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PubMed1997

Ischemic and excitotoxic damage to brain slices from normal and microencephalic rats.

Brain slices (olfactory cortex, fronto-parietal cortex and hippocampus) taken from normal or microencephalic rats, obtained by gestational administration of the DNA-alkylating agent methylazoxymethanol acetate (MAM), were subjected to in vitro simulated ischemia or exposed to glutamate (5 mM) or kainate (1 mM). All these neurotoxic insults resulted in decreased viability of the slices, as quantitatively assessed by decrease in the rate of protein synthesis. Hippocampal slices subjected to ischemia and olfactory cortex slices exposed to glutamate or kainate were significantly less sensitive to the neurotoxic insult in microencephalic rats than in controls. The increased efflux of neurotransmitter amino acids (glutamate, aspartate and GABA) in the medium from slices subjected to ischemia or exposed to kainate, showed no significant differences among microencephalic and control rats. The present results suggest that the decreased excitotoxic sensitivity of microencephalic rats is, at least in part, related to intrinsic structural and/or functional alterations of some brain regions which undergo decrease in size as a consequence of the gestational treatment.

Animals↗

PubMed1978

Physiological roles of adenosine derivatives which are released during neurotransmission in mammalian brain.

1. Experiments using synaptosome beds suggested that ATP was released from presynaptic sites and degraded to adenosine in the synaptic cleft and that the resulting adenosine was taken up again into nerve endings where it was re-phosphorylated to ATP. 2. Adenosine derivatives in the synaptic cleft inhibited the postsynaptic potentials in olfactory cortex slices in vitro, presumably by the inhibition of Ca2+ influx into nerve endings which resulted in the reduction of transmitter release. 3. The adenosine derivatives also increased the level of cyclic AMP in the slices under the same conditions as above. 4. Although the nature of the "adenosine receptors" for both functions was remarkably similar, the increase of cyclic AMP did not mediate the inhibitory action, but the presynaptic increase of cyclic AMP induced by adenosine derivatives might mediate the facilitation observed in the olfactory cortex. 5. Possible physiological roles of extracellular adenosine derivatives in mammalian brain were classified, at different sites of action around the synapses, with different time courses and modes of action, directly or via the increase of intracellular cyclic AMP.

Adenine Nucleotides↗

PubMedDate not supplied

[The role of endogenous peptides in the development of long-term posttetanic potentiation].

Using the model of long-term posttetanic potentiation (LTP) in slices of the olfactory cortex of rat brain, we have tested a hypothesis according to which activation of nerve cells results in a release of neuromodulatory factors into extracellular space; these factors, diffusing over significant distances, are capable of synchronously modifying the initial reactivity of neuronal populations. Using the technique of bioassay, i.e., transfer of perfusate from the tetanized donor slice to the recipient slice, in combination with pharmacological and neurochemical techniques, we found that in response to excitation, the cells of olfactory cortex slices secrete peptides. This observation confirms the above hypothesis. The spectrum of released peptides changes depending on the degree of cell excitation and, in addition, is frequency-dependent. It has been demonstrated that the key target of these peptides are N-methyl-D-aspartate and glutamate receptors. We propose that two peptide pools are involved in the initial and late phases of LTP. The possible significance of peptide cell regulation in mechanisms of neuronal plasticity is discussed.

Animals↗

PubMed1987

Cellular mechanisms of potassium homeostasis in the mammalian nervous system.

Double-barrelled ion-sensitive microelectrodes were used to measure changes in the intracellular activities of K+, Na+, and Cl- (aKi, aNai, aCli) in neurones of rat sympathetic ganglia and in glial cells of slices from guinea-pig olfactory cortex. In sympathetic neurones, carbachol and gamma-aminobutyric acid (GABA) produced a reversible decrease of aKi. The decrease of aKi during carbachol was accompanied by a rise of aNai, whereas in the presence of GABA decreases of aKi and aCli were seen. The reuptake of K+ released during the action of carbachol was completely blocked by ouabain, whereas furosemide inhibited the aKi recovery after the action of GABA. In glial cells, in contrast to the observations in the sympathetic neurones, aKi and aCli increased, whereas aNai decreased when neuronal activity was enhanced by repetitive stimulation of the lateral olfactory tract. It was found that barium ions and ouabain strongly reduced the activity-related rise of intraglial aKi in slices of guinea-pig olfactory cortex. These data show that mammalian neurones as well as glial cells possess several K+ uptake mechanisms that contribute to potassium homeostasis. Ouabain, furosemide, and Ba2+ are useful pharmacological tools to separate these mechanisms.

