scholarly journals Low-intensity ultrasound restores long-term potentiation and memory in senescent mice through pleiotropic mechanisms including NMDAR signaling

2021 ◽  
Author(s):  
Daniel G. Blackmore ◽  
Fabrice Turpin ◽  
Tishila Palliyaguru ◽  
Harrison T. Evans ◽  
Antony Chicoteau ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Long Term Potentiation ◽  
Functional Improvement ◽  
Learning Deficits ◽  
Non Invasive ◽  
Term Potentiation ◽  
Low Intensity Ultrasound ◽  
Electrophysiological Correlate ◽  
Elderly Humans

AbstractAdvanced physiological aging is associated with impaired cognitive performance and the inability to induce long-term potentiation (LTP), an electrophysiological correlate of memory. Here, we demonstrate in the physiologically aged, senescent mouse brain that scanning ultrasound combined with microbubbles (SUS+MB), by transiently opening the blood–brain barrier, fully restores LTP induction in the dentate gyrus of the hippocampus. Intriguingly, SUS treatment without microbubbles (SUSonly), i.e., without the uptake of blood-borne factors, proved even more effective, not only restoring LTP, but also ameliorating the spatial learning deficits of the aged mice. This functional improvement is accompanied by an altered milieu of the aged hippocampus, including a lower density of perineuronal nets, increased neurogenesis, and synaptic signaling, which collectively results in improved spatial learning. We therefore conclude that therapeutic ultrasound is a non-invasive, pleiotropic modality that may enhance cognition in elderly humans.

Hippocampal long-term potentiation and spatial learning in the rat: effects of GABAB receptor blockade

Neuroscience ◽  
1996 ◽  
Vol 74 (2) ◽  
pp. 331-339 ◽  
Author(s):  
F.H Brucato ◽  
E.D Levin ◽  
D.D Mott ◽  
D.V Lewis ◽  
W.A Wilson ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Gabab Receptor ◽  
Long Term Potentiation ◽  
Receptor Blockade ◽  
Term Potentiation

Dissociation between genes activated in long-term potentiation and in spatial learning in the rat

1998 ◽  
Vol 251 (1) ◽  
pp. 41-44 ◽  
Author(s):  
G Richter-Levin ◽  
K.L Thomas ◽  
S.P Hunt ◽  
T.V.P Bliss
Keyword(s):  
Spatial Learning ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 4195-4203 ◽  
Author(s):  
Li Sui ◽  
M. E. Gilbert
Keyword(s):  
Thyroid Hormone ◽  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Learning Deficits ◽  
Paired Pulse ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Paired Pulse Depression

Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and postnatally to 0, 3, or 10 ppm propylthiouracil (PTU), a thyroid hormone synthesis inhibitor, administered in the drinking water of dams from gestation d 6 until postnatal day (PN) 30. Excitatory postsynaptic potentials and population spikes were recorded from the stratum radiatum and the pyramidal cell layer, respectively, in area CA1 of hippocampal slices from offspring between PN21 and PN30. Baseline synaptic transmission was evaluated by comparing input-output relationships between groups. Paired-pulse facilitation, paired-pulse depression, long-term potentiation, and long-term depression were recorded to examine short- and long-term synaptic plasticity. PTU reduced thyroid hormones, reduced body weight gain, and delayed eye-opening in a dose-dependent manner. Excitatory synaptic transmission was increased by developmental exposure to PTU. Thyroid hormone insufficiency was also dose-dependently associated with a reduction paired-pulse facilitation and long-term potentiation of the excitatory postsynaptic potential and elimination of paired-pulse depression of the population spike. The results indicate that thyroid hormone insufficiency compromises the functional integrity of synaptic communication in area CA1 of developing rat hippocampus and suggest that these changes may contribute to learning deficits associated with developmental hypothyroidism.

Reduced hippocampal CA1 Ca2+-induced long-term potentiation is associated with age-dependent impairment of spatial learning

1995 ◽  
Vol 686 (1) ◽  
pp. 107-110 ◽  
Author(s):  
Giovanni Diana ◽  
Maria Rosaria Domenici ◽  
Arsenia Scotti de Carolis ◽  
Alberto Loizzo ◽  
Stefano Sagratella
Keyword(s):  
Spatial Learning ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Age Dependent

scholarly journals Long-Term Potentiation and Memory

2004 ◽  
Vol 84 (1) ◽  
pp. 87-136 ◽  
Author(s):  
M. A. LYNCH
Keyword(s):  
Animal Models ◽  
Cell Signaling ◽  
Spatial Learning ◽  
Gene Knockout ◽  
Transgenic Animals ◽  
Long Term Potentiation ◽  
Afferent Pathways ◽  
Term Potentiation ◽  
Signaling Events

Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

Sign in / Sign up

Export Citation Format

Share Document