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PubMed1994

Corticonigral degeneration with neuronal achromasia presenting with primary progressive aphasia: ultrastructural and immunocytochemical studies.

We describe a clinico-pathological variant of a degenerative disorder involving Broca's, Wernicke's, and supplementary motor areas, which presented as primary progressive aphasia, dysarthria, bucco-facial apraxia, and hearing loss as initial symptoms, followed by organic personality changes. Postmortem examination revealed severe focal atrophy of the cerebral convolutions in the frontal operculum, superior frontal gyrus, and superior and transverse temporal gyri in addition to diffuse atrophy of the frontal and temporal lobes in both hemispheres. Microscopical examination revealed argyrophilic neuronal inclusions (ANIs) in the neuronal perikarya and presynaptic terminal throughout the central nervous system, as well as neuronal loss and swollen chromatolytic neurons in the affected cortices. Neocortical ANIs showed a positive immunoreaction with an anti-tau antibody but only a weak reaction with an anti-ubiquitin antibody immunohistochemically. Ultrastructurally, neocortical ANIs consisted of 15-nm thick smooth-surfaced tubules and tubules with constrictions at 120-150-nm intervals; thus they were different from the typical paired helical filaments of the 80-nm interval constrictions observed in the subiculum. ANIs were also found in the basal ganglia, brain stem nuclei, and cervical cord. Accordingly, ANIs appear distinct from neurofibrillary tangles (NFTs) of progressive supranuclear palsy, NFTs of Alzheimer-type dementia, and Pick bodies. The authors consider that this case fits the histopathological criteria of corticonigral degeneration with neuronal achromasia except for the unusual extension to the temporal lobes.

Aphasia↗
PubMed1994

The role of intracellular free calcium in motor neuron disease.

The intracellular calcium (Ca2+) concentrations of motoneurons can be altered by the influx of Ca2+ into the cell by the opening of voltage-dependent Ca2+ channels and ligand-gated channels linked to Ca2+ influx, especially by the N-methyl-D-aspartate (NMDA) type of excitatory amino acid receptor. Intracellular Ca2+ concentration is also affected by the release of Ca2+ buffered in mitochondria and endoplasmic reticulum. Evidence that motoneurons may be selectively vulnerable to Ca(2+)-induced cell death include the following observations: (i) the presence of excitatory amino acid receptors on the cell membranes of motoneurons, some of which would permit Ca2+ influx (e.g. NMDA receptors); (ii) the availability of the presynaptic terminal for antibody-mediated effects leading to changes in cell permeability and Ca2+ influx; and (iii) the limited amounts of intracellular Ca(2+)-binding proteins such as calbindin D28K and parvalbumin in motoneurons. Elevation of intracellular free Ca2+ may also be a common event in a number of independent mechanisms leading to motoneuron death in motor neuron disease.

Animals↗
PubMed1983

Effects of localized applications of L-glutamate on the population spike in the hippocampal slice preparation.

L-Glutamate applied exclusively to the CA3 cell body region of the rat hippocampal slice resulted in long-term potentiation (LTP) of the CA1 population spike evoked by Schaffer collateral stimulation. The same localized glutamate application to the CA1 area caused a prolonged depression of the response. These observations are consistent with the possibility that LTP is at least partly presynaptic and that the depression is due to an effect of glutamate on the postsynaptic elements and/or the presynaptic terminals.

Action Potentials↗
PubMed1984

Neuropeptide Y: stimulation of feeding and drinking by injection into the paraventricular nucleus.

Neuropeptide Y (NPY), a peptide contained within numerous presynaptic terminals in the hypothalamic paraventricular nucleus (PVN), was injected directly into the PVN of satiated, brain-cannulated rats, and food and water intake were measured 0.5, 1, 2 and 4 hrs postinjection. Neuropeptide Y (24 and 78 pmoles/0.3 microliter isotonic saline) caused a dose-dependent increase in food intake, as well as a small, dose-dependent increase in water intake. This effect on feeding occurred even when food was not presented until 4 hrs postinjection. To determine the behavioral specificity of this effect, the impact of PVN injection of NPY (78 pmoles) on various behaviors was observed. With food available, only feeding and drinking behavior were affected. No change in other behaviors, including grooming, rearing, sleeping, resting or different levels of activity, was observed. With food absent, NPY still elicited drinking, suggesting that this is a primary effect, rather than secondary to the feeding. In addition to drinking, NPY reliably increased activity while decreasing sleep and grooming. These results suggest an important role for hypothalamic NPY, or a structurally-related peptide, in the regulation of feeding and drinking behavior.

