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PubMedDate not supplied

Distribution and coexistence of urotensin I and urotensin II peptides in the cerebral ganglia of Aplysia californica.

Urotensin I (UI) and urotensin II (UII) were demonstrated in the cerebral ganglia of Aplysia californica by applying immunocytochemical and radioimmunoassay procedures. Sequential analysis of adjacent sections of the cerebral ganglia of Aplysia demonstrated that the UI-immunoreactive (UI-IR) neurons of the F cluster of the cerebral ganglia also contained UII immunoreactivity (UII-IR). Both UI-IR and UII-IR were also observed in a cuff-like arrangement of fibers surrounding the proximal portion of the supralabial nerve, as well as in a few fibers in the anterior tentacular nerves. The UI-IR perikarya of the cerebral ganglia appeared to project to the entire CNS of Aplysia, but the UII-IR fibers appeared only in the neuropile and commissure of the cerebral ganglia. The UI-IR staining was abolished by previous immunoabsorption of the UI antiserum with sucker (Catastomus commersoni) UI, but not with ovine corticotropin-releasing factor (CRF), rat/human CRF, or goby (Gillichthys mirabilis) UII. Immunostaining with UII antiserum was quenched by goby UII, but not by sucker UII-A, UII-B, UII-A(6-12), or carp (Cyprinus carpio) UII-alpha and UII-gamma. The UII staining was not abolished by UI or somatostatin. The F cluster was not stained when a somatostatin antiserum was applied. Radioimmunoassay of dilutions of cerebral ganglia extract, using UII antiserum, revealed a parallel displacement curve to synthetic goby UII.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Lophotoxin: selective blockade of nicotinic transmission in autonomic ganglia by a coral neurotoxin.

Lophotoxin is a diterpene lactone isolated from gorgonian corals. The toxin has previously been shown to bind with high affinity to an acetylcholine recognition site located on skeletal muscle nicotinic receptors, producing an essentially irreversible blockade of neuromuscular transmission. Lophotoxin has also been shown to block nicotinic transmission in autonomic ganglia of the frog and in ileal strips of guinea pig and rabbit. The effects of lophotoxin have now been examined on neuronal nicotinic receptors in autonomic ganglia of the chick and rat. Low concentrations of lophotoxin (1 microM) produce a blockade of neuronal nicotinic transmission which is partially reversed by 3-5 h of washing out the toxin. The blockade produced by higher concentrations of lophotoxin (up to 32 microM) is not reversed during a similar washout period. Prior exposure to d-tubocurarine, a competitive nicotinic antagonist, can partially protect ganglia against exposure to lophotoxin. In contrast the local anesthetic QX-314, a noncompetitive nicotinic antagonist, does not protect ganglia against lophotoxin exposure. Lophotoxin binds to a site in ganglia identified by [125I]kappa-bungarotoxin which appears to be on the neuronal nicotinic receptor. Intracellular recordings reveal that lophotoxin has no effect on either muscarinic responses or on responses to gamma-aminobutyrate in autonomic ganglia. Passive and active membrane properties of the neurons are unaffected by lophotoxin except for the blockade of nicotinic responses. It is concluded that lophotoxin is a selective, high-affinity antagonist at the neuronal nicotinic receptor. The long-term nature of the blockade with lophotoxin suggests that the toxin will be of considerable value as a probe for characterizing the ganglionic nicotinic receptor.

Action Potentials↗
PubMed1992

Distribution of nicotinic receptors in cynomolgus monkey brain and ganglia: localization of alpha 3 subunit mRNA, alpha-bungarotoxin and nicotine binding sites.

