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Thirst Is Associated with Suppression of Habenula Output and Active Stress Coping: Is there a Role for a Non-canonical Vasopressin-Glutamate Pathway?

Zhang L, Hernández VS, Vázquez-Juárez E, Chay FK, Barrio RA - Front Neural Circuits (2016)

Bottom Line: We demonstrate a direct pathway from hypothalamic paraventricular VP-expressing, glutamatergic magnocellular neurons to the medial division of lateral habenula (LHbM), a region containing GABAergic neurons.In vivo recording and juxtacellular labeling revealed that GABAergic neurons in the LHbM had locally branching axons, and received VP-positive axon terminal contacts on their dendrites.Our results reveal a novel VP-expressing hypothalamus to the LHbM circuit that is likely to evoke GABA-mediated inhibition in the LHbM, which promotes escape behavior during stress coping.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México Ciudad de México, Mexico.

ABSTRACT
Water-homeostasis is a fundamental physiological process for terrestrial life. In vertebrates, thirst drives water intake, but the neuronal circuits that connect the physiology of water regulation with emotional context are poorly understood. Vasopressin (VP) is a prominent messenger in this circuit, as well as L-glutamate. We have investigated the role of a VP circuit and interaction between thirst and motivational behaviors evoked by life-threatening stimuli in rats. We demonstrate a direct pathway from hypothalamic paraventricular VP-expressing, glutamatergic magnocellular neurons to the medial division of lateral habenula (LHbM), a region containing GABAergic neurons. In vivo recording and juxtacellular labeling revealed that GABAergic neurons in the LHbM had locally branching axons, and received VP-positive axon terminal contacts on their dendrites. Water deprivation significantly reduced freezing and immobility behaviors evoked by innate fear and behavioral despair, respectively, accompanied by decreased Fos expression in the lateral habenula. Our results reveal a novel VP-expressing hypothalamus to the LHbM circuit that is likely to evoke GABA-mediated inhibition in the LHbM, which promotes escape behavior during stress coping.

No MeSH data available.


Related in: MedlinePlus

Most AVP+ axon terminals co-expressed vesicular glutamate transporter 2 (vGluT2) and established Gray type I synapses onto habenular neuron's dendrites. (A,B) Representative confocal photomicrographs of double immunofluorescence AVP (red) and vGluT2 (green) centered at the medio-central lateral habenular (LHbMC) subnucleus. Double arrowheads indicate the double-labeled axon terminals. (C,D) Electron microscopy photomicrographs showing the AVP+ dense core vesicles (dcv, thin white arrows) inside the axon terminals (AT) established Gray type I synapse (post-synaptic densities, PSD, were indicated with black arrowheads) onto habenular neuron's dendrites (dend). Asterisks are put adjacent to AVP+ dcv, which showed docking onto presynaptic membranes. Scale bars: A: 50 μm; B: 5 μm, C, D: 500 nm.
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Figure 2: Most AVP+ axon terminals co-expressed vesicular glutamate transporter 2 (vGluT2) and established Gray type I synapses onto habenular neuron's dendrites. (A,B) Representative confocal photomicrographs of double immunofluorescence AVP (red) and vGluT2 (green) centered at the medio-central lateral habenular (LHbMC) subnucleus. Double arrowheads indicate the double-labeled axon terminals. (C,D) Electron microscopy photomicrographs showing the AVP+ dense core vesicles (dcv, thin white arrows) inside the axon terminals (AT) established Gray type I synapse (post-synaptic densities, PSD, were indicated with black arrowheads) onto habenular neuron's dendrites (dend). Asterisks are put adjacent to AVP+ dcv, which showed docking onto presynaptic membranes. Scale bars: A: 50 μm; B: 5 μm, C, D: 500 nm.

Mentions: Vesicular glutamate transporter 2 (vGluT2 belongs to a family of three vesicular glutamate transporters (vGluT1, vGluT2, and vGluT3). The vGluT2 is the subtype expressed in the hypothalamic neuroendocrine magnocells and exhibit robust up-regulation in response to certain homeostatic challenges (Ziegler et al., 2002; Hrabovszky and Liposits, 2007, 2008). Using double immunofluorescence and confocal microscopy, we have observed that most of the VP+ axon terminals co-expressed vGluT2 (Figures 2A,B). At the level of electron microscopy, we found that VP containing axon terminals in the LHbMC region established Gray type I (asymmetric) synapses (10:10, n:N) onto dendrites of habenular neurons (Figures 2C,D). Interestingly, some VP+ dense core vesicles (dcv) were found in co-storage in the active zone, adjacent to the presynaptic membranes and some seemed to be docked onto the presynaptic membrane (Figures 2C,D asterisks).