Animals↗
PubMed1984

Effects of the selective noradrenergic neurotoxin DSP4 on cerebellar Purkinje neuron electrophysiology.

The effect of the adrenergic neurotoxin DSP4 on cerebellar electrophysiology was studied in the rat. DSP4, administered parenterally, depleted cerebellar norepinephrine by 76%. The depressant response of cerebellar Purkinje neurons to phencyclidine, a drug which acts on adrenergic presynaptic terminals to release NE, was markedly reduced after DSP4 pretreatment. In contrast with 6OHDA, which increased firing rates of the Purkinje cells, DSP4 did not change the rate or pattern of Purkinje cell discharge. Taken together these results suggest that DSP4 may be a valuable tool for studying central adrenergic pathways, but that this drug has properties which differ from 6OHDA.

Amines↗
PubMed1989

Influence of a carrier transport process on in vivo release and metabolism of dopamine: dependence on extracellular Na+.

In vivo microdialysis was utilized to evaluate the role of extracellular Na+ in regulating dopamine (DA) neurotransmission in the caudate-putamen of halothane-anaesthetized rats. Reduction of the extracellular Na+ concentration by introduction of a perfusion media containing 50mM Na+ (with choline replacement) produced an excessive release of DA that could be effectively blocked by nomifensine and Lu 19-005, potent inhibitors of an amine transport carrier. These results substantiate reports of a carrier-mediated efflux of DA from presynaptic terminals. Pretreatment with amphetamine, considered both a DA uptake inhibitor and releaser, did not, however, influence the efflux of DA induced by the low extracellular Na+ environment. Although the release of DA from an apparent non-granular cytosolic pool was greatly enhanced by the low extracellular Na+ environment, 3,4-dihydrophenylacetic acid (DOPAC) levels, which supposedly reflect metabolism of non-vesicular DA, were minimally effected. In contrast, homovanillic acid (HVA) was sensitive to extracellular Na+ and not directly related to extracellular levels of either DA or DOPAC, suggesting the possibility of a Na+-sensitive (carrier-mediated?) process involved in the formation of HVA. Overall, the results of this paper cannot be completely reconciled with the traditional concept of intracellular organization of DA pools and suggests the possibility of various non-granular pools being differentially sensitive to efflux and metabolism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Differing actions of convulsant and nonconvulsant barbiturates: an electrophysiological study in the isolated spinal cord of the rat.

The effects of various pairs of convulsant and nonconvulsant barbiturates on mono- and polysynaptic activity were studied in the isolated spinal cord of the immature rat, using extracellular recording. The convulsant barbiturates, 5-ethyl-5-(3-methylbut-2'-enyl) barbituric acid (3M2B), 5-ethyl-5-(1,3-dimethylbut-1'-enyl) barbituric acid (1,3M1B) and (+)-5-(1,3-dimethylbutyl)-5-ethyl barbituric acid [(+) DMBB] all increased the monosynaptic reflex at concentrations between 5 and 50 microM with no change in polysynaptic activity. When the concentration was raised to between 100 and 300 microM, however, the convulsants all reduced the monosynaptic reflex, thus producing a biphasic dose-response relationship. The nonconvulsant barbiturates phenobarbital, 5-ethyl-5-(3-methylbut-1'-enyl) barbituric acid (3M1B), amylobarbital (3MB) and (-)-5-(1,3-dimethylbutyl)-5-ethyl barbituric acid [(-)DMBB] produced only a decrease in mono- and polysynaptic reflexes. At concentrations which enhanced the monosynaptic reflex, the responses of motoneurones to glycine and eledoisin-related peptide (an analogue of substance P) were reduced by (+)DMBB, while 1,3M1B and 3M2B had no significant effects upon any of the neurotransmitters tested. At concentrations which depressed the monosynaptic reflex, the convulsants all reduced the response to glycine whereas the nonconvulsant barbiturates all increased the response to GABA. With the exception of phenobarbital, both convulsant and nonconvulsant barbiturates produced a direct depolarisation of the presynaptic terminal membrane, with only the convulsants producing a depolarisation of the membrane of the motoneurone. Using another convulsant barbiturate, 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB), this direct depolarising action was found to be calcium-dependent.