Animals↗

PubMed1982

Electrophysiological analysis of the presynaptic action of beta-bungarotoxin in the central nervous system.

In view of previously reported actions of beta-bungarotoxin (beta-BuTX) on central brain synaptosomes, the effects on this toxin on the electrical activity of two brain slice preparations have been examined in vitro. beta-BuTX initially suppresses the synaptic component of the field responses to electrical stimulation in olfactory cortex and hippocampal slices. Intracellular recordings demonstrate that this synaptic depression occurs without detectable reduction in the sensitivity of the postsynaptic neuron to putative neurotransmitters. Following longer exposure to the toxin, reduced neuronal excitability is observed both pre- and post-synaptically. Elimination of the phospholipase A2 activity of beta-BuTX, by chemical modification or removing the Ca2+ necessary for enzymic activity, greatly reduces but does not totally eradicate the toxin's ability to block neurotransmission in the olfactory cortex. In the absence of enzymic activity beta-BuTX has no obvious effect on axonal conduction. Pure phospholipases A2, such as that from Naja melanoleuca mimic the transmission-blocking action of beta-BuTX, but with lower potency and without the effects on fibre excitability. Collectively, these results are taken as evidence that beta-BuTX initially suppresses transmitter release, a notion supported by the observed loss of spontaneous synaptic activity in hippocampal cells. Prolonged exposure to the toxin induces apparently less specific effects on neuronal excitability which are dependent on phospholipase A2 activity and are discussed with reference to the selective action of beta-BuTX on hippocampal fibre systems which possess release sites.

Animals↗

PubMed1997

The 5-HT3 receptor is present in different subpopulations of GABAergic neurons in the rat telencephalon.

The type 3 serotonin receptor (5-HT3R) is a ligand-gated ion channel whose presence in the CNS has been established by radioligand binding, in situ hybridization, and immunohistochemical analysis. To analyze further the role of the 5-HT3R in the CNS, we used in situ hybridization and immunocytochemistry to determine that 5-HT3R-expressing neurons are mainly GABA-containing cells in the rat telencephalon. We determined that 5-HT3R/GABA-containing neurons do not exhibit somatostatin immunoreactivity but often contain cholecystokinin (CCK) immunoreactivity. 5-HT3R-expressing cells with CCK immunoreactivity were observed in the neocortex, olfactory cortex, hippocampus, and amygdala. The 5-HT3R/CCK interneurons represent between 35 and 66% of the total population of CCK-containing cells in the neocortex. Further characterization of the 5-HT3R/GABAergic neurons was based on their calcium-binding protein immunoreactivity and showed that these neurons lack parvalbumin (PV) and represent a subpopulation of calbindin (CB)-containing interneurons that were preferentially present in the CA1-CA3 subfield of the hippocampus. Although some 5-HT3R/GABAergic neurons with calretinin (CR) were found in the neocortex, olfactory cortex, hippocampus, and amygdala, these neurons were more often present in the agranular insular and piriform cortices. We conclude that the neuronal expression of the 5-HT3R is selective within the GABA neuron population in the rat telencephalon. These 5-HT3R-expressing interneurons might contain CCK, CB, and CR. We suggest that serotonin through the 5-HT3R may regulate GABA and CCK neurotransmission in the telencephalon.

Animals↗

PubMed1998

Cholinergic neurons and terminal fields revealed by immunohistochemistry for the vesicular acetylcholine transporter. I. Central nervous system.