The distribution of nicotinic receptors in the brain and ganglia of the Cynomolgus monkey was studied by in situ hybridization and receptor autoradiography. A 35S-labeled antisense riboprobe for the mRNA of the alpha 3 subunit of the human nicotinic receptor, [3H]L-nicotine and [125]alpha-bungarotoxin were used as markers. The highest levels of alpha 3-mRNA were observed in the hippocampus, the medial habenula, the lateral geniculate, the granular layer of the cerebellum, as well as in the pineal gland; moderate levels were found in other nuclei of the thalamus and in the deeper layers of the cerebral cortex. High-affinity binding sites for [3H]L-nicotine were observed mainly in the thalamus. The distribution of [125I]alpha-bungarotoxin binding sites was different from that observed for alpha 3-mRNA and [3H]L-nicotine; they were most abundant in a few specific thalamic nuclei, in the medial habenula and in lamina I of the cerebral cortex. The localization of these three markers was also investigated in the sympathetic, parasympathetic and sensory ganglia of the monkey. Intense labeling was observed for alpha 3-mRNA and for [125I]alpha-bungarotoxin in the sympathetic and parasympathetic ganglia, whereas no positive signal was seen in the ganglion of Gasser. [3H]L-nicotine binding was not detected in any of the ganglia examined. High levels of mRNA for the alpha 3 subunit of the nicotinic receptor were also detected in human sympathetic ganglia. Comparison between alpha 3-mRNA distribution and [3H]L-nicotine binding suggests that in the Cynomolgus monkey brain, the alpha 3 subunit may participate in the formation of more than one nicotinic receptor subtype: a high-affinity binding site for [3H]L-nicotine in the thalamus, and other sites with low affinity for nicotine in the medial habenula and cerebral cortex. Both the alpha 3-mRNA and the [125I]alpha-bungarotoxin are highly expressed in the sympathetic ganglia; however, since no information is presently available on the intraneuronal cellular localization, it cannot be established whether or not they are both present at synaptic sites.

Animals↗
PubMed1994

Permeation of proteins from the blood into peripheral nerves and ganglia.

We have attempted to resolve apparently conflicting observations of previous investigators regarding the penetration of proteins into peripheral ganglia and nerves of the rat. Horseradish peroxidase, which is largely cleared from the blood and extracellular fluids in less than 30 min, entered all the extracellular spaces of ganglia, including the clefts between glial cells and neurons, but it did not enter the endoneurium. Rhodamine B-conjugated bovine albumin quickly entered sensory and sympathetic ganglia, but its penetration into avascular enteric nervous tissue was arrested at the outer margin of each myenteric and submucosal ganglion. If injected daily for a week, this fluorescent protein was seen also in the endoneurium, but it was still absent from enteric ganglia. The failure to enter enteric ganglia may have been due to the entrapment of aggregates of dye-labelled albumin molecules in the basal lamina that encloses the enteric nervous system. Extracellular endogenous albumin immunoreactivity was seen in all parts of peripheral nerves and in all types of ganglion. Some neuronal perikarya contained albumin-immunoreactive material; the strongest staining was in enteric neurons. Albumin may reach these cell bodies by retrograde axonal transport from peripheral terminals. We conclude that all the extracellular spaces of the rat's peripheral nervous system are accessible to plasma proteins, though diffusion occurs more slowly into the endoneurium than into ganglia.

Animals↗
PubMed1994

The organization of the basal ganglia-thalamocortical circuits: open interconnected rather than closed segregated.

