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Related Concept Videos

Long-term Potentiation01:25

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Potentiation01:35

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Depression01:03

Long-term Depression

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Increased Body Temperature01:25

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A body temperature above  38°C  (100.4 °F) is known as fever or pyrexia, and a person with fever is termed 'febrile.' Typically, the hypothalamus, a part of the brain that acts as the body's thermostat, regulates body temperature through a thermoregulatory setpoint. It receives signals from cold and warm thermal receptors throughout the body and adjusts the body's temperature accordingly. Fever occurs when this hypothalamic setpoint is altered, usually in...
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Immunological memory, a pivotal pillar of the adaptive immune system, is responsible for the body's ability to remember and respond more swiftly and effectively to previously encountered pathogens. This remarkable feature is what makes vaccines so effective in preventing diseases.
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Related Experiment Video

Updated: Jan 17, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Fever Induces Long-Term Synaptic Enhancement and Protects Learning in an Accelerated Aging Model.

Fusheng Du1, Qi Wan2, Oleg O Glebov1,3

  • 1Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, Qingdao 266071, Shandong, China.

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Fever can enhance brain structure by strengthening synapses, a process involving AMPA-type glutamate receptors. This effect, observed in animal models, may offer long-term cognitive protection, especially during aging.

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Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice
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Area of Science:

  • Neuroscience
  • Physiology
  • Molecular Biology

Background:

  • The brain's response to fever, a common physiological state, is not fully understood.
  • Existing knowledge on fever's impact on brain structure and function is limited.

Purpose of the Study:

  • To investigate the physiological impact of fever on brain structure and function.
  • To explore the underlying mechanisms of fever-induced synaptic plasticity.
  • To assess the long-term effects of fever on cognitive function and aging.

Main Methods:

  • Induction of fever via yeast injection in rats and whole-body hyperthermia in mice.
  • Analysis of synaptic structure and function in the prefrontal cortex.
  • Investigation of the roles of AMPA-type glutamate receptors and protein translation.
  • Assessment of long-term effects in a D-galactose accelerated aging model.

Main Results:

  • Fever triggers structural synaptic enhancement in the prefrontal cortex.
  • This enhancement involves AMPA-type glutamate receptors and protein translation.
  • Repeated fever in juveniles leads to persistent synaptic strengthening into adulthood.
  • This strengthening mitigates learning deficits and synaptic loss in an aging model.

Conclusions:

  • Fever can induce long-lasting synaptic plasticity and cognitive benefits.
  • Thermal treatments may hold potential for cognitive protection in aging.
  • Environmental factors like temperature can shape long-term brain function.