Antibodies directed against the C-terminus of the rat vesicular acetylcholine transporter mark expression of this specifically cholinergic protein in perinuclear regions of the soma and on secretory vesicles concentrated within cholinergic nerve terminals. In the central nervous system, the vesicular acetylcholine transporter terminal fields of the major putative cholinergic pathways in cortex, hippocampus, thalamus, amygdala, olfactory cortex and interpeduncular nucleus were examined and characterized. The existence of an intrinsic cholinergic innervation of cerebral cortex was confirmed by both in situ hybridization histochemistry and immunohistochemistry for the rat vesicular acetylcholine transporter and choline acetyltransferase. Cholinergic interneurons of the olfactory tubercle and Islands of Calleja, and the major intrinsic cholinergic innervation of striatum were fully characterized at the light microscopic level with vesicular acetylcholine transporter immunohistochemistry. Cholinergic staining was much more extensive for the vesicular acetylcholine transporter than for choline acetyltransferase in all these regions, due to visualization of cholinergic nerve terminals not easily seen with immunohistochemistry for choline acetyltransferase in paraffin-embedded sections. Cholinergic innervation of the median eminence of the hypothalamus, previously observed with vesicular acetylcholine transporter immunohistochemistry, was confirmed by the presence of vesicular acetylcholine transporter immunoreactivity in extracts of median eminence by western blotting. Cholinergic projections to cerebellum, pineal gland, and to the substantia nigra were documented by vesicular acetylcholine transporter-positive punctate staining in these structures. Additional novel localizations of putative cholinergic terminals to the subependymal zone surrounding the lateral ventricles, and putative cholinergic cell bodies in the sensory mesencephalic trigeminal nucleus, a primary sensory afferent ganglion located in the brainstem, are documented here. The cholinergic phenotype of neurons of the sensory mesencephalic trigeminal nucleus was confirmed by choline acetyltransferase immunohistochemistry. A feature of cholinergic neurons of the central nervous system revealed clearly with vesicular acetylcholine transporter immunohistochemistry in paraffin-embedded sections is the termination of cholinergic neurons on cholinergic cell bodies. These are most prominent on motor neurons of the spinal cord, less prominent but present in some brainstem motor nuclei, and apparently absent from projection neurons of the telencephalon and brainstem, as well as from the preganglionic vesicular acetylcholine transporter-positive sympathetic and parasympathetic neurons visualized in the intermediolateral and intermediomedial columns of the spinal cord. In addition to the large puncta decorating motor neuronal perikarya and dendrites in the ventral horn, vesicular acetylcholine transporter-positive terminal fields are distributed in lamina X surrounding the central canal, where additional small vesicular acetylcholine transporter-positive cell bodies are located, and in the superficial layers of the dorsal horn. Components of the central cholinergic nervous system whose existence has been controversial have been confirmed, and the existence of new components documented, with immunohistochemistry for the vesicular acetylcholine transporter. Quantitative visualization of terminal fields of known cholinergic systems by staining for vesicular acetylcholine transporter will expand the possibilities for documenting changes in synaptic patency accompanying physiological and pathophysiological changes in these systems.

Acetylcholine↗

PubMed1970

Effects of nicotine and tobacco smoke on the electrical activity of the cerebral cortex and olfactory bulb.

1. Effects of nicotine, cigarette smoke and carbon monoxide have been compared in the cat encéphale isolé preparation, exhibiting a synchronized electrocorticogram (ECoG) and behavioural sleep.2. 2 ml samples of smoke, containing approximately 7 mug nicotine (approximately 2 mug nicotine/kg for a 3 kg cat), introduced into the lungs at 30 s intervals from a smoking simulator, caused desynchronization of the ECoG and behavioural arousal.3. Effects of smoke were matched in the same experiments by intravenous injections of nicotine, 2 mug/kg every 30 s.4. The use of specific nicotine antagonists, for example mecamylamine, and filters for removing nicotine, indicated the presence in smoke of other agents capable of exerting a pharmacological response.5. Cigarette smoke contains approximately 5.0% carbon monoxide. Introduced into the lungs of cats pretreated with mecamylamine (2 mg/kg), 2 ml samples of 5% carbon monoxide caused changes in the ECoG similar to those caused by smoke.6. Effects of nicotine or smoke were not modified by pretreatment with chlorpromazine (2.0-4.0 mg/kg). Atropine (0.3 mg/kg), however, prevented the cortical activation, but not the behavioural arousal.7. 2 ml samples of smoke applied to the nostrils caused the occurrence in the olfactory bulb of a discharge or burst of "induced" waves. This discharge was sometimes accompanied by a transient period of cortical activation.8. These studies demonstrate that in cats, nicotine is the principal pharmacological constituent of tobacco smoke as far as effects on the central nervous system are concerned, although other constituents of smoke may play a contributory role.

