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Biomedical subjects

Kazuhiro Nakamura

Publications and source records attributed to Kazuhiro Nakamura.

At least 37 records · Page 2Linked to original sources
PubMed2005

The relationship between esophagoscopic findings and total acid reflux time below pH 4 and pH 5 in the upper esophagus in patients with laryngopharyngeal reflux disease (LPRD).

OBJECTIVE: : To investigate the relationship between esophagoscopic findings and total acid reflux time in the upper esophagus in the patients of laryngopharyngeal reflux disease (LPRD), and to evaluate whether pH<5 holding time is appropriate for diagnosing LPRD. METHOD: : Esophagoscopy and 24-h pH monitoring in the upper esophagus were performed in 29 patients suspected of LPRD and 19 healthy volunteers participated as controls. The total acid reflux times below pH 4 and 5 in the upper esophagus were compared between the LPRD group and the controls. The LPRD group was divided into LPRD with reflux esophagitis (RE) and LPRD without RE, and the total acid reflux times below pH 4 and 5 of these two groups were compared. RESULTS: : Eight of the 29 (27.6%) LPRD patients had reflux esophagitis. The LPRD group showed a significantly longer acid reflux time than the control group at pH below 5 (P=0.009) but not at pH below 4 (P=0.48). The LPRD with RE had significantly longer acid reflux times below both pH 4 and 5 in the upper esophagus compared to those of the LPRD without RE. The P values using a cut-off value of pH 5 were smaller than that of pH 4 in all statistical results. CONCLUSION: : The LPRD patients showed significantly longer acid reflux time in the upper esophagus than the control group. In the LPRD group, the LPRD with RE patients had more frequent acid exposure in the upper esophagus than the LPRD without RE. A pH level of 5 could be appropriate as a cutoff level for the diagnosis of LPRD in upper esophagus pH monitoring.

Case-Control Studies↗
PubMed2005

Adenocarcinoma of the thymus: mucinous subtype.

Primary thymic adenocarcinoma, mucinous subtype, is extremely rare with only one case reported to date. We describe herein a case of thymic mucinous adenocarcinoma. A 59-year-old man was identified to have an anterior mediastinal tumor and was diagnosed as mucinous adenocarcinoma. Clinical and radiographic examinations disclosed no evidence of tumor elsewhere. The patient received radiotherapy, but the general condition deteriorated and died 11 months after tumor detection. Thoracic autopsy revealed an anterior mediastinal tumor measuring greater than 10 cm, uncapsulated, and white. The tumor had clear margins and was clearly isolated from the lung. Histologically, the tumor demonstrated papillary, acinar, and cribriform structure and produced abundant extracellular mucin. Immunohistochemically, most tumor cells were positive for cytokeratin 7, were partially positive for CD5, and were negative for TTF-1, Sp-A, CDX-2, MUC2, napsin A, and cytokeratin 20. Collectively, the diagnosis of the tumor was primary mucinous adenocarcinoma of the thymus. We propose that the mucinous subtype should be recognized as one of the histopathological entities of thymic adenocarcinoma.

Adenocarcinoma, Mucinous↗
PubMed2005

Sympathetic premotor neurons mediating thermoregulatory functions.

The sympathetic nervous system controls various homeostatic conditions, such as blood circulation, body temperature, and energy expenditure, through the regulation of diverse peripheral effector organs. In this system, sympathetic premotor neurons play a crucial role by mediating efferent signals from higher autonomic centers directly to sympathetic preganglionic neurons in the intermediolateral cell column of the spinal cord. The medulla oblongata is thought to subsume many sympathetic premotor neurons, and the rostral ventrolateral medulla (RVLM) has been established to contain the sympathetic premotor neurons responsible for cardiovascular control. Although premotor neurons controlling other effector organs than the cardiovascular system have been largely unknown, recent accumulating findings have suggested that medullary raphe regions including the raphe pallidus and raphe magnus nuclei are candidates for the pools of excitatory sympathetic premotor neurons involved in thermoregulation. Further recently, excitatory premotor neurons controlling the thermoregulatory effector organs, brown adipose tissue and tail, have been identified with expression of vesicular glutamate transporter (VGLUT)3, whereas those for cardiovascular control were characterized with VGLUT2 expression. The VGLUT3-expressing premotor neurons would mediate thermoregulation including fever induction, and could be also involved in the control of energy metabolism.