Animals↗
PubMed1983

Pre- and post-synaptic structures in insect CNS: intramembranous features and sites of alpha-bungarotoxin binding.

The central neuropile of thoracic ganglia in the central nervous system (CNS) of the cockroach Periplaneta americana contains synapses with characteristic pre- and post-synaptic membrane specializations and associated structures. These include dense pre-synaptic T-bars surrounded by synaptic vesicles, together with post-synaptic densities of varying electron opacity. Exocytotic release of synaptic vesicles is observed only rarely near presynaptic densities, but coated pits are seen at variable distances from them, and may be involved in membrane retrieval. After freeze-fracture, paralinear arrays of intramembranous articles (IMPs) are detected on the P face of many presynaptic terminals, with associated dimples indicative of vesicular release. The E face of these membranes exhibits protuberances complementary to the P face dimples, as well as scattered larger IMPs. Post-synaptic membranes possess dense IMP aggregates on the P face, some of which may represent receptor molecules. Electrophysiological studies with biotinylated alpha-bungarotoxin reveal that biotinylation does not inhibit the pharmacological effectiveness of the toxin in blocking acetylcholine receptors on an identified motoneurone in the metathoracic ganglion. Preliminary thin section ultrastructural analysis of this tissue post-treated with avidin-HRP or avidin-ferritin indicates that alpha-bungarotoxin-binding sites are localized at certain synapses in these insect thoracic ganglia.

Animals↗
PubMed1991

Dopamine and plasticity of horizontal cell function in the teleost retina: regulation of a spectral mechanism through D1-receptors.

The negative feed-back interaction between horizontal cells (HCs) and cones in the cyprinid fish retina is thought to be mediated by horizontal cell spinules. These are "plastic" structures, largely absent from the dark-adapted retina and formed anew during light adaptation. We have previously shown that horizontal cell feed-back is similarly enhanced by light adaptation. The role of the interplexiform cell transmitter dopamine in both processes has been studied in the roach retina. Application of dopamine to dark-adapted retinae induced spinule formation in a dose-dependent way. The effect of dopamine was mimicked by dibutyryl-cAMP and suppressed selectively by D1 receptor antagonists. The effect of light in inducing spinule formation was lost in retinae depleted of endogenous dopamine. However, application of exogenous dopamine to these retinae triggered normal spinule formation. For all pharmacological treatments used, there was a strong correlation between spinule number and degree of feed-back activity in biphasic horizontal cells. Thus, when the spinule content of the cone pedicles was high, biphasic horizontal cell responses exhibited strong depolarizing components and vice versa. It is concluded that light-evoked formation of spinules in HC dendrites involves the action of dopamine upon D1 receptors. Spinules, in turn, are likely to be presynaptic terminals mediating the dynamic negative feed-back effect of horizontal cells upon cones.

Animals↗
PubMed1981

Prolactin induces grooming in the rat: possible involvement of nigrostriatal dopaminergic system.

The possibility that Prolactin-induced grooming involves the nigrostriatal dopaminergic system was studied. Intracerebroventricular injection of rat Prolactin (PRL) in an amount of 10 micrograms induced grooming in male rats, and neostriatal injection of haloperidol (1 microgram/1 microliter) markedly suppressed this effect. Local administration of 6-OHDA in the substantia nigra also abolished the influence of intracerebroventricularly administered PRL. Bilateral injections of PRL (10 micrograms/l microliters) in the neostriatum failed to induce grooming, whereas bilateral injections of peptide into the substantia nigra (1 microgram/0.5 micrograms) elicited the behavioral response. It is probable that PRL induces grooming in the rat by interacting with the nigrostriatal dopaminergic transmission through an action on the cell bodies rather than in presynaptic terminals or at the postsynaptic level of this system.

Animals↗
PubMed1994

The selective dopamine uptake inhibitor GBR 12909: its effects on the microstructure of feeding in rats.

Previous experiments have investigated the anorectic effects of mazindol and cocaine, both of which can inhibit dopamine (DA) uptake into presynaptic terminals but do not do so selectively. GBR 12909, however, is an example of a potent and selective inhibitor of DA uptake and, therefore, the present study was concerned with investigating its possible effects on feeding behavior in nondeprived rats given access to a sweetened palatable diet. GBR 12909 (5-20 mg/kg, IP) was injected 2 h before a 60 min observation test. It produced a significant reduction in food intake, as a consequence of a reduction in the duration of feeding, without reducing the rate of eating. This anorectic profile is consistent with earlier findings for mazindol and cocaine. The other main behavioral effect of GBR 12909, observed in the present study, was to induce intense sniffing activity, but, unlike cocaine, it did not suppress grooming or induce hyperlocomotion. This selective behavioral effect of GBR 12909 indicates that sniffing can be isolated as one component of a broader array of components typically associated with DA-related stereotyped behavior.