Animals↗

PubMed1983

Effects of lithium on electrical activity and potassium ion distribution in the vertebrate central nervous system.

Three different regions of the vertebrate central nervous system maintained in vitro (frog spinal cord, guinea pig olfactory cortex and hippocampus) have been used to investigate how Li+ influences membrane potential, membrane resistance, action potentials, synaptic potentials and the transmembrane K+-distribution of neurons and glial cells. In view of the therapeutic action of Li+ in manic-depressive disease, a special effort was made to determine the threshold concentration for the actions of Li+ on the parameters described above. It was observed that Li+ induced a membrane depolarization of both neurons and glial cells, a decrease of action potential amplitudes, a facilitation of monosynaptic excitatory postsynaptic potentials and a depression of polysynaptic reflexes. The membrane resistance of neurons was not altered. Li+ also induced an elevation of the free extracellular potassium concentration and a decrease of the free intracellular potassium concentration. Furthermore, in the presence of Li+ a slowing of the recovery of the membrane potential of neurons and glial cells, and of the extracellular potassium concentration after repetitive synaptic stimulation was observed. The threshold concentrations for the effects of Li+ were below 5 mmol/l in the frog spinal cord and below 2 mmol/l in the guinea pig olfactory cortex and hippocampus. The basic mechanism underlying the action of Li+ may be an interaction with the transport-function of the Na+/K+ pump.

Animals↗

PubMed1997

Metabotropic glutamate receptor subtypes mediating slow inward tail current (IADP) induction and inhibition of synaptic transmission in olfactory cortical neurones.

1. The pharmacological features of the pre- and postsynaptic metabotropic glutamate receptors (mGluRs) present in the guinea-pig olfactory cortex, were examined in brain slices in vitro by use of a conventional intracellular current clamp/voltage clamp recording technique. 2. Bath-application of trans-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD) (50 microM) produced a sustained membrane depolarization, increase in cell excitability and induction of a post-stimulus inward (after depolarizing) tail current (IADP) (measured under 'hybrid' voltage clamp) similar to those evoked by the muscarinic receptor agonist oxotremorine-M (OXO-M, 2 microM). 3. L-Glutamate (0.25 1 mM. in the presence of 20 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 100 microM-DL-amino-5-phosphono valeric acid (DL-APV)) or the broad spectrum mGluR agonists 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD, 10 microM), 1S,3S-ACPD (50 microM), ibotenate (Ibo; 25 microM. in the presence of 100 microM DL-APV), the selective mGluR I agonists (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG, 10 microM), (S)-3-hydroxyphenylglycine ((S)-3HPG, 50 microM), or quisqualate (10 microM, in the presence of 20 microM CNQX), but not the mGluR II agonist 2S,1'S,2'S-2-(2'-carboxycyclopropyl)-glycine (L-CCG1,1 microM) or mGluR III agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4, 1 mM), were all effective in producing membrane depolarization and inducing a post-stimulus IADP. Unexpectedly, the proposed mGluR II-selective agonist (2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)-glycine (DCG-IV, 10 microM, in the presence of 100 microM DL-APV) was also active. 4. The excitatory effects induced by 10 microM 1S,3R-ACPD were reversibly antagonized by the mGluR I/II antagonist (1)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG, 0.5 1 mM), as well as the selective mGluR I antagonists (S)-4-carboxyphenylglycine ((S)-4CPG) and (S)-4-carboxy-3-hydroxyphenyl glycine ((S)-4C3HPG) (both at 1 mM), but not the nonselective mGluR antagonist L(+)-2-amino-3-phosphonopropionic acid (L-AP3, 1 mM) or the selective mGluR III antagonist (S)-alpha-methyl-L-AP4 (MAP4, 1 mM). 5. The excitatory postsynaptic potentials (e.p.s.ps), induced by single focal stimulation of cortical excitatory fibre tracts, were markedly reduced by 1S,3R-ACPD or L-AP4 (both at 10 microM), and by the selective mGluR II agonists (mGluR 1 antagonists) (S)-4CPG or (S)-4C3HPG (both at 1 mM) but not (S)-3,5-DHPG or (S)-3HPG (both at 100 microM). 6. The inhibitory effects of 1S-3R-ACPD, but not L-AP4, were reversibly blocked by (+)-MCPG (1 mM), whereas those produced by L-AP4, but not 1S,3R-ACPD, were blocked by the selective mGluR III antagonist MAP4 (1 mM). 7. It is concluded that a group I mGluR is most likely involved in mediating excitatory postsynaptic effects, whereas two distinct mGluRs (e.g. group II and III) might serve as presynaptic inhibitory autoreceptors in the guinea-pig olfactory cortex.

