scholarly journals Septal GABAergic Inputs to CA1 Govern Contextual Memory Retrieval

2019 ◽  
Author(s):  
Arnau Sans-Dublanc ◽  
Adrià Razzauti ◽  
Srinidhi Desikan ◽  
Marta Pascual ◽  
Jaime de la Rocha ◽  
...  
Keyword(s):  
Memory Retrieval ◽  
Pyramidal Cells ◽  
Fear Memory ◽  
Medial Septum ◽  
Gabaergic Neurons ◽  
Contextual Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Feed Forward Inhibition ◽  
Fear Behavior

AbstractWhether projections from the medial septum regulate the function of the CA1 hippocampus in episodic memory retrieval is not known. Here we show that septal GABAergic inputs to CA1 promote contextual fear memory, blocking the activation of parvalbumin-rich interneurons to facilitate Erk/MAP-kinase signaling in pyramidal cells during retrieval. Thus, suppression of feed-forward inhibition onto CA1 by septal GABAergic neurons gates contextual fear behavior.

scholarly journals Limited replicability of drug-induced amnesia after contextual fear memory retrieval in rats

2019 ◽  
Vol 166 ◽  
pp. 107105 ◽  
Author(s):  
Natalie Schroyens ◽  
Joaquín Matias Alfei ◽  
Anna Elisabeth Schnell ◽  
Laura Luyten ◽  
Tom Beckers
Keyword(s):  
Memory Retrieval ◽  
Fear Memory ◽  
Drug Induced ◽  
Contextual Fear ◽  
Contextual Fear Memory

scholarly journals GABAergic neurons are susceptible to BAX-dependent apoptosis following isoflurane exposure in the neonatal period

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0238799
Author(s):  
Andrew M. Slupe ◽  
Laura Villasana ◽  
Kevin M. Wright
Keyword(s):  
Spatial Memory ◽  
Neonatal Period ◽  
Apoptotic Cell ◽  
Fear Memory ◽  
Gabaergic Neurons ◽  
Memory Retention ◽  
Neuron Death ◽  
Neuroinflammatory Response ◽  
Contextual Fear ◽  
Contextual Fear Memory

Exposure to volatile anesthetics during the neonatal period results in acute neuron death. Prior work suggests that apoptosis is the dominant mechanism mediating neuron death. We show that Bax deficiency blocks neuronal death following exposure to isoflurane during the neonatal period. Blocking Bax-mediated neuron death attenuated the neuroinflammatory response of microglia following isoflurane exposure. We find that GABAergic interneurons are disproportionately overrepresented among dying neurons. Despite the increase in neuronal apoptosis induced by isoflurane exposure during the neonatal period, seizure susceptibility, spatial memory retention, and contextual fear memory were unaffected later in life. However, Bax deficiency alone led to mild deficiencies in spatial memory and contextual fear memory, suggesting that normal developmental apoptotic death is important for cognitive function. Collectively, these findings show that while GABAergic neurons in the neonatal brain undergo elevated Bax-dependent apoptotic cell death following exposure to isoflurane, this does not appear to have long-lasting consequences on overall neurological function later in life.

scholarly journals Contextual fear memory retrieval by correlated ensembles of ventral CA1 neurons

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jessica C. Jimenez ◽  
Jack E. Berry ◽  
Sean C. Lim ◽  
Samantha K. Ong ◽  
Mazen A. Kheirbek ◽  
...  
Keyword(s):  
Memory Retrieval ◽  
Fear Memory ◽  
Ca1 Neurons ◽  
Contextual Fear ◽  
Contextual Fear Memory

scholarly journals Limited replicability of drug-induced amnesia after contextual fear memory retrieval in rats

2019 ◽  
Author(s):  
Natalie Schroyens ◽  
Joaquin Matias Alfei Palloni ◽  
Anna Elisabeth Schnell ◽  
Laura Luyten ◽  
Tom Beckers
Keyword(s):  
Memory Retrieval ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Memory Retention ◽  
Conditioning Context ◽  
Drug Induced ◽  
Systemic Injection ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Systemic Drug

