scholarly journals Differential encoding of predator fear in the ventromedial hypothalamus and periaqueductal grey

2018 ◽  
Author(s):  
Maria Esteban Masferrer ◽  
Bianca A. Silva ◽  
Kensaku Nomoto ◽  
Susana Q. Lima ◽  
Cornelius T. Gross
Keyword(s):  
Internal State ◽  
Motor Pattern ◽  
Ventromedial Hypothalamus ◽  
Sympathetic Activation ◽  
Periaqueductal Grey ◽  
Differential Encoding ◽  
Defensive Responses ◽  
Electrophysiological Recordings ◽  
Mammalian Predator ◽  
Stimulation Of

AbstractThe ventromedial hypothalamus is a central node of the mammalian predator defense network. Stimulation of this structure in rodents and primates elicits abrupt defensive responses, including flight, freezing, sympathetic activation, and panic, while inhibition reduces defensive responses to predators. The major efferent target of the ventromedial hypothalamus is the dorsal periaqueductal grey, and stimulation of this structure also elicits flight, freezing, and sympathetic activation. However, reversible inhibition experiments suggest that the ventromedial hypothalamus and periaqueductal grey play distinct roles in the control of defensive behavior, with the former proposed to encode an internal state necessary for the motivation of defensive responses, while the latter serves as a motor pattern initiator. Here we used electrophysiological recordings of single units in behaving mice exposed to a rat to investigate the encoding of predator fear in the dorsomedial division of the ventromedial hypothalamus and the dorsal periaqueductal grey. Distinct correlates of threat intensity and motor responses were found in both structures, suggesting a distributed encoding of sensory and motor features in the medial hypothalamic-brainstem instinctive network.

scholarly journals Stimulus-specific neural encoding of a persistent, internal defensive state in the hypothalamus

2019 ◽  
Author(s):  
Ann Kennedy ◽  
Prabhat S. Kunwar ◽  
Lingyun Li ◽  
Daniel Wagenaar ◽  
David J. Anderson
Keyword(s):  
Neural Activity ◽  
Internal State ◽  
Stress Hormones ◽  
Ventromedial Hypothalamus ◽  
Persistent Activity ◽  
Neural Encoding ◽  
Population Activity ◽  
Defensive Responses ◽  
Neuroendocrine Mechanisms ◽  
Threatening Stimuli

SummaryPersistent neural activity has been described in cortical, hippocampal, and motor networks as mediating short-term working memory of transiently encountered stimuli1–4. Internal emotion states such as fear also exhibit persistence following exposure to an inciting stimulus5,6, but such persistence is typically attributed to circulating stress hormones7–9; whether persistent neural activity also plays a role has not been established. SF1+/Nr5a1+ neurons in the dorsomedial and central subdivision of the ventromedial hypothalamus (VMHdm/c) are necessary for innate and learned defensive responses to predators10–13. Optogenetic activation of VMHdmSF1 neurons elicits defensive behaviors that can outlast stimulation11,14, suggesting it induces a persistent internal state of fear or anxiety. Here we show that VMHdmSF1 neurons exhibit persistent activity lasting tens of seconds, in response to naturalistic threatening stimuli. This persistent activity was correlated with, and required for, persistent thigmotaxic (anxiety-like) behavior in an open-field assay. Microendoscopic imaging of VMHdmSF1 neurons revealed that persistence reflects dynamic temporal changes in population activity, rather than simply synchronous, slow decay of simultaneously activated neurons. Unexpectedly, distinct but overlapping VMHdmSF1 subpopulations were persistently activated by different classes of threatening stimuli. Computational modeling suggested that recurrent neural networks (RNNs) incorporating slow excitation and a modest degree of neurochemical or spatial bias can account for persistent activity that maintains stimulus identity, without invoking genetically determined “labeled lines”15. Our results provide causal evidence that persistent neural activity, in addition to well-established neuroendocrine mechanisms, can contribute to the ability of emotion states to outlast their inciting stimuli, and suggest a mechanism that could prevent over-generalization of defensive responses without the need to evolve hardwired circuits specific for each type of threat.

scholarly journals Differential Encoding of Predator Fear in the Ventromedial Hypothalamus and Periaqueductal Grey

2020 ◽  
Vol 40 (48) ◽  
pp. 9283-9292
Author(s):  
Maria Esteban Masferrer ◽  
Bianca A. Silva ◽  
Kensaku Nomoto ◽  
Susana Q. Lima ◽  
Cornelius T. Gross
Keyword(s):  
Ventromedial Hypothalamus ◽  
Periaqueductal Grey ◽  
Differential Encoding

Optimal Parameters for Eliciting Cardio-Acceleration by Electrical Stimulation of the Ventromedial Hypothalamus

1975 ◽  
Vol 94 (2) ◽  
pp. 189-197
Author(s):  
G. Johansson ◽  
R. Kalimo ◽  
T. Pääkkönen ◽  
S. Ruusunen
Keyword(s):  
Electrical Stimulation ◽  
Ventromedial Hypothalamus ◽  
Optimal Parameters ◽  
Stimulation Of

Chemical stimulation of visceral afferents activates medullary neurones projecting to the central amygdala and periaqueductal grey