Anatomical findings in primates and rodents have led to a description of several parallel segregated basal ganglia-thalamocortical circuits leading from a distinct frontocortical area, via separate regions in the basal ganglia and the thalamus, back to the frontocortical area from which the circuit originates. One of the questions raised by the concept of parallelism is whether and how the different circuits interact. The present Commentary proposes that interaction is inherent in the neural architecture of the basal ganglia-thalamocortical circuits. This proposal is based on the re-examination of the data on the topographical organization of the frontocortical-basal ganglia connections which indicates that each circuit-engaged striatal region sends divergent projections to parts of both substantia nigra pars reticulata and the internal segment of the globus pallidus (each ventral striatal region sends divergent projections to parts of ventral pallidum, substantia nigra pars reticulata and globus pallidus), and this segregation is maintained at subsequent thalamic and frontocortical levels. This results in an asymmetry in the frontal cortex-basal ganglia relationships, so that while each frontocortical subfield innervates one striatal region, each striatal region influences the basal ganglia output to two frontocortical subfields. Because of this asymmetry, at least one of the frontocortical targets of a given circuit-engaged striatal region is not the source of its frontocortical input. Since this organization is inconsistent with an arrangement in closed segregated circuits we introduce the concept of a "split circuit". A split circuit emanates from one frontocortical area, but terminates in two frontocortical areas. Thus, a split circuit contains at least one "open" striato-fronto-cortical pathway, that leads from a circuit-engaged striatal region to a frontocortical area which is a source of a different circuit. In this manner split circuits are interconnected via their open pathways. The second striato-fronto-cortical pathway of a split circuit can be another open pathway, or it can re-enter the frontocortical area of origin, forming a closed circuit. On the basis of the available anatomical data we tentatively identified a motor, an associative, and a limbic split circuit, each containing a closed circuit and an open pathway. The motor split circuit contains a closed motor circuit that re-enters the motor and premotor cortical areas and an open motor pathway that terminates in the associative prefrontal cortex. The associative split circuit contains a closed associative circuit that re-enters the associative prefrontal cortex and an open associative pathway that terminates in the premotor cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Serotonin is released from isolated leech ganglia by potassium-induced depolarization.

1. The quantities of serotonin that are released from isolated leech ganglia in vitro were measured with the sensitive neurochemical techniques of HPLC-EC. 2. Segmental ganglia were exposed to elevated concentrations of potassium that depolarize leech serotonin-containing neurons by approximately 35 mV per decade. 3. Each segmental ganglion released on average 0.20 pmol of serotonin during 10 min of incubation in a solution containing 64 mM K+. 4. The rate of serotonin release increased nearly four-fold to 0.74 pmol/10 min when ganglia were incubated in 120 mM K+. 5. The rates of ganglionic serotonin release in 120 mM K+ were quantitatively similar in these three, experimentally important species of leeches: Hirudo medicinalis, Macrobdella decora and Haementeria ghilianii. 6. Ionic substitution experiments with the divalent cations Mg2+ and Co2+ indicated that the release of serotonin from leech ganglia is mediated by a Ca2+ dependent process. 7. The serotonin-uptake blockers, imipramine and chlorimipramine, did not increase the amount of serotonin released in elevated potassium. 8. Vitally staining the identified serotonin-containing neurons with Neutral Red dye did not reduce the quantity of serotonin that was released from the ganglia in elevated potassium. 9. This study demonstrates the capacity of leech ganglia to release the neurochemical serotonin, and the rates of transmitter release increase with the degree of depolarization of serotonin-containing neurons.

Animals↗
PubMed2005

Short-term synaptic plasticity in rabbit pancreatic ganglia.

The extrinsic innervation of the pancreas converges on a plexus of intrinsic pancreatic ganglia whose cholinergic neurons innervate acini, ducts, islets and blood vessels. Therefore, understanding ganglionic transmission is essential for understanding neural control of pancreatic secretion. Intracellular recordings of nicotinic fast excitatory postsynaptic potentials (fEPSPs) and action potentials (APs) were used to characterize and compare transmission in ganglia from the head/neck and body regions of the rabbit pancreas. Paired-pulse facilitation (PPF) or depression (PPD) of fEPSPs was observed in ganglia from both regions with PPF peaking and disappearing at shorter inter-stimulus intervals than PPD. PPF was most frequent in the head/neck (60%) and PPD (50%) in the body. Repetitive stimulation (10 Hz/5 s) evoked multiple forms of mid- and post-train plasticity. Facilitation during the first 1-2 s of train stimulation was reduced or reversed with continued stimulation due to development of synaptic depression and mid-train depression was of greater magnitude in the head/neck region. A brief (approximately 10 s) post-train augmentation was followed by a 1-2 min post-train depression that appeared to result from inhibition of ACh release. Regional differences in the frequency, magnitude, or duration of all forms of synaptic plasticity suggested regional differences in the extrinsic innervation patterns and possibly the function of pancreatic ganglia. In conclusion, rabbit pancreatic ganglia exhibit multiple forms of short-term synaptic plasticity that markedly alter the probability of postsynaptic firing, consistent with these ganglia being critical sites of synaptic integration and autonomic regulation of pancreatic secretion.