Amino Acid Transport Systems, Acidic↗
PubMed2005

Direct pyrogenic input from prostaglandin EP3 receptor-expressing preoptic neurons to the dorsomedial hypothalamus.

Fever is induced by a neuronal mechanism in the brain. Prostaglandin (PG) E2 acts as a pyrogenic mediator in the preoptic area (POA) probably through the EP3 subtype of PGE receptor expressed on GABAergic neurons, and this PGE2 action triggers neuronal pathways for sympathetic thermogenesis in peripheral effector organs including brown adipose tissue (BAT). To explore pyrogenic efferent pathways from the POA, we determined projection targets of EP3 receptor-expressing POA neurons with a special focus on rat hypothalamic regions including the dorsomedial hypothalamic nucleus (DMH), which is known as a center for autonomic responses to stress. Among injections of cholera toxin b-subunit (CTb), a retrograde tracer, into hypothalamic regions at the rostrocaudal level of the DMH, injections into the DMH, lateral hypothalamic area (LH) and dorsal hypothalamic area (DH) resulted in EP3 receptor immunolabelling in substantial populations of CTb-labeled neurons in the POA. Bilateral microinjections of muscimol, a GABA(A) receptor agonist, into the DMH and a ventral region of the DH, but not those into the LH, inhibited thermogenic (BAT sympathetic nerve activity, BAT temperature, core body temperature and expired CO2) and cardiovascular (arterial pressure and heart rate) responses to an intra-POA PGE2 microinjection. Further immunohistochemical observations revealed a close association of POA-derived GABAergic axon swellings with DMH neurons projecting to the medullary raphe regions where sympathetic premotor neurons for febrile and thermoregulatory responses are localized. These results suggest that a direct projection of EP3 receptor-expressing POA neurons to the DMH/DH region mediates febrile responses via a GABAergic mechanism.

Adipose Tissue, Brown↗
PubMed2005

Ablation of MEKK4 kinase activity causes neurulation and skeletal patterning defects in the mouse embryo.

Skeletal disorders and neural tube closure defects represent clinically significant human malformations. The signaling networks regulating normal skeletal patterning and neurulation are largely unknown. Targeted mutation of the active site lysine of MEK kinase 4 (MEKK4) produces a kinase-inactive MEKK4 protein (MEKK4(K1361R)). Embryos homozygous for this mutation die at birth as a result of skeletal malformations and neural tube defects. Hindbrains of exencephalic MEKK4(K1361R) embryos show a striking increase in neuroepithelial cell apoptosis and a dramatic loss of phosphorylation of MKK3 and -6, mitogen-activated protein kinase kinases (MKKs) regulated by MEKK4 in the p38 pathway. Phosphorylation of MAPK-activated protein kinase 2, a p38 substrate, is also inhibited, demonstrating a loss of p38 activity in MEKK4(K1361R) embryos. In contrast, the MEK1/2-extracellular signal-regulated kinase 1 (ERK1)/ERK2 and MKK4-Jun N-terminal protein kinase pathways were unaffected. The p38 pathway has been shown to regulate the phosphorylation and expression of the small heat shock protein HSP27. Compared to the wild type, MEKK4(K1361R) fibroblasts showed significantly reduced phosphorylation of p38 and HSP27, with a corresponding heat shock-induced instability of the actin cytoskeleton. Together, these data demonstrate MEKK4 regulation of p38 and that substrates downstream of p38 control cellular homeostasis. The findings are the first demonstration that MEKK4-regulated p38 activity is critical for neurulation.

Animals↗
PubMed2005

A case of adolescent primary adrenal natural killer cell lymphoma.

Primary adrenal lymphoma is uncommon, and the majority cases of this disorder are found in elderly individuals. We describe a 17-year-old boy with persistent fever, hemophagocytic lymphohistiocytosis, and a bilateral tumor of the adrenal glands. The disease was progressive and did not respond to treatment such as immunosuppression therapy or plasma exchange. Postmortem analysis revealed nasal-type natural killer cell lymphoma in association with Epstein-Barr virus infection. To our knowledge, this case is the first of primary adrenal lymphoma with the natural killer cell phenotype to be reported. The characterization of this unusual case should be included in the differential diagnosis of adrenal gland tumors.

Adolescent↗
PubMed2005

A method for measuring the decay time of hyperpolarized 129Xe magnetization in rat brain without estimation of RF flip angles.

