scholarly journals Distribution of Vesicular Glutamate Transporter-2 Messenger Ribonucleic Acid and Protein in the Septum-Hypothalamus of the Rat

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 662-670 ◽  
Author(s):  
Winston Lin ◽  
Kyle McKinney ◽  
Liansheng Liu ◽  
Shruti Lakhlani ◽  
Lothar Jennes
Keyword(s):  
Glutamate Transporter ◽  
Brain Regions ◽  
Female Rats ◽  
Vesicular Glutamate Transporter ◽  
Excitatory Neurotransmitter ◽  
Adrenal Steroid ◽  
Messenger Ribonucleic Acid ◽  
Glutamatergic Neurons ◽  
Neurotransmitter Glutamate ◽  
Arcuate Nuclei

The excitatory neurotransmitter glutamate is involved in the control of most, perhaps all, neuroendocrine systems, yet the sites of glutamatergic neurons and their processes are unknown. Here, we used in situ hybridization and immunohistochemistry for the neuron-specific vesicular glutamate transporter-2 (VGLUT2) to identify the neurons in female rats that synthesize the neurotransmitter glutamate as well as their projections throughout the septum-hypothalamus. The results show that glutamatergic neurons are present in the septum-diagonal band complex and throughout the hypothalamus. The preoptic area and ventromedial and dorsomedial nuclei are particularly rich in glutamatergic neurons, followed by the supraoptic, paraventricular, and arcuate nuclei, whereas the suprachiasmatic nucleus does not express detectable amounts of VGLUT2 mRNA. Immunoreactive neurites are seen in very high densities in all regions analyzed, particularly in the preoptic region, followed by the ventromedial, dorsomedial, and arcuate nuclei as well as the external layer of the median eminence, whereas the mammillary complex does not exhibit VGLUT2 immunoreactivity. Many VGLUT2 immunoreactive fibers also contained synaptophysin, suggesting that the transporter is indeed localized to presynaptic terminals. Together, the results identify glutamatergic cell bodies throughout the septum-hypothalamus in region-specific patterns and show that glutamatergic nerve terminals are present in very large numbers such that most neurons in these brain regions can receive glutamatergic input. We examined the GnRH system as an example of a typical neuroendocrine system and could show that the GnRH perikarya are closely apposed by many VGLUT2-immunoreactive boutons, some of which also contained synaptophysin. The presence of VGLUT2 mRNA-containing cells in specific nuclei of the hypothalamus indicates that many neuroendocrine neurons coexpress glutamate as neurotransmitter, in addition to neuropeptides. These systems include the oxytocin, vasopressin, or CRH neurons as well as many others in the periventricular and mediobasal hypothalamus. The presence of VGLUT2 mRNA in steroid-sensitive regions of the hypothalamus, such as the anteroventral periventricular, paraventricular, or ventromedial nuclei indicates that gonadal and adrenal steroid can directly alter the functions of these glutamatergic neurons.

scholarly journals The Existence of a Second Vesicular Glutamate Transporter Specifies Subpopulations of Glutamatergic Neurons

2001 ◽  
Vol 21 (22) ◽  
pp. RC181-RC181 ◽  
Author(s):  
Etienne Herzog ◽  
Gian Carlo Bellenchi ◽  
Christelle Gras ◽  
Véronique Bernard ◽  
Philippe Ravassard ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter ◽  
Glutamatergic Neurons

scholarly journals Expression of Vesicular Glutamate Transporter 2 (vGluT2) on Large Dense-Core Vesicles within GnRH Neuroterminals of Aging Female Rats

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0129633 ◽  
Author(s):  
Weiling Yin ◽  
Zengrong Sun ◽  
John M. Mendenhall ◽  
Deena M. Walker ◽  
Penny D. Riha ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Dense Core ◽  
Female Rats ◽  
Vesicular Glutamate Transporter ◽  
Dense Core Vesicles ◽  
Large Dense Core Vesicles

scholarly journals Glutamatergic and GABAergic Innervation of Human Gonadotropin-Releasing Hormone-I Neurons

Endocrinology ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2766-2776 ◽  
Author(s):  
Erik Hrabovszky ◽  
Csilla S. Molnár ◽  
Róbert Nagy ◽  
Barbara Vida ◽  
Beáta Á. Borsay ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter ◽  
Glutamatergic Neurons ◽  
Relative Contribution ◽  
Paraventricular Nuclei ◽  
Gnrh Neurons ◽  
Immunohistochemical Studies ◽  
Dual Label ◽  
Formalin Fixed ◽  
Afferent Control

Amino acid (aa) neurotransmitters in synaptic afferents to hypothalamic GnRH-I neurons are critically involved in the neuroendocrine control of reproduction. Although in rodents the major aa neurotransmitter in these afferents is γ-aminobutyric acid (GABA), glutamatergic axons also innervate GnRH neurons directly. Our aim with the present study was to address the relative contribution of GABAergic and glutamatergic axons to the afferent control of human GnRH neurons. Formalin-fixed hypothalamic samples were obtained from adult male individuals (n = 8) at autopsies, and their coronal sections processed for dual-label immunohistochemical studies. GABAergic axons were labeled with vesicular inhibitory aa transporter antibodies, whereas glutamatergic axons were detected with antisera against the major vesicular glutamate transporter (VGLUT) isoforms, VGLUT1 and VGLUT2. The relative incidences of GABAergic and glutamatergic axonal appositions to GnRH-immunoreactive neurons were compared quantitatively in two regions, the infundibular and paraventricular nuclei. Results showed that GABAergic axons established the most frequently encountered type of axo-somatic apposition. Glutamatergic contacts occurred in significantly lower numbers, with similar contributions by their VGLUT1 and VGLUT2 subclasses. The innervation pattern was different on GnRH dendrites where the combined incidence of glutamatergic (VGLUT1 + VGLUT2) contacts slightly exceeded that of the GABAergic appositions. We conclude that GABA represents the major aa neurotransmitter in axo-somatic afferents to human GnRH neurons, whereas glutamatergic inputs occur somewhat more frequently than GABAergic inputs on GnRH dendrites. Unlike in rats, the GnRH system of the human receives innervation from the VGLUT1, in addition to the VGLUT2, subclass of glutamatergic neurons.