With the ultimate goal of investigating boundary conditions for post-reactivation amnesia, we set out to replicate studies in which systemic, post-reactivation administration of midazolam, propranolol, or cycloheximide resulted in amnesia for contextual fear memories. Our experiments involved conceptual as well as exact replications of previously published studies. In most of our experiments, we adopted a procedure that conformed to the standard 3-day protocol typically used in the literature, with contextual fear conditioning on day 1, unreinforced re-exposure to the conditioning context followed by systemic injection of the amnestic drug on day 2, and a memory retention test on day 3. Given the plethora of successful studies with large effects sizes and the absence of any failed replications in the literature, we were surprised to find that we were generally unable to replicate those findings. Our results suggest that post-reactivation amnesia by systemic drug administration in rats is more difficult to obtain than what would be expected based on published empirical reports. At present, it remains unclear which conditions determine the success of this procedure.

Contextual Fear Memory Retrieval Is Vulnerable to Hippocampal Noise

2020 ◽  
Author(s):  
Satoshi Iwasaki ◽  
Yuji Ikegaya
Keyword(s):  
Memory Retrieval ◽  
Basolateral Amygdala ◽  
Fear Memory ◽  
Memory Recall ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Hippocampal Ca1 ◽  
Recall Memory ◽  
Neuron Ensemble ◽  
Memory Engram

Abstract Memory retrieval depends on reactivation of memory engram cells. Inadvertent activation of these cells is expected to cause memory-retrieval failure, but little is known about how noisy activity of memory-irrelevant neurons impacts mnemonic processes. Here, we report that optogenetic nonselective activation of only tens of hippocampal CA1 cells (∼0.01% of the total cells in the CA1 pyramidal cell layer) impairs contextual fear memory recall. Memory recall failure was associated with altered neuronal reactivation in the basolateral amygdala. These results indicate that hippocampal memory retrieval requires strictly regulated activation of a specific neuron ensemble and is easily disrupted by the introduction of noisy CA1 activity, suggesting that reactivating memory engram cells as well as silencing memory-irrelevant neurons are both crucial for memory retrieval.

scholarly journals Septal GABAergic inputs to CA1 govern contextual memory retrieval

2020 ◽  
Vol 6 (44) ◽  
pp. eaba5003
Author(s):  
Arnau Sans-Dublanc ◽  
Adrià Razzauti ◽  
Srinidhi Desikan ◽  
Marta Pascual ◽  
Hannah Monyer ◽  
...  
Keyword(s):  
Memory Retrieval ◽  
Pyramidal Neurons ◽  
Medial Septum ◽  
Aminobutyric Acid ◽  
Contextual Fear ◽  
Extracellular Signal Regulated Kinase ◽  
Impaired Memory ◽  
Extracellular Signal ◽  
Episodic Memories ◽  
Feed Forward Inhibition

The CA1 output region of the hippocampus plays an essential role in the retrieval of episodic memories. γ-Aminobutyric acid–releasing (GABAergic) long-range projections from the medial septum (MS) densely innervate the hippocampus, but whether septal inputs regulate memory expression remains elusive. We found that the MS to CA1 connection is recruited during recall of a contextual fear memory. Chemogenetic silencing of CA1-projecting MS neurons or septal GABAergic terminals within CA1 blocked memory retrieval. Photostimulation of septal GABAergic terminals in CA1 selectively inhibited interneurons. Abrogating septal GABAergic cells during retrieval disinhibited parvalbumin-rich (PV+) cells in CA1. Direct activation of CA1 PV+ cells impaired memory and prevented the induction of extracellular signal–regulated kinase/mitogen-activated kinase signaling in postsynaptic pyramidal neurons. Opposing disinhibition of hippocampal PV+ cells reversibly restored memory. Our data indicate that suppression of feed-forward inhibition onto CA1 by septal GABAergic neurons is an important mechanism in gating contextual fear behavior.

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