PURPOSE: The decay time of hyperpolarized 129Xe in brain tissue depends on the cerebral blood flow (CBF) as well as the longitudinal relaxation time in the tissue (T(1,tissue)). Therefore, the decay time is an important parameter for investigating the potential of Xe for cerebral studies. Previous attempts to measure the decay time have been performed after correction of the MR signal for the costheta decay induced by multiple radiofrequency (RF) excitation pulses. However, since this method requires accurate knowledge of the RF pulse flip angle, the use of a surface coil is restricted because of its nonuniform RF power, distribution. We present a two-pulse protocol for estimating the decay time without the need for flip-angle estimation and demonstrate it in the rat brain. METHOD: After rat inhalation of hyperpolarized Xe, two MR spectra of the rat head were obtained at various delay times (4-16 s) and the logarithmic ratio of the two amplitudes was calculated. The decay time was obtained from the slope of the logarithmic ratio against the delay time. The MR measurements were performed with a 4.7T imaging spectrometer with a surface coil located over the head of the anesthetized rat. The gas (25 cc) was smoothly introduced to the lung for 40 s before each measurement began. RESULT: From 18 experiments on 11 rats, the decay time was estimated to be 17.7+/-1.9 s. DISCUSSION: Assuming a normal rat CBF value, T(1,tissue) can be estimated from the decay time to be 26+/-4 s.

Administration, Inhalation↗
PubMed2005

[The advantage of our original straight cannula for tracheostoma].

Patients with head and neck cancers often require use of a tracheal cannula due to stenosis of the permanent tracheostoma following total laryngectomy. However, a cannula that is designed for a multi-purpose tracheotomy frequently presents a problem, when placed in a permanent tracheostoma. To resolve this difficulty, we developed a straight cannula that fits most permanent tracheostomas. We achieved a straight design by removing the curvature of a cuffed tracheostomy single cannula (size 12: Koken Co., Ltd.). To facilitate installation by the patient without assistance, silicone was used because it is softer than similar conventional products. By making the cannula diameter slightly larger, immobilization with a strap is lomger needed. Our cannula was used in 14 patients following surgery for the laryngeal, hypopharyngel, esophageal carcinomas. The cannula fit well and reduced the respiratory discomfort in all patients.

Aged↗
PubMed2005

A comparison of the defective granulopoiesis in childhood cyclic neutropenia and in severe congenital neutropenia.

BACKGROUND AND OBJECTIVES: Cyclic neutropenia (CyN) in childhood and severe congenital neutropenia (SCN) are congenital disorders that cause chronic neutropenia. Mutations in the neutrophil elastase gene, ELA2, have been reported in patients with CyN and in those with SCN. We examined granulopoietic defects in CyN patients with those in SCN patients. DESIGN AND METHODS: Three patients with CyN and four with SCN were enrolled in this study. Bone marrow cells were enriched based on the expression of CD34, Kit, and granulocyte colony-stimulating factor receptor (G-CSFR). The purified cells were assayed for colony formation, proliferation, and mRNA expression of granular enzymes. RESULTS: All patients showed heterozygous mutations of ELA2. Flow cytometric analysis demonstrated no differences in the frequency of CD34, Kit, and G-CSFR expression between CyN patients and normal subjects. Significant differences in granulocyte/macrophage (GM)-colony formation of CD34(+)/Kit(+) cells were observed among CyN patients, SCN patients, and normal subjects in response to hematopoietic factors. Impaired granulopoiesis was found in both CD34(+)/Kit(+)/G-CSFR(+) and CD34(+)/Kit(+)/G-CSFR- cells in patients with CyN, whereas this impairment was observed only in CD34(+)/Kit(+)/G-CSFR(+) cells in SCN patients, as previously reported. The mRNA expression of granular enzymes in myeloid precursors and the transcription levels during myeloid cell differentiation in CyN patients were comparable to those in normal subjects, in contrast to the abnormal transcription of granular enzymes in SCN patients. INTERPRETATION AND CONCLUSIONS: These results suggest that the underlying granulopoietic abnormalities differ between CyN and SCN, and emphasize the presence of additional genetic pathophysiology specific to each disease.

Agranulocytosis↗
PubMed2005

[A 60-year-old man with intention tremor as an initial symptom followed by cerebellar ataxia, peripheral neuropathy and dementia].

