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Related Concept Videos

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
Antiprotozoal Agents01:21

Antiprotozoal Agents

Leishmaniasis is a widespread parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. First-line treatment relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. Even so, how these drugs work has not been fully clear, especially their interaction with parasite-specific biochemical pathways. One key target is trypanothione reductase (TR), an enzyme that...
Long-term Potentiation01:35

Long-term Potentiation

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.
Long-term Potentiation01:25

Long-term Potentiation

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.
Hebbian LTP
LTP can occur when presynaptic neurons...
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...

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Related Experiment Video

Updated: Jul 7, 2026

Selective Depletion of Microglia from Cerebellar Granule Cell Cultures Using L-leucine Methyl Ester
08:10

Selective Depletion of Microglia from Cerebellar Granule Cell Cultures Using L-leucine Methyl Ester

Published on: July 7, 2015

Leptin as a neuroprotective agent.

Bor Luen Tang1

  • 1Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, Singapore 117597, Singapore. bchtbl@nus.edu.sg

Biochemical and Biophysical Research Communications
|January 29, 2008
PubMed
Summary

Leptin, a hormone regulating energy balance, shows neuroprotective effects. It enhances neuronal survival in models of brain injury and neurodegeneration, suggesting therapeutic potential.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Leptin is an adipocyte-derived hormone crucial for regulating satiety and energy homeostasis.
  • Leptin receptors are present in key brain regions, including the hypothalamus, hippocampus, and cerebral cortex, influencing neural development and neuroendocrine functions.

Purpose of the Study:

  • To investigate the neuroprotective potential of leptin.
  • To explore leptin's role in enhancing neuronal survival in vitro and in vivo.
  • To examine leptin's efficacy in animal models of neurological damage.

Main Methods:

  • In vitro and in vivo studies assessing neuronal survival.
  • Administration of leptin in animal models of cerebral ischemic injury and hemiparkinsonism.
  • Analysis of downstream signaling pathways including JAK-STAT, PI3K, and ERK.

Related Experiment Videos

Last Updated: Jul 7, 2026

Selective Depletion of Microglia from Cerebellar Granule Cell Cultures Using L-leucine Methyl Ester
08:10

Selective Depletion of Microglia from Cerebellar Granule Cell Cultures Using L-leucine Methyl Ester

Published on: July 7, 2015

Main Results:

  • Leptin administration demonstrated neuroprotective effects, enhancing neuronal survival.
  • Leptin treatment mitigated neuronal death in animal models of ischemic injury and hemiparkinsonism.
  • Leptin receptor signaling activates pro-survival and anti-apoptotic pathways.

Conclusions:

  • Leptin exhibits significant neuroprotective properties, promoting neuronal survival.
  • Leptin's ability to cross the blood-brain barrier peripherally supports its therapeutic potential for brain injuries.
  • Leptin is a promising drug candidate for neurodegenerative diseases and brain injury treatment.