scholarly journals Impaired EAT-4 Vesicular Glutamate Transporter Leads to Defective Nocifensive Response of Caenorhabditis elegans to Noxious Heat

2019 ◽  
Author(s):  
Sophie Leonelli ◽  
Bruno Nkambeu ◽  
Francis Beaudry
Keyword(s):  
Glutamate Receptors ◽  
Glutamate Transporter ◽  
Mechanical Stimuli ◽  
Pain Sensation ◽  
Noxious Heat ◽  
Excitatory Neurotransmitter ◽  
Glutamate Signaling ◽  
C Elegans ◽  
Avoidance Behaviors ◽  
Neurotransmitter Glutamate

AbstractIn mammals, glutamate is an important excitatory neurotransmitter. Glutamate and glutamate receptors are found in areas specifically involved in pain sensation, transmission and transduction such as peripheral nervous system, spinal cord and brain. In C. elegans, several studies have suggested glutamate pathways are associated with withdrawal responses to mechanical stimuli and to chemical repellents. However, few evidences demonstrate that glutamate pathways are important to mediate nocifensive response to noxious heat. The thermal avoidance behavior of C. elegans was studied and results illustrated that mutants of glutamate receptors (glr-1, glr-2, nmr-1, nmr-2) behaviors was not affected. However, results revealed that all strains of eat-4 mutants, C. elegans vesicular glutamate transporters, displayed defective thermal avoidance behaviors. Due to the interplay between the glutamate and the FLP-18/FLP-21/NPR-1 pathways, we analyzed the effectors FLP-18 and FLP-21 at the protein level, we did not observebiologically significant differences compared to N2 (WT) strain (fold-change < 2) except for the IK602 strain. The data presented in this manuscript reveals that glutamate signaling pathways are essential to elicit a nocifensive response to noxious heat in C. elegans.

scholarly journals Elimination of glutamatergic transmission from Hb9 interneurons does not impact treadmill locomotion

2021 ◽  
Author(s):  
Lina M. Koronfel ◽  
Kevin C. Kanning ◽  
Angelita Alcos ◽  
Christopher E. Henderson ◽  
Robert M. Brownstone
Keyword(s):  
Motor Neurons ◽  
Neural Circuits ◽  
Glutamate Transporter ◽  
Homeobox Gene ◽  
Vesicular Glutamate Transporter ◽  
Glutamatergic Neurotransmission ◽  
Glutamatergic Transmission ◽  
Glutamatergic Neurons ◽  
Treadmill Locomotion

ABSTRACTThe spinal cord contains neural circuits that can produce the rhythm and pattern of locomotor activity. It has previously been postulated that a rhythmogenic population of glutamatergic neurons, termed Hb9 interneurons, contributes to this rhythmogenesis. The homeobox gene, Hb9, is expressed in these interneurons as well as motor neurons. We developed a mouse line in which cre recombinase activity is inducible in neurons expressing Hb9. We then used this line to eliminate vesicular glutamate transporter 2 from Hb9 interneurons, and found that there were no deficits in treadmill locomotion. We conclude that glutamatergic neurotransmission by Hb9 interneurons is not required for locomotor rhythmogenesis. The role of these neurons in neural circuits remains elusive.

scholarly journals Elimination of Glutamatergic Transmission From Hb9 Interneurons Does Not Impact Treadmill Locomotion

2021 ◽  
Author(s):  
Lina M Koronfel ◽  
Kevin C Kanning ◽  
Angelita Alcos ◽  
Christopher E Henderson ◽  
Robert M Brownstone
Keyword(s):  
Motor Neurons ◽  
Neural Circuits ◽  
Glutamate Transporter ◽  
Homeobox Gene ◽  
Vesicular Glutamate Transporter ◽  
Glutamatergic Neurotransmission ◽  
Glutamatergic Transmission ◽  
Glutamatergic Neurons ◽  
Treadmill Locomotion

Abstract The spinal cord contains neural circuits that can produce the rhythm and pattern of locomotor activity. It has previously been postulated that a rhythmogenic population of glutamatergic neurons, termed Hb9 interneurons, contributes to this rhythmogenesis. The homeobox gene, Hb9, is expressed in these interneurons as well as motor neurons. We developed a mouse line in which cre recombinase activity is inducible in neurons expressing Hb9. We then used this line to eliminate vesicular glutamate transporter 2 from Hb9 interneurons, and found that there were no deficits in treadmill locomotion. We conclude that glutamatergic neurotransmission by Hb9 interneurons is not required for locomotor rhythmogenesis. The role of these neurons in neural circuits remains elusive.

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