We report a 60-year-old man with a 6-year history of tremor in his hands. He noted the onset of short of breath and gait disturbance in 1994; both of these symptoms were slowly progressive. Then recently he developed fever two months prior to the present admission. He was admitted to the rheumatology department of our hospital and neurological consultation was asked on December 13, 2000. On neurologic examination, he showed Gottron sign and fine crackle in both lungs. Pertinent neurological findings were bilateral dysmetria in finger-to-nose and heel-to-knee tests and a broad-based gait. In addition, he showed intention tremor in upper extremities more on the left. Romberg sign was positive. Deep tendon reflexes were decreased. Vibratory sensation was reduced at the wrists. The patient's hemoglobin was 11.1 g/dl, with a mean corpuscular volume of 92.0 fl. Vitamin B12 level was 190 (reference range, >230 pg/ml). Serum lactic acid, pyruvic acid and ceruloplasmin were slightly elevated. Chest X-ray showed interstitial pneumonia. Muscle biopsy showed grouping of small angular fiber. Brain MRI showed diffuse atrophy of the cerebral cortex and the cerebellum hemisphere. Thalamotomy did not improve his tremor. He was admitted again in November 2001. General worsening of his neurological findings was observed. IL2-receptor was markedly elevated. Serum anti-Hu, Yo and Ri antibodies were negative. An anaplastic carcinoma was found in his jejunum. He died from respiratory failure in February 2002. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had paraneoplastic syndrome. Other diagnosis entertained included MERRF, GSS, Ramsay Hunt syndrome, subacute combined degeneration, spinocerebellar degeneration. Majority of the participants thought that paraneoplastic syndrome was most likely. Post-mortem examination revealed poorly differentiated carcinoma in the small intestine. Myeline pallor was noted in the posterior and the lateral columns in the thoracic spine. Neuronal cell loss was observed in the Purkinje cell and granular cell layer in the cerebellum. Sural nerve demonstrated loss of myelinated fibers and grouping of small fibers. Neuropathological findings were consistent with Friedreich ataxia; nevertheless, no mutation was reported in frataxin in Japan. The neuropathologist concluded that neuropathological diagnosis was a spinocerebellar ataxia with neuropathological similarities to Friedreich ataxia.

Aged↗
PubMed2005

[A 54-year-old man with familial parkinsonism, gaze palsy, and dementia].

We report a Japanese man with familial parkinsonism who died at age 54. His younger brother, his mother, the mother's 4 brothers, and their mother were also affected with similar parkinsonism. The patient had had nystagmus since adolescence. He noticed difficulty in walking and micrographia at age 42. Neurological examination at age 45 in our hospital revealed pendular nystagmus, moderate rigidity in his neck and upper limbs, postural tremor in hands and shuffling gait. He received L-dopa/benzerazide 200 mg and his movement was mildly improved. Then he developed forced closing of eyelids suggesting either blepharospasms or apraxia of eye lid opening. He became apathetic at age 48. He was admitted to our hospital at age 49. On admission, he showed mild dementia and sexually disinhibited behaviours. Moderate downward gaze palsy and rigidity were seen. Increase of L-dopa/benzerazide and pergolide did not improve his parkinsonism and his disinhibited behaviors became worse. L-dopa/benzerazide and pergolide were decreased and he received electroconvulsive therapy at a psychiatric hospital with temporally improvement in his movement. He became unable to walk at age 52 and he was mutic and bedridden. He died of pneumonia at age 54. The patient was discussed in a neurological CPC, and a chief discussant arrived at the conclusion that the patient had a familial form of dementia with Lewy bodies. Many participants thought that he had frontotemporal dementia and parkinsonism linked to chromosome 17. The pathological examination of his brain showed severe neuronal loss in the substantia nigra, subthalamus, and pallidum. Ballooned neurons were observed in the cerebral cortex. Immunohistochemistry using anti-tau antibodies revealed tau-positive neurons, glial cells and threads in the cerebral cortex, white matter and subcortical nuclei; these tau deposition reacted with an anti-4-repeat tau antibody, but not reacted to an anti-3-repeat tau antibody. Sequencing of genomic DNA of the patient showed a missense mutation in exon 10 of tau that caused a substitution at codon N279K. These neuropathological and molecular studies revealed the diagnosis of the patient was FTDP-17 with N279K mutation.

Dementia↗
PubMed2005

Studies on the amount of aluminum and calcium in urine following aluminum administration with and without amino acids.