Animals↗
PubMed1996

FS stress induces long-lasting memory facilitation: involvement of cholinergic pathways.

We tested in vivo the hypothesis that foot-shock (FS) stress-induced prolongation of latencies in the one-trial step-through passive avoidance learning task in mice occurred through a long-term facilitation process. Whereas behavioral responses in control mice lasted for 24 h, decreasing progressively in the subsequent days, FS-stress exposure for 15 min before training (pretraining), immediately after training (posttraining), or 15 min before the test (pretest) resulted in a profound and sustained enhancement of test latencies that lasted for at least 96 h. These facilitating effects disappeared when FS exposure was delivered with a 2- or 3-h difference with respect to the training trial. Scopolamine (Scop) (1 mg/kg, intraperitoneally) 30 min before the training session caused impairment of test latencies in control and pretest stressed animals, but failed to affect both pre- and posttraining FS stress-induced enhancement. Our working hypothesis is that FS stress may increase the levels of acetylcholine in the presynaptic terminal or the firing rate of cholinergic input. Animals pretreated with FS stress daily for 1 or 4 days followed by the acute schedule described above showed no enhancements of test latencies. Pretraining Scop impaired test latencies in pre- and posttraining and pretest stressed animals, suggesting that unpredictability is a critical factor in activating behavioral long-term facilitation.

Animals↗
PubMed1992

HRP reacted with the chromogen o-tolidine produces whole-cell reaction product at light and electron microscope levels: negative effects of sucrose and Golgi staining on benzidine reactions.

Studies of pathway microcircuitry often require electron microscope analysis. To facilitate these analyses, methods for labeling cells in their entirety are extremely useful. Furthermore, such a method would be most useful if the label would be completely confined by the cell membrane so that second labels for synapse identification could be used. No existing method reliably and repeatably produces this kind of a result. In seeking to develop such a method, a seldom-used chromogen for horseradish peroxidase (HRP) was found which produced superlative results for light and electron microscope analysis. o-Tolidine (3,3'-dimethylbenzidine) reacted with HRP produces a very electron-dense reaction product distributed uniformly throughout the cytoplasm and nucleoplasm; membranes are unobscured so that mitochondria, lysosomes, Golgi apparati and endoplasmic reticula are well defined. The reaction product extends into cellular processes of all sizes, including processes with cell bodies not within the plane of section, and is easily visualized at even the lowest electron microscope magnification. The HRP reaction product is completely confined by the cell membrane, thus terminals presynaptic to labeled cells remain distinct. However, the o-tolidine/HRP reaction product is negatively affected by exposure to oxidizers. In tissue exposed to sucrose before or after being reacted with o-tolidine, the HRP reaction product is less electron dense and is found only in lysosomes outside the nucleus or occasionally in proximal cellular processes. The o-tolidine/HRP reaction product is similarly affected when exposed to potassium dichromate for Golgi staining. For some other benzidine compounds, the chromogen/HRP reaction product is also negatively affected by exposure to these chemicals. Therefore, o-tolidine is a superior chromogen for HRP, labeling cells with details similar to that found for cells intracellularly injected with HRP.

Animals↗
PubMed1993

Real-time imaging of neurons retrogradely and anterogradely labelled with calcium-sensitive dyes.

Membrane-impermeant calcium indicator dyes were used to retrogradely label dorsal root ganglia, spinal motoneurons and interneurons in the spinal cord of the chick embryo. The dyes were also used to label anterogradely primary afferent axons in the spinal cord and synaptic endings in the ciliary ganglion. Labelled neurons were imaged using digital videomicroscopy. Motoneurons and dorsal root ganglion cells exhibited a frequency-dependent change in fluorescence during antidromic stimulation. Single antidromic stimuli resulted in fluorescence transients that could be resolved in individual cells in real time. In addition, fluorescence changes could be recorded in motoneurons during episodes of bursting generated by rhythmic synaptic inputs from premotor networks. Stimulus-induced fluorescence signals were also detected in axons and synaptic endings labelled anterogradely. Optical signals were largely abolished in the absence of extracellular calcium. The results show that calcium changes can now be measured in identified populations of neurons and presynaptic terminals. The strong dependence of these signals on impulse activity suggests that the technique will be useful for monitoring the activity of identified neuronal populations. The calcium-dependent fluorescence signal probably results from cytosolic dye derived from diffusion which may limit the technique to situations in which the dye can be applied close (< 1 cm) to cell bodies.

