Satb2 Ablation Impairs Hippocampus-Based Long-Term Spatial Memory and Short-Term Working Memory and Immediate Early Genes (IEGs)-Mediated Hippocampal Synaptic Plasticity

Author(s):  
Ying Li ◽  
Qiang-Long You ◽  
Sheng-Rong Zhang ◽  
Wei-Yuan Huang ◽  
Wen-Jun Zou ◽  
...  
2022 ◽  
Vol 15 ◽  
Author(s):  
Violeta-Maria Caragea ◽  
Denise Manahan-Vaughan

Dopamine is a key factor in the enablement of cognition and hippocampal information processing. Its action in the hippocampus is mediated by D1/D5 and D2-like (D2, D3, D4) receptors. While D1/D5-receptors are well recognized as strong modulators of hippocampal synaptic plasticity and information storage, much less is known about the role of D2-like receptors (D2R) in these processes. Here, we explored to what extent D2R contribute to synaptic plasticity and cumulative spatial memory derived from semantic and episodic-like information storage. In freely behaving adult rats, we also assessed to what extent short and long-term forms of synaptic plasticity are influenced by pharmacological activation or blockade of D2R. Antagonism of D2R by means of intracerebral treatment with remoxipride, completely prevented the expression of both short-term (<1 h) and long-term potentiation (>4 h), as well as the expression of short-term depression (STD, <1 h) in the hippocampal CA1 region. Scrutiny of involvement of D2R in spatial learning revealed that D2R-antagonism prevented retention of a semantic spatial memory task, and also significantly impaired retention of recent spatiotemporal aspects of an episodic-like memory task. Taken together, these findings indicate that D2R are required for bidirectional synaptic plasticity in the hippocampal CA1 region. Furthermore, they are critically involved in enabling cumulative and episodic-like forms of spatial learning.


1991 ◽  
Vol 5 (2-4) ◽  
pp. 297-314 ◽  
Author(s):  
Wickliffe C. Abraham ◽  
Michael Dragunow ◽  
Warren P. Tate

1989 ◽  
Vol 13 (4) ◽  
pp. 301-313 ◽  
Author(s):  
M. Dragunow ◽  
R.W. Currie ◽  
R.L.M. Faull ◽  
H.A. Robertson ◽  
K. Jansen

Neuroreport ◽  
1993 ◽  
Vol 4 (1) ◽  
pp. 37-40 ◽  
Author(s):  
Jari Koistinaho ◽  
Markku Pelto-Huikko ◽  
Stephen M. Sagar ◽  
Åke Dagerlind ◽  
Reina Roivainen ◽  
...  

Author(s):  
Andrea de Bartolomeis ◽  
Elisabetta F. Buonaguro ◽  
Gianmarco Latte ◽  
Rodolfo Rossi ◽  
Federica Marmo ◽  
...  

1991 ◽  
Vol 11 (1) ◽  
pp. 89-91 ◽  
Author(s):  
Steven S. Schreiber ◽  
Stephen Maren ◽  
Georges Tocco ◽  
Tracey Jo Shors ◽  
Richard F. Thompson

1998 ◽  
Vol 119 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Ottavio Pompeiano

Experiments performed either in decerebrate cats or in intact rabbits have shown that functional inactivation of the cerebellar anterior vermis or the flocculus decreased the basic gain of the vestibulospinal or the vestibulo-ocular reflex, respectively. These findings were attributed to the fact that a proportion of the vermal or floccular Purkinje cells, which are inhibitory in function, discharge out of phase with respect to the vestibulospinal or the vestibulo-ocular neurons during sinusoidal animal rotation, thus exerting a facilitatory influence on the gain of the vestibular reflexes. Intravermal injection of a β-noradrenergic agonist slightly increased the gain of the vestibulospinal reflex, whereas the opposite result was obtained after injection of β-antagonists. Similarly, intrafloccular injection of a β-noradrenergic agonist slightly facilitated the gain of the vestibulo-ocular reflex in darkness (but not in light), whereas a small decrease of the reflex occurred after injection of a β-antagonist. It was postulated that the noradrenergic system acts on Purkinje cells by enhancing their amplitude of modulation to a given labyrinth signal, thus increasing the basic gain of the vestibular reflexes. The Purkinje cells of the cerebellar anterior vermis and the flocculus also exert a prominent role on the adaptation of vestibulospinal and vestibulo-ocular reflexes, respectively. In particular, intravermal or intrafloccular injection of β-noradrenergic antagonists decreased or suppressed the adaptive capacity of the vestibulospinal and vestibulo-ocular reflexes that always occurred during sustained out-of-phase neck-vestibular or visual-vestibular stimulation, whereas the opposite result was obtained after local injection of a β-noradrenergic agonist. The noradrenergic innervation of the cere-bellar cortex originates from the locus coeruleus complex, whose neurons respond to vestibular, neck, and visual signals. It was postulated that this structure acts through β-adrenoceptors to increase the expression of immediate-early genes, such as c- fos and Jun-B, in the Purkinje cells during vestibular adaptation. Induction of immediate-early genes could then represent a mechanism by which impulses elicited by sustained neck-vestibular or visuovestibular stimulation are transduced into long-term biochemical changes that are required for cerebellar long-term plasticity. (Otolaryngol Head Neck Surg 1998;119:93-105.)


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