Animals↗

PubMed2005

Dynamics of learning-induced cellular modifications in the cortex.

This aim of this review is to describe the dynamics of learning-induced cellular modifications in the rat piriform (olfactory) cortex after olfactory discrimination learning and to describe their functional significance to long-term memory consolidation. The first change to occur is in the intrinsic properties of the neurons. One day after learning, pyramidal neurons show enhanced neuronal excitability. This enhancement results from reduction in calcium-dependent conductance that mediates the post burst after-hyperpolarization. Such enhanced excitability lasts for 3 days and is followed by a series of synaptic modifications. Several forms of long-term enhancement in synaptic connections between layer II pyramidal neurons in the piriform cortex accompany olfactory learning. Enhanced synaptic release is indicated by reduced paired-pulse facilitation. Post-synaptic enhancement of synaptic transmission is indicated by reduced rise time of post-synaptic potentials and formation of new synaptic connections is indicated by increased spine density along dendrites of these neurons. Such modifications last for up to 5 days. Thus, olfactory discrimination rule learning is accompanied by a series of cellular modifications which occur and then disappear at different times. These modifications overlap partially, allowing the maintenance of the cortical system in a 'learning mode' in which memories for specific odors can be acquired rapidly and efficiently.

Animals↗

PubMed1982

Neocortical and basal telencephalic origins of the anterior commissure of the cat.

The neocortical and basal telencephalic origins of the anterior commissure of the cat have not been described in earlier studies of the great cerebral commissures. In this anatomical study, all cerebral commissures, except the anterior commissure, of twelve cats were first transected. Subsequent unilateral injections of large quantities of horseradish peroxidase throughout the right hemisphere revealed the entire origins of the three branches of the anterior commissure in the left hemisphere. Since the anterior commissure was the only interhemispheric fibre system remaining, only the cells, fibres and anterogradely-labelled terminals of the anterior commissure were labelled by horseradish peroxidase in the uninjected hemisphere. Approximately three-quarters of the neurons of the anterior commissure are in the neocortex, mostly in layers V and VI. These neocortical cells occupy an extensive field stretching from gyrus proreus to the posterior ectosylvian gyrus and from the rhinal sulcus to the suprasylvian sulcus. Other fibres of the anterior commissure, however, were found to have their cell bodies in regions not considered part of the neocortex, and these included the anterior olfactory nucleus, the pyriform cortex, olfactory tubercles, nucleus of the lateral olfactory tract, part of the amygdaloid nuclei, the periamygdaloid nucleus and the lateral entorhinal area. Finally, it was found that the fibres of the anterior commissure do not have an exclusive neocortical territory from which cells of other commissural fibres are excluded. Rather, there appears to be a substantial overlap between the field of origin of fibres of the anterior commissure and those of the largest cerebral commissure, the corpus callosum. The disposition of this field may help to explain why visual information fails to transfer between the hemispheres in cats whose corpus callosum has been cut, in contrast to the success of such transfer in primates.

