scholarly journals The Role and Mechanisms of Action of Glucocorticoid Involvement in Memory Storage

1998 ◽  
Vol 6 (3) ◽  
pp. 41-52 ◽  
Author(s):  
Carmen Sandi

Adrenal steroid hormones modulate learning and memory processes by interacting with specific glucocorticoid receptors at different brain areas. In this article, certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation. By reviewing the work carried out in different learning models in chicks (passive avoidance learning) and rats (spatial orientation in the Morris water maze and contextual fear conditioning), a role for brain corticosterone action through the glucocorticoid receptor type on the mechanisms of memory consolidation is hypothesized. Evidence is also presented to relate post-training corticosterone levels to the strength of memory storage. Finally, the possible molecular mechanisms that might mediate the influences of glucocorticoids in synaptic plasticity subserving long-term memory formation are considered, mainly by focusing on studies implicating a steroid action through (i) glutamatergic transmission and (ii) cell adhesion molecules.

Author(s):  
Tanisse Teale

A majority of research into memory formation and consolidation is commonly focused on adult brains and organisms. Our work focuses on the mechanisms of memory within the developing, juvenile brain in an attempt to provide a more full understanding of the underlying neural mechanisms of memory formation, consolidation and storage. During juvenile development, the brain undergoes important remodeling and synaptic pruning towards shaping the adult brain. Thus, during this time, memories may be lost through the remodeling of hippocampal-neocortical connections. The significance of comparing juvenile and adult memory processes is critical in understanding the structural changes that occur within memory-specific circuits associated with long-term memory formation. To provide a comparison of the neurobehavioral aspects of long-term memory formation in juveniles and adults, we trained Long Evan’s rats on a spatial task on postnatal days 16, 18, 20, 25, 30 or 50 (adults). Each age group was then tested for memory recall 24 hours or 3 weeks later. We noted that memory recall showed a dramatic change at postnatal day 20 such that memory recall at postnatal day 25 was similar to adult levels. We then used immunohistochemistry to quantify and analyze neural activity patterns in brain regions thought to underlie the short- and long-term storage of spatial memories. Identification of these regional activity changes during juvenile periods and comparison with adults allows us to explore the function and organization of interacting brain regions in long-term spatial memory storage during development.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Baker ◽  
Ryan Y. Wong

AbstractLearning to anticipate potentially dangerous contexts is an adaptive behavioral response to coping with stressors. An animal’s stress coping style (e.g. proactive–reactive axis) is known to influence how it encodes salient events. However, the neural and molecular mechanisms underlying these stress coping style differences in learning are unknown. Further, while a number of neuroplasticity-related genes have been associated with alternative stress coping styles, it is unclear if these genes may bias the development of conditioned behavioral responses to stressful stimuli, and if so, which brain regions are involved. Here, we trained adult zebrafish to associate a naturally aversive olfactory cue with a given context. Next, we investigated if expression of two neural plasticity and neurotransmission-related genes (npas4a and gabbr1a) were associated with the contextual fear conditioning differences between proactive and reactive stress coping styles. Reactive zebrafish developed a stronger conditioned fear response and showed significantly higher npas4a expression in the medial and lateral zones of the dorsal telencephalon (Dm, Dl), and the supracommissural nucleus of the ventral telencephalon (Vs). Our findings suggest that the expression of activity-dependent genes like npas4a may be differentially expressed across several interconnected forebrain regions in response to fearful stimuli and promote biases in fear learning among different stress coping styles.


2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Nicolette Ognjanovski ◽  
Samantha Schaeffer ◽  
Jiaxing Wu ◽  
Sima Mofakham ◽  
Daniel Maruyama ◽  
...  

Abstract Activity in hippocampal area CA1 is essential for consolidating episodic memories, but it is unclear how CA1 activity patterns drive memory formation. We find that in the hours following single-trial contextual fear conditioning (CFC), fast-spiking interneurons (which typically express parvalbumin (PV)) show greater firing coherence with CA1 network oscillations. Post-CFC inhibition of PV+ interneurons blocks fear memory consolidation. This effect is associated with loss of two network changes associated with normal consolidation: (1) augmented sleep-associated delta (0.5–4 Hz), theta (4–12 Hz) and ripple (150–250 Hz) oscillations; and (2) stabilization of CA1 neurons’ functional connectivity patterns. Rhythmic activation of PV+ interneurons increases CA1 network coherence and leads to a sustained increase in the strength and stability of functional connections between neurons. Our results suggest that immediately following learning, PV+ interneurons drive CA1 oscillations and reactivation of CA1 ensembles, which directly promotes network plasticity and long-term memory formation.


2006 ◽  
Vol 210 (3) ◽  
pp. 174-191 ◽  
Author(s):  
Robert D. Hawkins ◽  
Eric R. Kandel ◽  
Craig H. Bailey

1991 ◽  
Vol 5 (2-4) ◽  
pp. 333-350 ◽  
Author(s):  
K. T. Ng ◽  
M. E. Gibbs ◽  
S. F. Crowe ◽  
G. L. Sedman ◽  
F. Hua ◽  
...  

1998 ◽  
Vol 5 (4) ◽  
pp. 365-374 ◽  
Author(s):  
Roussoudan Bourtchouladze ◽  
Ted Abel ◽  
Nathaniel Berman ◽  
Rachael Gordon ◽  
Kyle Lapidus ◽  
...  

We have used a combined genetic and pharmacological approach to define the time course of the requirement for protein kinase A (PKA) and protein synthesis in long-term memory for contextual fear conditioning in mice. The time course of amnesia in transgenic mice that express R(AB) and have genetically reduced PKA activity in the hippocampus parallels that observed both in mice treated with inhibitors of PKA and mice treated with inhibitors of protein synthesis. This PKA- and protein synthesis-dependent memory develops between 1 hr and 3 hr after training. By injecting the protein synthesis inhibitor anisomycin or the PKA inhibitor Rp-cAMPs at various times after training, we find that depending on the nature of training, contextual memory has either one or two brief consolidation periods requiring synthesis of new proteins, and each of these also requires PKA. Weak training shows two time periods of sensitivity to inhibitors of protein synthesis and PKA, whereas stronger training exhibits only one. These studies underscore the parallel dependence of long-term contextual memory on protein synthesis and PKA and suggest that different training protocols may recruit a common signaling pathway in distinct ways.


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