Animals↗
PubMed2006

A hypothetical role of cortico-basal ganglia-thalamocortical loops in visual processing.

The goal of the present work was to define the mechanisms underlying the contribution of sensory and limbic cortico-basal ganglia-thalamocortical loops to visual processing and its attentional modulation. We proposed that visual processing is promoted by dopamine-dependent long-term modifications of synaptic transmission in the basal ganglia that favour a selection of neocortical patterns representing a visual stimulus. This selection is the result of the opposite sign of modulation of strong and weak cortico-basal ganglia inputs and subsequent activity reorganization in each loop. Reorganization leads to disinhibition/inhibition of cortical neurons strongly/weakly excited by stimulus during dopamine release. Recruitment of the thalamo-basal ganglia-collicular pathway is proposed to be necessary for stimulus-evoked dopamine release that underlies bottom-up attentional effects. Visual excitation of the prefrontal cortex and hippocampus (via the thalamus), their cooperation in control of the basal ganglia and dopaminergic cell firing, and simultaneous modulation of activity in diverse cortico-basal ganglia-thalamocortical loops is proposed to underlie top-down attentional effects. It follows from our model that only those components of cortical responses can be modulated by attention, whose onset exceeds the latency of visual responses of dopaminergic cells (50-110 ms). This and other consequences of the model are in accordance with known experimental data.

Animals↗
PubMed2005

Peptide 19 in the rat vagal and glossopharyngeal sensory ganglia.

Peptide 19 (PEP 19) is a 7.6-kDa polypeptide which binds to calmodulin and inhibits calcium-calmodulin signaling. In this study, PEP 19-immunoreactivity (PEP 19-IR) was examined in the rat vagal and glossopharyngeal sensory ganglia. Twenty-nine percent, 59%, and 41% of sensory neurons contained PEP 19-IR in the jugular, petrosal, and nodose ganglia, respectively. These neurons were of various sizes (jugular, mean +/- SD = 635.8 +/- 392.6 microm2, range = 105.9-1695.9 microm2; petrosal, mean +/- SD = 370.9 +/- 228.5 microm2, range = 57.7-1662.7 microm2; nodose, mean +/- SD = 380.5 +/- 157 microm2, range = 87.5-950.4 microm2) and scattered throughout these ganglia. Double immunofluorescence method revealed that PEP 19-IR neurons which had parvalbumin-IR were rare in the ganglia (jugular, 4%; petrosal, 10%; nodose, 8%). PEP 19-IR neurons which contained calbindin D-28k were abundant in the petrosal (20%) and nodose (22%) ganglia but not in the jugular ganglion (8%). Retrograde tracing method indicated that many PEP 19-IR neurons projected to the circumvallate papilla and soft palate. In the soft palate, taste buds were innervated by PEP 19-IR nerve fibers. The present study suggests that PEP 19-IR neurons include chemoreceptors in the vagal and glossopharyngeal sensory ganglia.

Animals↗
PubMedDate not supplied

Anatomical funneling, sparse connectivity and redundancy reduction in the neural networks of the basal ganglia.

The major anatomical characteristics of the main axis of the basal ganglia are: (1) Numerical reduction in the number of neurons across layers of the feed-forward network, (2) lateral inhibitory connections within the layers, and (3) neuro-modulatory effects of dopamine and acetylcholine, both on the basal ganglia neurons and on the efficacy of information transmission along the basal ganglia axis. We recorded the simultaneous activity of neurons in the output stages of the basal ganglia as well as the activity of dopaminergic and cholinergic neurons during the performance of a probability decision-making task. We found that the functional messages of the cholinergic and dopaminergic neurons differ, and that the cholinergic message is less specific than that of the dopaminergic neurons. The output stage of the basal ganglia showed uncorrelated neuronal activity. We conclude that despite the huge numerical reduction from the cortex to the output nuclei of the basal ganglia, the activity of these nuclei represents an optimally compressed (uncorrelated) version of distinctive features of cortical information.

Animals↗
PubMed2006

Temporal dynamics of basal ganglia response and connectivity during verbal working memory.