2006 ◽  
Vol 71 (1-3) ◽  
pp. 51-59 ◽  
Author(s):  
Odile Viltart ◽  
Daniela M. Sartor ◽  
Anthony J.M. Verberne
Keyword(s):  
Chemical Stimulation ◽  
Visceral Afferents ◽  
Central Amygdala ◽  
Periaqueductal Grey ◽  
Stimulation Of

Autonomic changes associated with analgesia produced by stimulation of the periaqueductal grey

Pain ◽  
1984 ◽  
Vol 18 ◽  
pp. S328 ◽  
Author(s):  
T. A. Lovick ◽  
J. Cairns
Keyword(s):  
Periaqueductal Grey ◽  
Autonomic Changes ◽  
Stimulation Of

scholarly journals Multimodal Medullary Neurons and Correlational Linkages of the Respiratory Network

1999 ◽  
Vol 82 (1) ◽  
pp. 188-201 ◽  
Author(s):  
Zhongzeng Li ◽  
Kendall F. Morris ◽  
David M. Baekey ◽  
Roger Shannon ◽  
Bruce G. Lindsey
Keyword(s):  
Firing Rate ◽  
Nucleus Tractus Solitarius ◽  
Motor Pattern ◽  
Sensory Modality ◽  
Spike Trains ◽  
Negative Feedback Regulation ◽  
Firing Rates ◽  
Respiratory Network ◽  
Cross Correlation Analysis ◽  
Stimulation Of

This study addresses the hypothesis that multiple sensory systems, each capable of reflexly altering breathing, jointly influence neurons of the brain stem respiratory network. Carotid chemoreceptors, baroreceptors, and foot pad nociceptors were stimulated sequentially in 33 Dial-urethan–anesthetized or decerebrate vagotomized adult cats. Neuronal impulses were monitored with microelectrode arrays in the rostral and caudal ventral respiratory group (VRG), nucleus tractus solitarius (NTS), and n. raphe obscurus. Efferent phrenic nerve activity was recorded. Spike trains of 889 neurons were analyzed with cycle-triggered histograms and tested for respiratory-modulated firing rates. Responses to stimulus protocols were assessed with peristimulus time and cumulative sum histograms. Cross-correlation analysis was used to test for nonrandom temporal relationships between spike trains. Spike-triggered averages of efferent phrenic activity and antidromic stimulation methods provided evidence for functional associations of bulbar neurons with phrenic motoneurons. Spike train cross-correlograms were calculated for 6,471 pairs of neurons. Significant correlogram features were detected for 425 pairs, including 189 primary central peaks or troughs, 156 offset peaks or troughs, and 80 pairs with multiple peaks and troughs. The results provide evidence that correlational medullary assemblies include neurons with overlapping memberships in groups responsive to different sets of sensory modalities. The data suggest and support several hypotheses concerning cooperative relationships that modulate the respiratory motor pattern. 1) Neurons responsive to a single tested modality promote or limit changes in firing rate of multimodal target neurons. 2) Multimodal neurons contribute to changes in firing rate of neurons responsive to a single tested modality. 3) Multimodal neurons may promote responses during stimulation of one modality and “limit” changes in firing rates during stimulation of another sensory modality. 4) Caudal VRG inspiratory neurons have inhibitory connections that provide negative feedback regulation of inspiratory drive and phase duration.

Higher order neurons in buccal ganglia of Pleurobranchaea elicit vomiting motor activity

1983 ◽  
Vol 50 (3) ◽  
pp. 658-670 ◽  
Author(s):  
A. D. McClellan
Keyword(s):  
High Frequency ◽  
Motor Pattern ◽  
Higher Order ◽  
Root Activity ◽  
Command Neurons ◽  
Sensory Inputs ◽  
Buccal Ganglia ◽  
Output Pattern ◽  
Stimulation Of

The buccal mass of the gastropod Pleurobranchaea is used during a regurgitation response that consists of a writhing phase interrupted by brief periodic bouts of a vomiting phase (17, 20). During transitions from writhing to vomiting, specific changes occur in the motor pattern (19, 20). Evidence is presented suggesting that at least some of the initiation or "command" neurons for vomiting reside in the buccal ganglia. The present paper examines the role of two candidate vomiting-initiation cells, the ventral white cells (VWC) and midganglionic cells (MC), in the buccal ganglia of isolated nervous systems. Stimulation of single VWCs activates a vomiting motor pattern, consisting in part of alternating buccal root activity. Furthermore, the VWCs fire in high-frequency bursts during episodes (i.e., bouts) of this same vomiting pattern. Mutual reexcitation between the VWCs and motor pattern generator (MPG) appears to produce the accelerated buildup and maintenance of vomiting rhythms. Brief stimulation of single MCs "triggers" bouts of a vomiting motor pattern, but the membrane potential of this cell is only modulated during this same pattern, at least in the isolated nervous system. It is proposed that in intact animals the MCs are activated by sensory inputs and briefly excite the VWC-MPG network, thereby turning on the mutual reexcitatory mechanism mentioned above and switching the output pattern. A general implication for gastropod research is that higher order neurons that activate buccal root activity cannot automatically be given the function of "feeding command neuron," as some cells clearly control other responses, such as vomiting.

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