The evidence implicating aluminum as a neurotoxin is mounting. Research with animals and humans has linked aluminum with neuro-cognitive dysfunction and, in some cases, death. Although the relationship between aluminum intake and Alzheimer's disease is still unclear, some experts have recently issued a strong warning that human exposure to aluminum should be limited. The results indicate that the amount of aluminum decreased in the urine in mice that were administered glycine or glutamic acid together with aluminum ion. In the mice in which the amounts of aluminum decreased in the urine, the amount of calcium conversely increased.

Aluminum↗
PubMed2004

Dissection of the role of MHC class II A and E genes in autoimmune susceptibility in murine lupus models with intragenic recombination.

Systemic lupus erythematosus (SLE) is a multigenic autoimmune disease, and the major histocompatibility complex (MHC) class II polymorphism serves as a key genetic element. In SLE-prone (NZB x NZW)F(1) mice, the MHC H-2(d/z) heterozygosity (H-2(d) of NZB and H-2(z) of NZW) has a strong impact on disease; thus, congenic H-2(d/d) homozygous F(1) mice do not develop severe disease. In this study, we used Ea-deficient intra-H-2 recombination to establish A(d/d)-congenic (NZB x NZW)F(1) mice, with or without E molecule expression, and dissected the role of class II A and E molecules. Here we found that A(d/d) homozygous F(1) mice lacking E molecules developed severe SLE similar to that seen in wild-type F1 mice, including lupus nephritis, autoantibody production, and spontaneously occurring T cell activation. Additional evidence revealed that E molecules prevent the disease in a dose-dependent manner; however, the effect is greatly influenced by the haplotype of A molecules, because wild-type H-2(d/z) F(1) mice develop SLE, despite E molecule expression. Studies on the potential of dendritic cells to present a self-antigen chromatin indicated that dendritic cells from wild-type F(1) mice induced a greater response of chromatin-specific T cells than did those from A(d/d) F(1) mice, irrespective of the presence or absence of E molecules, suggesting that the self-antigen presentation is mediated by A, but not by E, molecules. Our mouse models are useful for analyzing the molecular mechanisms by which MHC class II regions regulate the process of autoimmune responses.

Animals↗
PubMed2004

Activation of EP4 receptors contributes to prostaglandin E2-mediated stimulation of renal sensory nerves.

Induction of cyclooxygenase-2 (COX-2) in the renal pelvic wall increases prostaglandin E(2) (PGE(2)) leading to stimulation of cAMP production, which results in substance P (SP) release and activation of renal mechanosensory nerves. The subtype of PGE receptors involved, EP2 and/or EP4, was studied by immunohistochemistry and renal pelvic administration of agonists and antagonists of EP2 and EP4 receptors. EP4 receptor-like immunoreactivity (LI) was colocalized with calcitonin gene-related peptide (CGRP)-LI in dorsal root ganglia (DRGs) at Th(9)-L(1) and in nerve terminals in the renal pelvic wall. Th(9)-L(1) DRG neurons also contained EP3 receptor-LI and COX-2-LI, each of which was colocalized with CGRP-LI in some neurons. No renal pelvic nerves contained EP3 receptor-LI and only very few nerves COX-2-LI. The EP1/EP2 receptor antagonist AH-6809 (20 microM) had no effect on SP release produced by PGE(2) (0.14 microM) from an isolated rat renal pelvic wall preparation. However, the EP4 receptor antagonist L-161,982 (10 microM) blocked the SP release produced by the EP2/EP4 receptor agonist butaprost (10 microM) 12 +/- 2 vs. 2 +/- 1 and PGE(2), 9 +/- 1 vs. 1 +/- 0 pg/min. The SP release by butaprost and PGE(2) was similarly blocked by the EP4 receptor antagonist AH-23848 (30 microM). In anesthetized rats, the afferent renal nerve activity (ARNA) responses to butaprost 700 +/- 100 and PGE(2).780 +/- 100%.s (area under the curve of ARNA vs. time) were unaffected by renal pelvic perfusion with AH-6809. However, 1 microM L-161,982 and 10 microM AH-23848 blocked the ARNA responses to butaprost by 94 +/- 5 and 78 +/- 10%, respectively, and to PGE(2) by 74 +/- 16 and 74 +/- 11%, respectively. L-161,982 also blocked the ARNA response to increasing renal pelvic pressure 10 mmHg, 85 +/- 5%. In conclusion, PGE(2) increases renal pelvic release of SP and ARNA by activating EP4 receptors on renal sensory nerve fibers.

Afferent Pathways↗
PubMed2004

Identification of sympathetic premotor neurons in medullary raphe regions mediating fever and other thermoregulatory functions.

