Suppression of ventral hippocampal CA1 pyramidal neuronal activities enhances water intake

2021 ◽  
Author(s):  
Bingxuan Han ◽  
Shuang Cui ◽  
Feng-Yu Liu ◽  
You Wan ◽  
Yan Shi ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Water Intake ◽  
Water Consumption ◽  
Pyramidal Neurons ◽  
Electrophysiological Recording ◽  
Water Restriction ◽  
Hippocampal Ca1 ◽  
Hypertonic Saline Injection

Thirst is an important interoceptive response and drives water consumption. The hippocampus actively modulates food intake and energy metabolism, but direct evidence for the exact role of the hippocampus in modulating drinking behaviors is lacking. We observed decreased number of c-Fos-positive neurons in the ventral hippocampal CA1 (vCA1) after water restriction or hypertonic saline injection in rats. Suppressed vCA1 neuronal activities under the hypertonic state were further confirmed with in vivo electrophysiological recording and the level of suppression paralleled both the duration and the total amount of water consumption. Chemogenetic inhibition of vCA1 pyramidal neurons increased water consumption in rats injected with both normal and hypertonic saline. These findings suggest that suppression of vCA1 pyramidal neuronal activities enhances water intake.

Abstract WP329: The Role of miR-34b/c in Global Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Hyae-Ran Byun ◽  
Morgan Porch ◽  
Fabrizio Pontarelli ◽  
Brenda L Court Vazquez ◽  
R.Suzanne Zukin ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Deficits ◽  
Neuronal Death ◽  
Target Genes ◽  
Pyramidal Neurons ◽  
Unmet Need ◽  
Global Ischemia ◽  
Hippocampal Ca1

Transient global ischemia arising as a consequence of cardiac arrest in humans causes selective, delayed death of hippocampal CA1 pyramidal neurons and cognitive impairment. Effective treatments to ameliorate the neurodegeneration and cognitive dysfunction associated with global ischemia are an unmet need. Emerging evidence points to a widespread role for microRNAs (miRNAs) as key modulators of target gene expression in neurons. Accordingly, dysregulation of miRNAs are implicated in the pathophysiology of neurodegenerative disease and neurological disorders. Our findings, derived via miRNA-seq, indicate that expression of a subset of microRNAs are altered in postischemic CA1 including miR-34b/c, miR-21, miR-331, miR-181 and miR-29. Ingenuity pathway analysis reveals that miR-34b/c is the leading miR candidate implicated in cell death and survival. A role for miR-34 in the pathogenesis of global ischemia is, as yet, unclear. Here we show ischemia induces p53-dependent activation of miR-34b/c and downregulation of its target genes Bcl-2 and Sirt1, which together promote neuronal death in selectively vulnerable hippocampal CA1 in vivo . Consistent with this, inhibition of miR-34b/c affords neuroprotection, rescues impaired synaptic plasticity and reduces memory deficits in global ischemia. These findings document a causal role for p53-dependent activation of miR-34b/c in neuronal death and identify a novel therapeutic target for amelioration of the neurodegeneration and cognitive deficits associated with ischemic stroke.

scholarly journals Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthieu Raveau ◽  
Denis Polygalov ◽  
Roman Boehringer ◽  
Kenji Amano ◽  
Kazuhiro Yamakawa ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Pyramidal Neurons ◽  
Chromosome 21 ◽  
Network Activity ◽  
Inhibitory Neurons ◽  
Spatial Coding ◽  
Extra Copy ◽  
Hippocampal Ca1

Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models, most studies have relied on in vitro measures. Here, using in vivo recording in the Dp(16)1Yey model, we find alterations in the organization of spiking of hippocampal CA1 pyramidal neurons, including deficits in the generation of complex spikes. These changes lead to poorer spatial coding during exploration and less coordinated activity during sharp-wave ripples, events involved in memory consolidation. Further, the density of CA1 inhibitory neurons expressing neuropeptide Y, a population key for the generation of pyramidal cell bursts, were significantly increased in Dp(16)1Yey mice. Our data refine the ‘over-suppression’ theory of Down syndrome pathophysiology and suggest specific neuronal subtypes involved in hippocampal dysfunction in these model mice.

scholarly journals Role of Glycine Receptors in Glycine-Induced LTD in Hippocampal CA1 Pyramidal Neurons

2011 ◽  
Vol 36 (9) ◽  
pp. 1948-1958 ◽  
Author(s):  
Rong-Qing Chen ◽  
Shan-Hui Wang ◽  
Wen Yao ◽  
Jing-Jing Wang ◽  
Fang Ji ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Glycine Receptors ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1

scholarly journals Hippocampal ghrelin signalling informs the decision to eat

2021 ◽  
Author(s):  
Ryan WS Wee ◽  
Karyna Mishchanchuk ◽  
Rawan AlSubaie ◽  
Andrew F MacAskill
Keyword(s):  
Calcium Imaging ◽  
Feeding Behaviour ◽  
Pyramidal Neurons ◽  
Internal State ◽  
Ventral Hippocampus ◽  
Direct Role ◽  
Induced Changes ◽  
In Vivo Calcium Imaging

