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Article ; Online: Glutamate Spillover Dynamically Strengthens Gabaergic Synaptic Inhibition of the Hypothalamic Paraventricular Nucleus.

Yamaguchi, Junya / Andrade, Mary Ann / Truong, Tamara T / Toney, Glenn M

The Journal of neuroscience : the official journal of the Society for Neuroscience

2024 Volume 44, Issue 7

Abstract: The hypothalamic paraventricular nucleus (PVN) is strongly inhibited by γ-aminobutyric acid (GABA) from the surrounding peri-nuclear zone (PNZ). Because glutamate mediates fast excitatory transmission and is substrate for GABA synthesis, we tested its ... ...

Abstract	The hypothalamic paraventricular nucleus (PVN) is strongly inhibited by γ-aminobutyric acid (GABA) from the surrounding peri-nuclear zone (PNZ). Because glutamate mediates fast excitatory transmission and is substrate for GABA synthesis, we tested its capacity to dynamically strengthen GABA inhibition. In PVN slices from male mice, bath glutamate applied during ionotropic glutamate receptor blockade increased PNZ-evoked inhibitory postsynaptic currents (eIPSCs) without affecting GABA-A receptor agonist currents or single-channel conductance, implicating a presynaptic mechanism(s). Consistent with this interpretation, bath glutamate failed to strengthen IPSCs during pharmacological saturation of GABA-A receptors. Presynaptic analyses revealed that glutamate did not affect paired-pulse ratio, peak eIPSC variability, GABA vesicle recycling speed, or readily releasable pool (RRP) size. Notably, glutamate-GABA strengthening (GGS) was unaffected by metabotropic glutamate receptor blockade and graded external Ca
MeSH term(s)	Male ; Mice ; Animals ; Paraventricular Hypothalamic Nucleus/metabolism ; Glutamic Acid/metabolism ; Neurons/physiology ; gamma-Aminobutyric Acid/metabolism ; Neuroglia/metabolism ; Synaptic Transmission/physiology
Chemical Substances	Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1851-22.2023
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Article ; Online: Anterior basolateral amygdala neurons comprise a remote fear memory engram.

Hammack, Robert J / Fischer, Victoria E / Andrade, Mary Ann / Toney, Glenn M

Frontiers in neural circuits

2023 Volume 17, Page(s) 1167825

Abstract: Introduction: Threatening environmental cues often generate enduring fear memories, but how these are formed and stored remains actively investigated. Recall of a recent fear memory is thought to reflect reactivation of neurons, in multiple brain ... ...

Abstract	Introduction: Threatening environmental cues often generate enduring fear memories, but how these are formed and stored remains actively investigated. Recall of a recent fear memory is thought to reflect reactivation of neurons, in multiple brain regions, activated during memory formation, indicating that anatomically distributed and interconnected neuronal ensembles comprise fear memory engrams. The extent to which anatomically specific activation-reactivation engrams persist during long-term fear memory recall, however, remains largely unexplored. We hypothesized that principal neurons in the anterior basolateral amygdala (aBLA), which encode negative valence, acutely reactivate during remote fear memory recall to drive fear behavior. Methods: Using adult offspring of TRAP2 and Ai14 mice, persistent tdTomato expression was used to "TRAP" aBLA neurons that underwent Fos-activation during contextual fear conditioning (electric shocks) or context only conditioning (no shocks) ( Results: TRAPed (tdTomato +), Fos +, and reactivated (double-labeled) neuronal ensembles were larger in fear- than context-conditioned mice, with the middle sub-region and middle/caudal dorsomedial quadrants of aBLA displaying the greatest densities of all three ensemble populations. Whereas tdTomato + ensembles were dominantly glutamatergic in context and fear groups, freezing behavior during remote memory recall was not correlated with ensemble sizes in either group. Discussion: We conclude that although an aBLA-inclusive fear memory engram forms and persists at a remote time point, plasticity impacting electrophysiological responses of engram neurons, not their population size, encodes fear memory and drives behavioral manifestations of long-term fear memory recall.
MeSH term(s)	Basolateral Nuclear Complex/cytology ; Basolateral Nuclear Complex/physiology ; Neurons/physiology ; Fear/physiology ; Memory, Long-Term/physiology ; Animals ; Mice ; Mice, Transgenic ; Conditioning, Operant ; Mental Recall/physiology ; Proto-Oncogene Proteins c-fos/genetics ; Gene Knock-In Techniques
Chemical Substances	Proto-Oncogene Proteins c-fos
Language	English
Publishing date	2023-04-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2452968-0
ISSN	1662-5110 ; 1662-5110
ISSN (online)	1662-5110
ISSN	1662-5110
DOI	10.3389/fncir.2023.1167825
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Article ; Online: Presence of a remote fear memory engram in the central amygdala.

