scholarly journals Hippocampal Stimulation of Fornical-lesioned Rats Improves Working Memory

1994 ◽  
Vol 21 (2) ◽  
pp. 100-103 ◽  
Author(s):  
J. Turnbull ◽  
F. Jiang ◽  
R. Racine
Keyword(s):  
Working Memory ◽  
Memory Impairment ◽  
Theta Rhythm ◽  
Rhythmic Activity ◽  
Hippocampal Theta Rhythm ◽  
Disease States ◽  
Hippocampal Stimulation ◽  
Hippocampal Theta ◽  
The Brain ◽  
Normal Cognition

Abstract:Intrinsic rhythmic electrical activity in the brain, such as the hippocampal theta rhythm, might serve important roles in normal cognition. Lesions to the medial septal nuclei, or to the fimbria/fornix, disrupt the hippocampal theta rhythm and lead to memory impairment. We have superimposed an artifical stimulating rhythm to the hippocampus of rats with prior lesion of the fornix, during testing in the Morris water maze. This intervention improves performance in a test of working memory, and lends support to the view that intrinsic rhythmic activity may play an important role in normal physiology, and in certain disease states.

Two populations of rhythmically bursting neurons in rat medial septum are revealed by atropine

1989 ◽  
Vol 61 (5) ◽  
pp. 982-993 ◽  
Author(s):  
M. Stewart ◽  
S. E. Fox
Keyword(s):  
Time Course ◽  
Theta Rhythm ◽  
Rhythmic Activity ◽  
Medial Septum ◽  
Hippocampal Theta Rhythm ◽  
Diagonal Band ◽  
Septohippocampal System ◽  
Rhythmic Firing ◽  
Hippocampal Theta ◽  
Resistant Cells

1. Previous findings, such as the sensitivity of the hippocampal theta rhythm to cholinergic manipulation, support a "pacemaker" role for the cholinergic cells of the medial septal nucleus and the vertical limb of the nucleus of the diagonal band (MSN-NDB). To explore the mechanism(s) of action of systemic antimuscarinic drugs in eliminating the theta rhythm, recordings of hippocampal EEG and rhythmic MSN-NDB neurons that fired in phase with the hippocampal theta rhythm were taken during the administration of atropine in urethane-anesthetized rats. 2. Twenty-two of 33 rhythmic MSN-NDB cells continued to burst at the theta rhythm frequency after administration of a dose of atropine (25 mg/kg iv) that was sufficient to eliminate the theta rhythm (atropine-resistant cells). The remaining 11 cells lost their rhythmic firing pattern over the same time course as the loss of the theta rhythm (atropine-sensitive cells). 3. Both types of rhythmic MSN-NDB cells could be antidromically driven from the fimbria/fornix with similar latencies (range, 0.5-4.0 ms). The extracellularly recorded spike waveforms were not useful in predicting the atropine sensitivity of a given cell. Atropine-resistant cells frequently had higher firing rates than atropine-sensitive cells, but there was sufficient overlap of the two groups to make this a poor predictor of sensitivity. 4. Cooling the fimbria/fornix reversibly eliminated the hippocampal theta rhythm, but had no effect on 21/25 rhythmic MSN-NDB cells tested. This indicates that the atropine-sensitive MSN-NDB cells do not depend on the periodic output from the hippocampus for their rhythmic firing. Recordings from pairs of rhythmic MSN-NDB cells during cooling and/or atropine administration showed unchanged phase relations at the theta rhythm frequency. In rats in which the septohippocampal system was exposed by aspirating the overlying brain tissue, direct application of atropine (10 mg/ml) to the septal nuclei reversibly eliminated the hippocampal theta rhythm. 5. The rhythmic cells of the MSN-NDB are apparently composed of at least two distinct types, both of which potentially contribute to the production of the theta rhythm in the hippocampus. Elimination of hippocampal theta rhythm after local septal atropine application suggests that the loss of rhythmic activity in the group of atropine-sensitive septal cells is sufficient for the elimination of the theta rhythm. A model of the septohippocampal connections necessary for the theta rhythm is presented.

scholarly journals Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

2021 ◽  
Author(s):  
Simone N. De Luca ◽  
Kurt Brassington ◽  
Stanley M. H. Chan ◽  
Aleksandar Dobric ◽  
Kevin Mou ◽  
...  
Keyword(s):  
Working Memory ◽  
Cognitive Dysfunction ◽  
Memory Impairment ◽  
Microglial Activation ◽  
Pulmonary Inflammation ◽  
Systemic Circulation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Memory Impairments ◽  
The Brain

Abstract Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods: Male BALB/c mice were exposed CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase (Gpx) mimetic, ebselen (10mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results: CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation.Conclusion: We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximizing the benefit of cessation.

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