Hunger is an internal state that not only invigorates behaviour towards feeding, but also acts as a contextual cue for the higher-order control of anticipatory feeding-related behaviour. The ventral hippocampus is a brain region important in encoding context, but how internal contexts such as hunger are represented in hippocampal circuits is not known. Pyramidal neurons in the ventral hippocampus, and in particular within the ventral CA1/subiculum border (vS) express the receptor for the peripheral hunger hormone ghrelin, and ghrelin is known to cross the blood brain barrier and directly influence hippocampal circuitry. However, what role vS neurons play during feeding related behaviour, and how ghrelin influences this role has not been directly investigated. In this study, we used a combination of whole-cell electrophysiology, optogenetics and molecular knockdown together with in vivo calcium imaging in mice to investigate the role of vS during feeding behaviour across different states of hunger. We found that activity of a unique subpopulation of vS neurons that project to the nucleus accumbens (vS-NAc) were active specifically when animals approached and investigated food, and that that this activity inhibited the transition to begin eating. Increases in peripheral ghrelin reduced vS-NAc activity during this anticipatory phase of feeding behaviour, by increasing the influence of synaptic inhibition. Furthermore, this effect required postsynaptic GHSR1a expression in vS-NAc neurons, suggesting a direct role of ghrelin signalling. Consistent with this role of hippocampal ghrelin signalling, removal of GHSR1a from vS-NAc neurons impaired ghrelin-induced changes in feeding-related behaviour. Together, these experiments define a ghrelin-sensitive hippocampal circuit that informs the decision to eat based on internal state.

scholarly journals Ischemic Neuronal Injury is Ameliorated by Astrocyte Activation

1998 ◽  
Vol 25 (2) ◽  
pp. 102-107 ◽  
Author(s):  
Deon F. Louw ◽  
Tetsuy Masada ◽  
Garnette R. Sutherland
Keyword(s):  
Ethidium Bromide ◽  
Neuronal Injury ◽  
Contralateral Side ◽  
Forebrain Ischemia ◽  
Astrocyte Activation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Sector ◽  
Ischemic Neuronal Injury

ABSTRACT:Background:The motivation of this study was to more precisely define the in vivo role of astrocytes in forebrain ischemia. Controversy exists in the literature as to whether they protect or injure neurons in this setting.Methods:Astrocytes in the rat hippocampus were disabled with stereotactic administration of a gliotoxin, ethidium bromide, 3 days prior to induction of forebrain ischemia. The extent of neuronal injury in this group was compared to a control category receiving intrahippocampal saline only.Results:Saline-injected animals demonstrated decreased hippocampal CA1 sector injury, and increased gliosis on the side of the injection compared to the contralateral side (P < 0.01) or ethidium bromide-treated animals (P < 0.05).Conclusion:The results suggest that activated astrocytes are protective to neurons subjected to an ischemic insult. This may result from their ability to elaborate neurotrophic factors, buffer potassium and metabolize a variety of neurotransmitters.

scholarly journals GSG1L regulates the strength of AMPA receptor-mediated synaptic transmission but not AMPA receptor kinetics in hippocampal dentate granule neurons

2017 ◽  
Vol 117 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Xia Mao ◽  
Xinglong Gu ◽  
Wei Lu
Keyword(s):  
Ampa Receptor ◽  
Pyramidal Neurons ◽  
Granule Cells ◽  
Granule Neurons ◽  
Ca1 Pyramidal Neurons ◽  
Auxiliary Subunit ◽  
Hippocampal Ca1 ◽  
Ampar Trafficking ◽  
And Function

GSG1L is an AMPA receptor (AMPAR) auxiliary subunit that regulates AMPAR trafficking and function in hippocampal CA1 pyramidal neurons. However, its physiological roles in other types of neurons remain to be characterized. Here, we investigated the role of GSG1L in hippocampal dentate granule cells and found that GSG1L is important for the regulation of synaptic strength but is not critical for the modulation of AMPAR deactivation and desensitization kinetics. These data demonstrate a neuronal type-specific role of GSG1L and suggest that physiological function of AMPAR auxiliary subunits may vary in different types of neurons. NEW & NOTEWORTHY GSG1L is a newly identified AMPA receptor (AMPAR) auxiliary subunit and plays a unique role in the regulation of AMPAR trafficking and function in hippocampal CA1 pyramidal neurons. However, its role in the regulation of AMPARs in hippocampal dentate granule cells remains to be characterized. The current work reveals that GSG1L regulates strength of AMPAR-mediated synaptic transmission but not the receptor kinetic properties in hippocampal dentate granule neurons.

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