Hammack, Robert J / Fischer, Victoria E / Andrade, Mary Ann / Toney, Glenn M

Learning & memory (Cold Spring Harbor, N.Y.)

2023 Volume 30, Issue 10, Page(s) 250–259

Abstract: Fear memory formation and recall are highly regulated processes, with the central amygdala (CeA) contributing to fear memory-related behaviors. We recently reported that a remote fear memory engram is resident in the anterior basolateral amygdala (aBLA). ...

Abstract	Fear memory formation and recall are highly regulated processes, with the central amygdala (CeA) contributing to fear memory-related behaviors. We recently reported that a remote fear memory engram is resident in the anterior basolateral amygdala (aBLA). However, the extent to which downstream neurons in the CeA participate in this engram is unknown. We tested the hypothesis that CeA neurons activated during fear memory formation are reactivated during remote memory retrieval such that a CeA engram participates in remote fear memory recall and its associated behavior. Using contextual fear conditioning in TRAP2;Ai14 mice, we identified, by persistent Cre-dependent tdTomato expression (i.e., "TRAPing"), CeA neurons that were
MeSH term(s)	Mice ; Animals ; Central Amygdaloid Nucleus ; Memory/physiology ; Memory, Long-Term ; Fear/physiology ; Mental Recall/physiology
Language	English
Publishing date	2023-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1204777-6
ISSN	1549-5485 ; 1072-0502
ISSN (online)	1549-5485
ISSN	1072-0502
DOI	10.1101/lm.053833.123
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Article ; Online: Central AT1 receptor signaling by circulating angiotensin II is permissive to acute intermittent hypoxia-induced sympathetic neuroplasticity.

Shimoura, Caroline G / Andrade, Mary Ann / Toney, Glenn M

Journal of applied physiology (Bethesda, Md. : 1985)

2020 Volume 128, Issue 5, Page(s) 1329–1337

Abstract: Acute intermittent hypoxia (AIH) triggers sympathetic long-term facilitation (sLTF), a progressive increase in sympathetic nerve activity (SNA) linked to central AT1 receptor (AT1R) activation by circulating angiotensin II (ANG II). Here, we investigated ...

Abstract	Acute intermittent hypoxia (AIH) triggers sympathetic long-term facilitation (sLTF), a progressive increase in sympathetic nerve activity (SNA) linked to central AT1 receptor (AT1R) activation by circulating angiotensin II (ANG II). Here, we investigated AIH activation of the peripheral renin-angiotensin system (RAS) and the extent to which the magnitude of RAS activation predicts the magnitude of AIH-induced sLTF. In anesthetized male Sprague-Dawley rats, plasma renin activity (PRA) increased in a linear fashion in response to 5 (
MeSH term(s)	Angiotensin II/blood ; Animals ; Blood Pressure ; Hypoxia ; Losartan/pharmacology ; Male ; Neuronal Plasticity ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; Renin-Angiotensin System ; Sympathetic Nervous System
Chemical Substances	Receptor, Angiotensin, Type 1 ; Angiotensin II (11128-99-7) ; Losartan (JMS50MPO89)
Language	English
Publishing date	2020-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00094.2020
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Article ; Online: Intermittent hypercapnic hypoxia induces respiratory hypersensitivity to fentanyl accompanied by tonic respiratory depression by endogenous opioids.