Research on the neural basis of working memory (WM) has generally focused on neocortical regions; comparatively little is known about the role of subcortical structures. There is growing evidence that the basal ganglia are involved in WM, but their contribution to different component processes of WM is poorly understood. We examined the temporal dynamics of basal ganglia response and connectivity during the encoding, maintenance and response phases of a Sternberg WM task. During the encoding and maintenance phases, WM-load-dependent activation was observed in the left anterior caudate, anterior putamen and globus pallidus; activation in the right anterior caudate was observed only during the maintenance phase. During the response phase, the basal ganglia were equally active in both the high-load and low-load WM conditions. Caudate and putamen activations were primarily localized to the (rostral) associative parts of the basal ganglia, consistent with the putative role of these regions in cognitive processing. Effective connectivity analyses revealed increased WM-load-dependent interaction of the left anterior caudate with the left posterior parietal cortex during all three phases of the task; with the visual association cortex, including the fusiform gyrus and inferior temporal gyrus, only during the encoding phase; with the ventrolateral prefrontal cortex during the encoding and maintenance phases; with the pre-supplementary motor area during the maintenance and response phases; and with the dorsolateral prefrontal and anterior cingulate cortices only during the response phase. Taken together with known neuroanatomy of the basal ganglia, these results suggest that the anterior caudate helps to link signals in distinct functional networks during different phases of the WM task. Our study offers new insight into the integrative and adaptive role of the basal ganglia in higher cognitive function.

Adolescent↗
PubMed2004

Number processing and basal ganglia dysfunction: a single case study.

Numerical processing has never been investigated in a case of Fahr's disease (FD) and only rarely in cases of basal ganglia dysfunction. The study describes the cognitive decline of a pre-morbidly high-functioning patient (medical doctor) affected by FD and his difficulties in number processing. A MRI scan revealed bilateral calcifications in the basal ganglia and a brain PET showed a massive reduction of glucose metabolism in the basal ganglia and both frontal lobes, but no other brain abnormalities. The patient's cognitive deficits included impairments in problem solving, in cognitive set shifting and in mental flexibility, as well as in verbal memory. These deficits are attributed to the disruption of the dorsolateral prefrontal circuit involving the basal ganglia. In number processing, the patient showed a severe deficit in the retrieval of multiplication facts, deficits in all tasks of numerical problem solving and in the execution of complex procedures. Importantly, he also showed a dense deficit in conceptual knowledge, which concerned all test conditions and all operations. The findings confirm the predictions of the triple code model in so far, as a disruption of cortico-subcortical loops involving the basal-ganglia may lead to specific deficits in fact retrieval. However, no verbal deficit, as assumed in the triple code model and reported in similar cases, could be observed. The present findings further add to current knowledge on numerical processing, showing how fronto-executive dysfunction may disrupt conceptual understanding of arithmetic. This study shows that not only parietal lesions may lead to severe deficits in conceptual understanding, but that basal ganglia lesions leading to frontal dysfunction may have a devastating effect.

Basal Ganglia Diseases↗
PubMed2005

The enhancement of cell adherence and inducement of neurite outgrowth of dorsal root ganglia co-cultured with hyaluronic acid hydrogels modified with Nogo-66 receptor antagonist in vitro.

Hyaluronic acid hydrogels modified with polyclonal anti-Nogo-66 receptor antibody were developed in order to promote regeneration in the injured CNS. These modified hydrogels were intended not only to deliver antibodies, but also to serve as a scaffold for neural regeneration following their implantation into injured tissue. Since unmodified hyaluronic acid-hydrogels do not support cell attachment, the gels were modified with polyclonal anti-Nogo-66 receptor with the aim of altering the surface properties of the gels in such a way as to improve neuronal adherence and survival. After evaluating the immobilization efficiency of the system, chicken dorsal root ganglia and dorsal root ganglia cells were planted on the surface of the modified gels to determine cell viability. Dorsal root ganglia were also cultured close to the gels in order to assay the inducement of neurite outgrowth. In dorsal root ganglia and cell viability assay, dorsal root ganglia and neuron cells could adhere to the modified hydrogels and survive well, but it did not happen to unmodified hydrogels. After 72 h, these attached cells were stained positively with immuno-staining for neurofilament. Neurite outgrowth inducement assay showed that the number and length of dorsal root ganglia neurites on the side toward modified hydrogels were significantly more than that on the opposite side (both P<0.01). The results reveal that hyaluronic acid-hydrogels modified with anti-Nogo-66 receptor can support neural cell attachment and survival in vitro. Furthermore, this system can greatly induce neurite outgrowth. The results also indicate that this modified hydrogels have potential to repair injury in the CNS.