Thirst Is Associated with Suppression of Habenula Output and Active Stress Coping: Is there a Role for a Non-canonical Vasopressin-Glutamate Pathway?

Zhang L, Hernández VS, Vázquez-Juárez E, Chay FK, Barrio RA - Front Neural Circuits (2016)

Most AVP+ axon terminals co-expressed vesicular glutamate transporter 2 (vGluT2) and established Gray type I synapses onto habenular neuron's dendrites. (A,B) Representative confocal photomicrographs of double immunofluorescence AVP (red) and vGluT2 (green) centered at the medio-central lateral habenular (LHbMC) subnucleus. Double arrowheads indicate the double-labeled axon terminals. (C,D) Electron microscopy photomicrographs showing the AVP+ dense core vesicles (dcv, thin white arrows) inside the axon terminals (AT) established Gray type I synapse (post-synaptic densities, PSD, were indicated with black arrowheads) onto habenular neuron's dendrites (dend). Asterisks are put adjacent to AVP+ dcv, which showed docking onto presynaptic membranes. Scale bars: A: 50 μm; B: 5 μm, C, D: 500 nm.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4814529&req=5

Figure 2: Most AVP+ axon terminals co-expressed vesicular glutamate transporter 2 (vGluT2) and established Gray type I synapses onto habenular neuron's dendrites. (A,B) Representative confocal photomicrographs of double immunofluorescence AVP (red) and vGluT2 (green) centered at the medio-central lateral habenular (LHbMC) subnucleus. Double arrowheads indicate the double-labeled axon terminals. (C,D) Electron microscopy photomicrographs showing the AVP+ dense core vesicles (dcv, thin white arrows) inside the axon terminals (AT) established Gray type I synapse (post-synaptic densities, PSD, were indicated with black arrowheads) onto habenular neuron's dendrites (dend). Asterisks are put adjacent to AVP+ dcv, which showed docking onto presynaptic membranes. Scale bars: A: 50 μm; B: 5 μm, C, D: 500 nm.
Mentions: Vesicular glutamate transporter 2 (vGluT2 belongs to a family of three vesicular glutamate transporters (vGluT1, vGluT2, and vGluT3). The vGluT2 is the subtype expressed in the hypothalamic neuroendocrine magnocells and exhibit robust up-regulation in response to certain homeostatic challenges (Ziegler et al., 2002; Hrabovszky and Liposits, 2007, 2008). Using double immunofluorescence and confocal microscopy, we have observed that most of the VP+ axon terminals co-expressed vGluT2 (Figures 2A,B). At the level of electron microscopy, we found that VP containing axon terminals in the LHbMC region established Gray type I (asymmetric) synapses (10:10, n:N) onto dendrites of habenular neurons (Figures 2C,D). Interestingly, some VP+ dense core vesicles (dcv) were found in co-storage in the active zone, adjacent to the presynaptic membranes and some seemed to be docked onto the presynaptic membrane (Figures 2C,D asterisks).

Bottom Line: We demonstrate a direct pathway from hypothalamic paraventricular VP-expressing, glutamatergic magnocellular neurons to the medial division of lateral habenula (LHbM), a region containing GABAergic neurons.In vivo recording and juxtacellular labeling revealed that GABAergic neurons in the LHbM had locally branching axons, and received VP-positive axon terminal contacts on their dendrites.Our results reveal a novel VP-expressing hypothalamus to the LHbM circuit that is likely to evoke GABA-mediated inhibition in the LHbM, which promotes escape behavior during stress coping.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México Ciudad de México, Mexico.

ABSTRACT
Water-homeostasis is a fundamental physiological process for terrestrial life. In vertebrates, thirst drives water intake, but the neuronal circuits that connect the physiology of water regulation with emotional context are poorly understood. Vasopressin (VP) is a prominent messenger in this circuit, as well as L-glutamate. We have investigated the role of a VP circuit and interaction between thirst and motivational behaviors evoked by life-threatening stimuli in rats. We demonstrate a direct pathway from hypothalamic paraventricular VP-expressing, glutamatergic magnocellular neurons to the medial division of lateral habenula (LHbM), a region containing GABAergic neurons. In vivo recording and juxtacellular labeling revealed that GABAergic neurons in the LHbM had locally branching axons, and received VP-positive axon terminal contacts on their dendrites. Water deprivation significantly reduced freezing and immobility behaviors evoked by innate fear and behavioral despair, respectively, accompanied by decreased Fos expression in the lateral habenula. Our results reveal a novel VP-expressing hypothalamus to the LHbM circuit that is likely to evoke GABA-mediated inhibition in the LHbM, which promotes escape behavior during stress coping.

No MeSH data available.


Related in: MedlinePlus