Brackley, Allison D / Andrade, Mary Ann / Toney, Glenn M

The Journal of physiology

2020 Volume 598, Issue 15, Page(s) 3239–3257

Abstract: Key points: Sleep apnoea increases susceptibility to opioid-induced respiratory depression (OIRD). Endogenous opioids are implicated as a contributing factor in sleep apnoea. Rats exposed to sleep-phase chronic intermittent hypercapnic hypoxia (CIHH) ... ...

Abstract	Key points: Sleep apnoea increases susceptibility to opioid-induced respiratory depression (OIRD). Endogenous opioids are implicated as a contributing factor in sleep apnoea. Rats exposed to sleep-phase chronic intermittent hypercapnic hypoxia (CIHH) for 7 days exhibited exaggerated OIRD to systemic fentanyl both while anaesthetized and artificially ventilated and while conscious and breathing spontaneously, implicating heightened CNS inhibitory efficacy of fentanyl. CIHH also induced tonic endogenous opioid suppression of neural inspiration. Sleep-related episodes of hypercapnic hypoxia, as in sleep apnoea, promote hypersensitivity to OIRD, with tonic respiratory depression by endogenous opioids implicated as a potential underlying cause. Abstract: Sleep apnoea (SA) increases opioid-induced respiratory depression (OIRD) and lethality. To test the hypothesis that this results from chronic intermittent bouts of hypercapnic hypoxia (CIHH) accompanying SA, we compared OIRD across continuously normoxic control rats and rats exposed to sleep-phase (8 h/day) CIHH for 1 week. OIRD sensitivity was first assessed in anaesthetized (urethane/α-chloralose), vagotomized and artificially ventilated rats by recording phrenic nerve activity (PNA) to index neural inspiration and quantify PNA burst inhibition to graded doses (0, 2, 20, 50 μg kg
MeSH term(s)	Analgesics, Opioid ; Animals ; Fentanyl/toxicity ; Hypoxia ; Rats ; Rats, Sprague-Dawley ; Respiratory Hypersensitivity ; Respiratory Insufficiency
Chemical Substances	Analgesics, Opioid ; Fentanyl (UF599785JZ)
Language	English
Publishing date	2020-06-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP280021
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Article ; Online: Early central cardiovagal dysfunction after high fat diet in a murine model.

Strain, Misty M / Espinoza, Liliana / Fedorchak, Stephanie / Littlejohn, Erica L / Andrade, Mary Ann / Toney, Glenn M / Boychuk, Carie R

Scientific reports

2023 Volume 13, Issue 1, Page(s) 6550

Abstract: High fat diet (HFD) promotes cardiovascular disease and blunted cardiac vagal regulation. Temporal onset of loss of cardiac vagal control and its underlying mechanism are presently unclear. We tested our hypothesis that reduced central vagal regulation ... ...

Abstract	High fat diet (HFD) promotes cardiovascular disease and blunted cardiac vagal regulation. Temporal onset of loss of cardiac vagal control and its underlying mechanism are presently unclear. We tested our hypothesis that reduced central vagal regulation occurs early after HFD and contributes to poor cardiac regulation using cardiovascular testing paired with pharmacology in mice, molecular biology, and a novel bi-transgenic mouse line. Results show HFD, compared to normal fat diet (NFD), significantly blunted cardio/pulmonary chemoreflex bradycardic responses after 15 days, extending as far as tested (> 30 days). HFD produced resting tachycardia by day 3, reflected significant loss of parasympathetic tone. No differences in bradycardic responses to graded electrical stimulation of the distal cut end of the cervical vagus indicated diet-induced differences in vagal activity were centrally mediated. In nucleus ambiguus (NA), surface expression of δ-subunit containing type A gamma-aminobutyric acid receptors (GABA
MeSH term(s)	Mice ; Animals ; Disease Models, Animal ; Diet, High-Fat/adverse effects ; Medulla Oblongata/metabolism ; Vagus Nerve/physiology ; Bradycardia ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2023-04-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-32492-w
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Article ; Online: Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation.

