Substantia nigra, nucleus basalis magnocellularis and basolateral amygdala roles in extinction of contextual fear conditioning in the rat

2010 ◽  
Vol 94 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Elisabetta Baldi ◽  
Corrado Bucherelli
Keyword(s):  
Substantia Nigra ◽  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Contextual Fear Conditioning ◽  
Nucleus Basalis ◽  
Nucleus Basalis Magnocellularis ◽  
Contextual Fear

scholarly journals Histaminergic ligands injected into the nucleus basalis magnocellularis differentially affect fear conditioning consolidation

2013 ◽  
Vol 16 (3) ◽  
pp. 575-582 ◽  
Author(s):  
Fernando Benetti ◽  
Elisabetta Baldi ◽  
Corrado Bucherelli ◽  
Patrizio Blandina ◽  
Maria Beatrice Passani
Keyword(s):  
Fear Conditioning ◽  
Memory Consolidation ◽  
Present Report ◽  
Fear Memory ◽  
Brain Regions ◽  
Contextual Fear Conditioning ◽  
Nucleus Basalis ◽  
Nucleus Basalis Magnocellularis ◽  
Endogenous Histamine ◽  
Male Wistar Rats

Abstract The role of the nucleus basalis magnocellularis (NBM) in fear conditioning encoding is well established. In the present report, we investigate the involvement of the NBM histaminergic system in consolidating fear memories. The NBM was injected bilaterally with ligands of histaminergic receptors immediately after contextual fear conditioning. Histaminergic compounds, either alone or in combination, were stereotaxically administered to different groups of adult male Wistar rats and memory was assessed as conditioned freezing duration 72 h after administration. This protocol prevents interference with NBM function during either acquisition or retrieval phases, hence restricting the effect of pharmacological manipulations to fear memory consolidation. The results presented here demonstrate that post-training H3 receptors (H3R) blockade with the antagonist/inverse agonist thioperamide or activation with immepip in the NBM potentiates or decreases, respectively, freezing response at retrieval. Thioperamide induced memory enhancement seems to depend on H2R, but not H1R activation, as the H2R antagonist zolantidine blocked the effect of thioperamide, whereas the H1R antagonist pyrilamine was ineffective. Furthermore, the H2R agonist ampthamine improved fear memory expression independently of the H3R agonist effect. Our results indicate that activation of post-synaptic H2R within the NBM by endogenous histamine is responsible for the potentiated expression of fear responses. The results are discussed in terms of activation of H3 auto- and heteroreceptors within the NBM and the differential effect of H3R ligands on fear memory consolidation in distinct brain regions.

scholarly journals The BigLEN-GPR171 Peptide Receptor System Within the Basolateral Amygdala Regulates Anxiety-Like Behavior and Contextual Fear Conditioning

2017 ◽  
Vol 42 (13) ◽  
pp. 2527-2536 ◽  
Author(s):  
Erin N Bobeck ◽  
Ivone Gomes ◽  
Darlene Pena ◽  
Kirstie A Cummings ◽  
Roger L Clem ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Contextual Fear Conditioning ◽  
Receptor System ◽  
Contextual Fear ◽  
Peptide Receptor

Histamine H3receptor-mediated impairment of contextual fear conditioning andin-vivoinhibition of cholinergic transmission in the rat basolateral amygdala

2001 ◽  
Vol 14 (9) ◽  
pp. 1522-1532 ◽  
Author(s):  
M. Beatrice Passani ◽  
Iacopo Cangioli ◽  
Elisabetta Baldi ◽  
Corrado Bucherelli ◽  
Pier Francesco Mannaioni ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Contextual Fear Conditioning ◽  
Cholinergic Transmission ◽  
Contextual Fear
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