Animals↗
PubMed2006

Interleukin-1 beta contributes to the upregulation of kappa opioid receptor mrna in dorsal root ganglia in response to peripheral inflammation.

During local painful inflammation, axonal transport of opioid receptors from dorsal root ganglia toward the periphery is increased, associated with a higher receptor density and enhanced efficacy of opioid analgesics at the injured site. To examine whether this increase is related to transcription, mRNA of the kappa opioid receptor in lumbar dorsal root ganglia was quantified by real time light cycler polymerase chain reaction. In dorsal root ganglia of naive rats, kappa opioid receptor mRNA expression was three-fold higher than previously shown for delta opioid receptor and two times lower than mu opioid receptor mRNA, respectively. After induction of unilateral paw inflammation by Freund's complete adjuvant, kappa opioid receptor mRNA was significantly upregulated with a peak at 12 h in ipsilateral dorsal root ganglia. This effect could be mimicked by intraplantar injection of the proinflammatory cytokine interleukin-1 beta. Kappa opioid receptor mRNA upregulation lasted longer in interleukin-1 beta-treated rats compared with Freund's complete adjuvant-treated rats. Furthermore, a significant increase in kappa opioid receptor positive neurons was detected by immunohistochemistry 24 h after local injection of Freund's complete adjuvant or interleukin-1 beta. In Freund's complete adjuvant-induced inflammation, kappa opioid receptor upregulation was blocked by treatment with interleukin-1 receptor antagonist without changing the leukocyte infiltration in the paw. In conclusion, kappa opioid receptor mRNA and protein in dorsal root ganglia are upregulated in response to peripheral inflammation. This effect can be mimicked by a single local injection of interleukin-1 beta, and Freund's complete adjuvant-induced upregulation in kappa opioid receptor mRNA and protein can be prevented by treatment with interleukin-1 receptor antagonist. These data suggest that the peripheral production of the proinflammatory cytokine interleukin-1 beta is a specific inducer of kappa opioid receptor expression in the dorsal root ganglia.

Animals↗
PubMed2005

Birdbrains could teach basal ganglia research a new song.

Recent advances in anatomical, physiological and histochemical characterization of avian basal ganglia neurons and circuitry have revealed remarkable similarities to mammalian basal ganglia. A modern revision of the avian anatomical nomenclature has now provided a common language for studying the function of the cortical-basal-ganglia-cortical loop, enabling neuroscientists to take advantage of the specialization of basal ganglia areas in various avian species. For instance, songbirds, which learn their vocal motor behavior using sensory feedback, have specialized a portion of their cortical-basal ganglia circuitry for song learning and production. This discrete circuit dedicated to a specific sensorimotor task could be especially tractable for elucidating the interwoven sensory, motor and reward signals carried by basal ganglia, and the function of these signals in task learning and execution.

Animals↗
PubMed2002

Basal ganglia volumes in first-episode schizophrenia and healthy comparison subjects.