Blackburn, Megan B / Andrade, Mary Ann / Toney, Glenn M

Journal of applied physiology (Bethesda, Md. : 1985)

2017 Volume 124, Issue 5, Page(s) 1233–1243

Abstract: Blackburn MB, Andrade MA, Toney GM. Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation. J Appl Physiol 124: 1233-1243, 2018. First published December 19, 2017; doi: 10.1152/japplphysiol ... ...

Abstract	Blackburn MB, Andrade MA, Toney GM. Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation. J Appl Physiol 124: 1233-1243, 2018. First published December 19, 2017; doi: 10.1152/japplphysiol.00743.2017 .- Acute intermittent hypoxia (AIH) repetitively activates the arterial chemoreflex and triggers a progressive increase of sympathetic nerve activity (SNA) and phrenic nerve activity (PNA) referred to as sympathetic and phrenic long-term facilitation (S-LTF and P-LTF), respectively. Neurons of the hypothalamic paraventricular nucleus (PVN) participate in the arterial chemoreflex, but their contribution to AIH-induced LTF is unknown. To determine this, anesthetized rats were vagotomized and exposed to 10 cycles of AIH, each consisting of ventilation for 3 min with 100% O
MeSH term(s)	Animals ; Hypoxia/physiopathology ; Long-Term Potentiation/physiology ; Male ; Paraventricular Hypothalamic Nucleus/physiopathology ; Phrenic Nerve/physiopathology ; Rats ; Rats, Sprague-Dawley ; Respiration ; Sympathetic Nervous System/physiopathology
Language	English
Publishing date	2017-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00743.2017
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Article ; Online: High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons.

Levi, David I / Wyrosdic, Joshua C / Hicks, Amirah-Iman / Andrade, Mary Ann / Toney, Glenn M / Prager-Khoutorsky, Masha / Bourque, Charles W

Cell reports

2021 Volume 34, Issue 11, Page(s) 108866

Abstract: High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells ( ... ...

Abstract	High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells (MNC
MeSH term(s)	Angiotensin II ; Animals ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cytoskeleton/drug effects ; Cytoskeleton/metabolism ; Disease Models, Animal ; Excitatory Postsynaptic Potentials/drug effects ; Hypertension/pathology ; Male ; Mechanotransduction, Cellular/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Osmosis ; Probability ; Rats, Wistar ; Sodium Chloride, Dietary/adverse effects ; Synapses/drug effects ; Synapses/metabolism ; Vasopressins/metabolism ; Rats
Chemical Substances	Sodium Chloride, Dietary ; Vasopressins (11000-17-2) ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2021-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.108866
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Article ; Online: Local ionotropic glutamate receptors are required to trigger and sustain ramping of sympathetic nerve activity by hypothalamic paraventricular nucleus TNF

Mourão, Aline A / Shimoura, Caroline G / Andrade, Mary Ann / Truong, Tamara T / Pedrino, Gustavo R / Toney, Glenn M

American journal of physiology. Heart and circulatory physiology

2021 Volume 321, Issue 3, Page(s) H580–H591

Abstract: Tumor necrosis factor-α (TNFα) in the hypothalamic paraventricular nucleus (PVN) contributes to increased sympathetic nerve activity (SNA) in cardiovascular disease models, but mechanisms are incompletely understood. As previously reported, bilateral PVN ...

Abstract	Tumor necrosis factor-α (TNFα) in the hypothalamic paraventricular nucleus (PVN) contributes to increased sympathetic nerve activity (SNA) in cardiovascular disease models, but mechanisms are incompletely understood. As previously reported, bilateral PVN TNFα (0.6 pmol, 50 nL) induced acute ramping of splanchnic SNA (SSNA) that averaged +64 ± 7% after 60 min and +109 ± 17% after 120 min (
MeSH term(s)	2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Excitatory Amino Acid Antagonists/pharmacology ; GABA-A Receptor Agonists/pharmacology ; Male ; Muscimol/pharmacology ; Paraventricular Hypothalamic Nucleus/metabolism ; Paraventricular Hypothalamic Nucleus/physiology ; Quinoxalines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Splanchnic Nerves/drug effects ; Splanchnic Nerves/metabolism ; Splanchnic Nerves/physiology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Excitatory Amino Acid Antagonists ; GABA-A Receptor Agonists ; Quinoxalines ; Receptors, AMPA ; Receptors, GABA-A ; Receptors, N-Methyl-D-Aspartate ; Tumor Necrosis Factor-alpha ; 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline (118876-58-7) ; Muscimol (2763-96-4) ; 2-Amino-5-phosphonovalerate (76726-92-6)
Language	English
Publishing date	2021-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00322.2021
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Article ; Online: Burst patterning of hypothalamic paraventricular nucleus-driven sympathetic nerve activity in ANG II-salt hypertension.