Animals↗

PubMed1988

Entorhinal projections to the hippocampal CA1 region in the rat: an underestimated pathway.

The projections of the entorhinal cortex to CA1 in relation to the entorhinal-dentate projections were studied in the rat, using the anterograde transport of Phaseolus vulgaris leucoagglutinin. It was observed that the entorhinal cortex is heterogeneous with respect to the origin of these projections. Caudomedial portions of the entorhinal cortex mainly distribute fibers to the fascia dentata, whereas only a minor projection reaches CA1. Progressively more rostral and lateral parts of the entorhinal cortex project more strongly to CA1, at the expense of the number of fibers that terminate in the fascia dentata. The rostrolateral part of the entorhinal cortex, adjacent to the olfactory cortex and the amygdaloid complex, projects only to CA1.

Animals↗

PubMed1993

The localization of cholecystokinin mRNA in embryonic striatal tissue grafts: further evidence for the presence of non-striatal cells.

We have studied by in situ hybridization histochemistry the mRNA expression of preprocholecystokinin (CCK) in grafts of foetal striatal tissue neurones implanted into the ibotenic acid lesioned adult rat neostriatum. Animals were studied at 30 and 90 days after implantation. Using a 35S-labelled 'antisense' oligonucleotide (45-mer) probe complementary to the rat CCK cDNA we observed a dense hybridization signal for CCK mRNA in the striatal eminence in developing embryos and in all the striatal grafts examined; no CCK mRNA expressing cells were found in the normal neonatal or adult rat neostriatum. However, CCK mRNA was heavily expressed in other areas of the host brain including the somatosensory cortex, the claustrum, primary olfactory cortex and endopiriform cortex. The germinal cell layer of the striatal eminence is the source of origin for these non-striatal cell groups as well as for cells destined to form the neostriatum. The present results suggest that CCK mRNA expression provides an unambiguous marker for many of the non-striatal cells in 'striatal' grafts.

Animals↗

PubMed2003

Blockade of phencyclidine-induced cortical apoptosis and deficits in prepulse inhibition by M40403, a superoxide dismutase mimetic.

Repetitive administration of phencyclidine (PCP) in the perinatal period results in cortical apoptosis and a long-lasting deficit in sensorimotor gating. Because these changes are olanzapine-sensitive, we have suggested that the effects of perinatal PCP could be used to model certain aspects of schizophrenia. Studies of PCP and N-methyl-D-aspartate-induced cell death suggested that superoxide could play a role in the pathway leading to death after PCP administration. The purpose of the current study was to determine whether the in vivo administration of M40403, a superoxide dismutase mimetic, could prevent PCP-induced cortical apoptosis and/or deficits in prepulse inhibition. Perinatal rat pups were administered 10 mg/kg PCP on postnatal (PN) days 7, 9, and 11 with or without treatment with 10 mg/kg M40403. Pups were either killed on PN 12 for analysis of various apoptotic markers or they were assessed for prepulse inhibition on PN 24 to 26. Treatment with M40403 2 and 24 h after each PCP treatment prevented PCP-induced increases in two measures of apoptosis in the dorsolateral frontal cortex and in the olfactory cortex. PCP-induced proapoptotic changes in Bax and Bcl-X(L) were also prevented by M40403 treatment. This regimen did not prevent the deficit in prepulse inhibition caused by PCP treatment, but when the treatment regimen was extended through PN 23, M40403 completely prevented the PCP-induced deficit in prepulse inhibition. These data suggest that perinatal PCP treatment leads to long-lasting changes in the pathway(s), leading to cell death and behavioral deficits, and that the superoxide radical plays a critical role in the underlying mechanism.

Acoustic Stimulation↗

PubMed1987

Relation of olfactory bulb and cortex. II. Model for driving of cortex by bulb.