BACKGROUND: Previous studies suggest that dysfunction of cortico-striato-pallido-thalamic (CSPT) circuitry may be involved in the pathophysiology of schizophrenia but also show that basal ganglia structure is highly plastic and may be influenced by antipsychotic treatments. Controversy remains about whether basal ganglia pathology can be detected in vivo among treatment-naïve patients. We conducted a magnetic resonance imaging (MRI) study to examine basal ganglia structures and the limbic forebrain in first episode schizophrenia and healthy comparison subjects. METHODS: Fifty-one patients with first-episode schizophrenia and 28 healthy comparison subjects participated in the study. A high-resolution, special contrast (white matter nulling) MRI sequence was used to measure the caudate nucleus, nucleus accumbens, putamen, and subcommissural limbic forebrain. RESULTS: Volumes of the basal ganglia regions of interest (adjusted for total brain volume and age) did not differ significantly between the groups. Age correlated significantly with caudate and putamen volumes bilaterally in the healthy comparison group, but not among patients. CONCLUSIONS: The findings suggest that there are no volumetric abnormalities in basal ganglia before treatment in first-episode schizophrenia. The lack of a negative correlation between age and striatal volume among patients may implicate illness-associated factors that alter normal age-related changes in basal ganglia size.

Adult↗
PubMed1994

The distribution of excitatory amino acid receptors in the normal human midbrain and basal ganglia with implications for Parkinson's disease: a quantitative autoradiographic study using [3H]MK-801, [3H]glycine, [3H]CNQX and [3H]kainate.

Quantitative receptor autoradiography using [3H]MK-801, [3H]glycine, [3H]CNQX and [3H]kainate was employed to determine the distribution and density of excitatory amino acid (EAA) binding sites in the midbrain and basal ganglia of the normal human nervous system. Detailed knowledge of the anatomy and subtype specificity of glutamate receptors is important both in understanding the normal physiology of basal ganglia neurotransmission and the pathophysiological changes occurring in diseases affecting the basal ganglia such as Parkinson's disease (PD). In PD, glutamate receptor activation may contribute to cell death of dopaminergic neurones in the substantia nigra. In addition, perturbation of glutamate neurotransmission resulting from dopamine depletion in the basal ganglia is likely to contribute to the clinical manifestations of motor dysfunction. The distribution and density of ligand binding representing N-methyl-D-aspartate (NMDA), AMPA (2-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) and kainate receptors has a heterogeneous distribution in the human midbrain and basal ganglia. In the substantia nigra relatively high densities of [3H]MK-801 and strychnine-insensitive [3H]glycine binding sites representing NMDA receptors were present, whereas only moderate densities of [3H]CNQX and [3H]kainate binding sites were present, compared to other regions. In both the medial globus pallidus and subthalamic nucleus, binding sites representing NMDA, AMPA and kainate receptors were all present at low density. These findings suggest that the clinical usefulness of modifying glutamatergic neurotransmission in these basal ganglia nuclei may be limited by the relatively low density of EAA binding sites present.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2002

Diabetes is not a potent inducer of neuronal cell death in mouse sensory ganglia, but it enhances neurite regeneration in vitro.

We examined the effects of diabetes on the morphological features and regenerative capabilities of adult mouse nodose ganglia (NG) and dorsal root ganglia (DRG). By light and electron microscopy, no apoptotic cell death was detected in the ganglia obtained from either streptozotocin (STZ)-induced diabetic or normal C57BL/6J mice in vivo. Neurite regeneration from transected nerve terminals of NG and DRG explants in culture at normal (10 mM) and high (30 mM) glucose concentrations was significantly enhanced in the diabetic mice. Chromatolytic changes (i.e. swelling and migration of the nucleus to an eccentric position in the neurons, and a loss of Nissl substance in the neuronal perikarya) and apoptotic cell death (less than one-fifth of the neurons) in the cultured ganglia were present, but neither hyperglycemia in vivo nor high glucose conditions in vitro altered the morphological features of the ganglia or the ratios of apoptotic cells at 3 days in culture. By semiquantitative RT-PCR analysis, the mRNA expressions of ciliary neurotrophic factor (CNTF) in DRG from both mice were down-regulated at 1 day in culture. The expression in diabetic DRG, but not in control DRG, was significantly up-regulated at later stages (3 and 7 days) in culture. In summary, hyperglycemia is unlikely to induce cell death in the sensory ganglia, but enhances the regenerative capability of vagal and spinal sensory nerves in vitro. The up-regulation of CNTF mRNA expression during the culture of diabetic DRG may play a role in the enhanced neurite regeneration.

Animals↗