Holbein, Walter W / Blackburn, Megan B / Andrade, Mary Ann / Toney, Glenn M

American journal of physiology. Heart and circulatory physiology

2017 Volume 314, Issue 3, Page(s) H530–H541

Abstract: ANG II-salt hypertension selectively increases splanchnic sympathetic nerve activity (sSNA), but the extent to which this reflects increased respiratory versus cardiac rhythmic bursting is unknown. Here, integrated sSNA was elevated in ANG II-infused ... ...

Abstract	ANG II-salt hypertension selectively increases splanchnic sympathetic nerve activity (sSNA), but the extent to which this reflects increased respiratory versus cardiac rhythmic bursting is unknown. Here, integrated sSNA was elevated in ANG II-infused rats fed a high-salt (2% NaCl) diet (ANG II-HSD) compared with vehicle-infused rats fed a normal-salt (0.4% NaCl) diet (Veh-NSD; P < 0.01). Increased sSNA was not accompanied by increased inspiratory or expiratory bursting, consistent with no group difference in central inspiratory drive. Consistent with preserved inhibitory baroreflex entrainment of elevated sSNA in ANG II-HSD rats, the time integral ( P < 0.05) and amplitude ( P < 0.01) of cardiac rhythmic sSNA were increased. Consistent with activity of hypothalamic paraventricular nucleus (PVN) neurons supporting basal SNA in ANG II-salt hypertension, inhibition of PVN with the GABA-A receptor agonist muscimol reduced mean arterial pressure (MAP) and integrated sSNA only in the ANG II-HSD group ( P < 0.001). PVN inhibition had no effect on respiratory rhythmic sSNA bursting in either group but reduced cardiac rhythmic sSNA in ANG II-HSD rats only ( P < 0.01). The latter likely reflected reduced inhibitory baroreflex entrainment subsequent to the fall of MAP. Of note is that MAP as well as integrated and rhythmic burst patterns of sSNA were similar in vehicle-infused rats whether they were fed a normal or high-salt diet. Findings indicate that PVN neurons support elevated sSNA in ANG II-HSD rats by driving a tonic component of activity without altering respiratory or cardiac rhythmic bursting. Because sSNA was unchanged in Veh-HSD rats, activation of PVN-driven tonic sSNA appears to require central actions of ANG II. NEW & NOTEWORTHY ANG II-salt hypertension is strongly neurogenic and depends on hypothalamic paraventricular nucleus (PVN)-driven splanchnic sympathetic nerve activity (sSNA). Here, respiratory and cardiac bursts of sSNA were preserved in ANG II-salt rats and unaltered by PVN inhibition, suggesting that PVN neurons drive a tonic component of sSNA rather than modulating dominant patterns of burst discharge.
MeSH term(s)	Angiotensin II ; Animals ; Arterial Pressure ; Baroreflex/drug effects ; Disease Models, Animal ; GABA-A Receptor Agonists/pharmacology ; Heart/innervation ; Heart Rate ; Hypertension/chemically induced ; Hypertension/physiopathology ; Male ; Paraventricular Hypothalamic Nucleus/drug effects ; Paraventricular Hypothalamic Nucleus/physiopathology ; Periodicity ; Phrenic Nerve/physiopathology ; Rats, Sprague-Dawley ; Respiratory Rate ; Sodium Chloride, Dietary ; Splanchnic Nerves/physiopathology ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/physiopathology ; Time Factors
Chemical Substances	GABA-A Receptor Agonists ; Sodium Chloride, Dietary ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2017-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00560.2017
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