The major projection pathway of the olfactory bulb is by way of the lateral olfactory tract (LOT) to the olfactory cortex. Oscillatory bursts of extracellular potential appear during inspiration in both bulb and cortex. Based on anatomical and physiological considerations, a model was proposed, consisting of a bulbar transmitter, a conduction line representing axons in the LOT, and a cortical receiver. The model predicted the relation between phase and frequency of bulbar and cortical burst pairs, based on the expectation that the bulb drives the cortex. Experimental phase-frequency plots were computed from bursts of 9 bulbocortical electrode site pairs from each of 10 rabbits. For each site pair, the model predicted the expected range of the joint variation of phase and frequency, using the known distance between the bulbar and cortical sites. The model was highly successful (greater than 95% prediction accuracy) for one quarter of the total number of site pairs examined. The wide range of variation for the rest of the data suggested that higher order interactions are responsible for the phase relation between bulb and cortex. Convergence of input, independence of the cortical generator, cortical feedback to the bulb and synchronization by an outside source are all discussed as possible contributors to this variation.

Animals↗

PubMed1990

Systemic injection of kainic acid: gliosis in olfactory and limbic brain regions quantified with [3H]PK 11195 binding autoradiography.

Neurodegenerative diseases may result from excessive stimulation of excitatory amino acid receptors by endogenous ligands. Because neuronal degeneration is associated with glial proliferation and hypertrophy, the degenerative changes throughout rat brain following the systemic administration of kainic acid (12 mg/kg) were mapped with quantitative autoradiography of [3H]PK 11195. This radioligand binds to a mitochondrial benzodiazepine binding site (MBBS) on microglia and astrocytes. Analysis of eight horizontal and four coronal brain levels revealed up to 16-fold increases in [3H]PK 11195 binding from 1 to 5 weeks but not 1 day after kainate injection. Increases in [3H]PK 11195 binding were predominantly in ventral limbic brain regions and olfactory projections to neocortical areas, with the olfactory cortex greater than subiculum/CA1 greater than anterior olfactory nucleus, medial thalamic nucleus, and piriform cortex greater than cingulate cortex and rostral hippocampus greater than dentate gyrus, septum, and amygdala greater than entorhinal cortex and temporal cortex. Little or no enhancement of [3H]PK 11195 binding was observed in numerous regions including the caudate-putamen, substantia nigra, nucleus accumbens, olfactory tubercle, cerebellum, thalamic nuclei, choroid plexus, medulla, parietal or occipital cortex, or pons. A 2-fold greater extent of neurodegeneration was obtained in ventral portions of the olfactory bulb, entorhinal cortex, temporal cortex, and dentate gyrus compared with the dorsal portions of these structures. The pattern of increase in [3H]PK 11195 binding closely matched the patterns of neuronal degeneration reported following parenteral kainate injection. These findings strengthen the notion that quantitative autoradiography of [3H]PK 11195 is a valuable tool to quantify the extent of neuronal degeneration. Furthermore, the quantitative changes in [3H]PK 11195 binding in different limbic structures parallel their relative variation in neuropathology observed in Alzheimer's disease but not Huntington's chorea. These findings are in agreement with the idea that excessive stimulation of excitatory amino receptors may contribute to the etiology of Alzheimer's disease.

Animals↗

PubMed1984

The ventral pallidal projection to the mediodorsal thalamus: a study with fluorescent retrograde tracers and immunohistofluorescence.

We have examined rat basal forebrain projections to the mediodorsal thalamic nucleus (MD) by making injections of retrogradely transported fluorescent tracers into the MD. Additionally, in some animals, we also stained sections for glutamate decarboxylase (GAD) by the indirect fluorescent antibody technique. Our results demonstrate that the following basal forebrain areas project to the MD: lateral orbital cortex, agranular insular cortex superficial to claustrum, primary olfactory cortex, diagonal band nuclei, ventral pallidum, and amygdala. A large number of labeled cells are present in the olfactory tubercle, and these cells are almost without exception located in dense GAD-positive ventral pallidal areas rather than in striatal regions of the tubercle. This ventral pallidal projection to the MD strengthens the concept of a ventral striatal-pallidal system in parallel to the classic striatal-pallidal system which projects to the ventral thalamus. These results are also discussed in relationship to the olfactory system.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