Sympathetic premotor neurons directly control sympathetic preganglionic neurons (SPNs) in the intermediolateral cell column (IML) of the thoracic spinal cord, and many of these premotor neurons are localized in the medulla oblongata. The rostral ventrolateral medulla contains premotor neurons controlling the cardiovascular conditions, whereas rostral medullary raphe regions are a candidate source of sympathetic premotor neurons for thermoregulatory functions. Here, we show that these medullary raphe regions contain putative glutamatergic neurons and that these neurons directly control thermoregulatory SPNs. Neurons expressing vesicular glutamate transporter 3 (VGLUT3) were distributed in the rat medullary raphe regions, including the raphe magnus and rostral raphe pallidus nuclei, and mostly lacked serotonin immunoreactivity. These VGLUT3-positive neurons expressed Fos in response to cold exposure or to central administration of prostaglandin E2, a pyrogenic mediator. Transneuronal retrograde labeling after inoculation of pseudorabies virus into the interscapular brown adipose tissue (BAT) or the tail indicated that those VGLUT3-expressing medullary raphe neurons innervated these thermoregulatory effector organs multisynaptically through SPNs of specific thoracic segments, and microinjection of glutamate into the IML of the BAT-controlling segments produced BAT thermogenesis. An anterograde tracing study further showed a direct projection of those VGLUT3-expressing medullary raphe neurons to the dendrites of SPNs. Furthermore, intra-IML application of glutamate receptor antagonists blocked BAT thermogenesis triggered by disinhibition of the medullary raphe regions. The present results suggest that VGLUT3-expressing neurons in the medullary raphe regions constitute excitatory neurons that could be categorized as a novel group of sympathetic premotor neurons for thermoregulatory functions, including fever.

Adipose Tissue, Brown↗
PubMed2004

Conditional activation of RhoA suppresses the epithelial to mesenchymal transition at the primitive streak during mouse gastrulation.

Gastrulation is a pivotal event of mouse early embryogenesis. In telencephalin (TLCN)-Cre mice carrying the Cre recombinase gene inserted into the translational initiation site of the TLCN gene, Cre-mediated recombination took place at the postimplantation stage. To examine the role of RhoA signaling in early embryogenesis, we produced Rho36 mice carrying constitutively active RhoA(G14V) gene inducible by Cre recombinase and crossed with TLCN-Cre mice. In doubly transgenic embryos at the gastrulation stage, there appeared an abnormal bulge of cells protruded from the primitive streak region into the amniotic cavity. The bulged cell mass expressed the epiblast marker gene Oct3 and E-cadherin, but not the primitive streak marker gene T except for the basal portion. These results suggest that the conditional activation of RhoA signaling suppressed the epithelial to mesenchymal transition at the primitive streak during mouse gastrulation.

Allantois↗
PubMed2004

Chemically specific circuit composed of vesicular glutamate transporter 3- and preprotachykinin B-producing interneurons in the rat neocortex.

The third vesicular glutamate transporter, VGLUT3, is distributed in cell bodies of neocortical neurons and axon terminals mainly in the superficial part of layer II/III of the cerebral cortex. We examined the chemical characteristics of VGLUT3-expressing neurons by immunohistochemistry in the rat neocortex. Since the vast majority of VGLUT3-immunoreactive neurons showed immunoreactivities for GABA, preprotachykinin B (PPTB) and cholecystokinin, VGLUT3-immunoreactive neocortical neurons were considered to constitute a subgroup of GABAergic interneurons. VGLUT3-immunoreactive axon terminals were immunopositive for either vesicular GABA transporter (VGAT) or serotonin. These results together with anterograde tracer injection and chemical lesion experiments in the dorsal and median raphe nuclei revealed that the neocortex contains at least two kinds of VGLUT3-laden axon terminals: one is serotonergic and derived from the raphe nuclei, and the other is GABAergic and intrinsic in the neocortex. Furthermore, many VGLUT3/VGAT-immunoreactive terminals formed axon baskets and made axosomatic symmetric synapses on neocortical neurons, most of which were immunoreactive for PPTB. VGLUT3-immunopositive axon baskets surrounded about a half of PPTB-positive and almost all VGLUT3-positive neurons. Thus, VGLUT3-expressing GABAergic interneurons form a chemically specific circuit within the PPTB-producing interneuron group and it is likely that glutamate is used within the chemically specific circuit.

Amino Acid Transport Systems, Acidic↗