Animals↗
PubMed1994

A new cytochemical method for the ultrastructural localization of calcium in the central nervous system.

We have developed a new cytochemical method for the localization of calcium at the ultrastructural level in the central nervous system (CNS). The method is based on the use of phosphate buffer in the primary fixation followed by a mixture of a complex of chromium(III)-trisoxalate and osmium tetroxide (OsO4) which precipitates calcium and results in the formation of a high electron-dense reaction product. Calcium selectivity was verified by reactions made in test tube, by EGTA treatment of the tissue, by electron spectroscopic imaging (ESI) and electron energy loss spectroscopy (EELS). The technique was found to be reproducible, yielding similar results in acutely prepared hippocampal slices or organotypic cultures fixed by immersion and in brain areas fixed by perfusion. In hippocampal slices, calcium deposits were found to accumulate in different subcellular compartments such as endoplasmic reticulum, mitochondria and synaptic vesicles. Interestingly, electron-dense reaction products were also visualized in smooth endoplasmic reticulum structures localized in presynaptic terminals or post-synaptic spines as well as in synaptic clefts and active zones. This new method may thus be of interest for studying the metabolism of calcium, specifically with regard to synaptic activity, in the CNS.

Animals↗
PubMed1982

Facilitatory effect of some drugs on transmission in the frog sympathetic ganglion.

Effects of 3,4-diaminopyridine and dimethylsulfoxide on transmission in frog sympathetic ganglion were analyzed. In the presence of either drug repetitive waves appeared in the compound action potential. Intracellular recording revealed a repetitive firing of certain populations of ganglionic neurons following each orthodromic stimulus. Antidromic stimulation did not evoke any repetitive response. Dependence of the repetitive response on drug concentration and stimulation rate is described. An enhancement and prolongation of fast EPSP was observed in the presence of both drugs. It is assumed that by interference with changes in membrane potassium permeability the drugs prolong the action potential in presynaptic terminals with a resulting increase in synaptic output of transmitter. The repetitive firing of the postsynaptic membrane subsequent to activation of the synapse is a consequence of its prolonged and more profound depolarization. Presumably, this is one of several mechanisms of drug-induced increase in efficacy of synaptic transmission in frog sympathetic ganglion known as stimulus-bound repetition.

4-Aminopyridine↗
PubMed1982

Modulation of nicotinic transmission by biogenic amines in bullfrog sympathetic ganglia.

Studies of transmission in isolated paravertebral sympathetic ganglia of the bullfrog and at the sciatic-sartarius muscle synapse in the frog yielded evidence that biogenic amines such as catecholamines or 5-hydroxytryptamine can modulate transmission in sympathetic ganglia and at the neuromyal junction. These two transmitter substances are able to modulate transmission by affecting the amount of ACh release from presynaptic terminals and also by affecting the sensitivity of nicotinic Ach receptors of the subsynaptic membrane. Information is presented as to how these compounds exert their modulatory effects on these synapses.

Acetylcholine↗
PubMed1984

Muscarinic agonists depress calcium-dependent gK in bullfrog sympathetic neurons.

Intracellular recordings were made from 'fast B' [9] neurons in bullfrog sympathetic ganglia. A single soma action potential was followed by a prolonged after-hyperpolarization lasting for several hundred milliseconds up to 2 s. The spike afterhyperpolarization, which is generated by calcium-dependent potassium conductance increase (gKCa) [3,20-24], was shortened by the muscarinic action of acetylcholine and oxotremorine (30-300 nM). These concentrations of muscarinic agonists were too low to cause any detectable changes in resting membrane potential, input resistance or action potential wave form. ACh released from presynaptic terminal under a physiological condition also caused the shortening of the calcium-dependent hyperpolarization. The results suggested that the shortening of calcium-dependent spike afterhyperpolarization may permit the neuron to pass the high frequency of discharge during the muscarinic excitation.

Acetylcholine↗