventricular zone to the brain surface and exhibit an increasingly rostrocaudal orientation as development proceeds. Individual polyclones contribute cells to several of the distinct auditory, visual, somatosensory, and olfactory regions within the neostriatum. A comparative analysis suggests that the avian neostriatum develops from a precursor region that in other vertebrates gives rise to olfactory cortex and, when present, to other components of the piriform lobe, such as the endopiriform claustrum and basolateral amygdala. Conclusions about lateral pallial homologies between birds and mammals remain uncertain, however, primarily because so little is known about the development of the lateral pallium in mammals. This lacuna might be filled by applying to mammals the novel fate-mapping method described in the present paper.

Animals↗