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Related Concept Videos

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...
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CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...
Plasticity00:58

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...
Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...

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Endocannabinoids in striatal plasticity.

David M Lovinger1, Brian N Mathur

  • 1Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA.

Parkinsonism & Related Disorders
|December 15, 2011
PubMed
Summary
This summary is machine-generated.

Endocannabinoids (eCBs) modulate brain plasticity via cannabinoid 1 (CB1) receptors. Dopamine depletion impacts these pathways, suggesting eCB signaling as a therapeutic target for Parkinson's disease (PD).

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Last Updated: May 26, 2026

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Preparation of Acute Brain Slices Using an Optimized N-Methyl-D-glucamine Protective Recovery Method

Published on: February 26, 2018

Area of Science:

  • Neuroscience
  • Neurophysiology
  • Molecular Biology

Background:

  • Endocannabinoids (eCBs) are lipid signaling molecules regulating synaptic plasticity in the nervous system, primarily through cannabinoid 1 (CB1) receptors.
  • In the striatum, eCBs and CB1Rs mediate synaptic depression at both GABAergic and glutamatergic synapses.
  • Dopamine (DA) signaling influences eCB-mediated synaptic plasticity, particularly at corticostriatal synapses.

Purpose of the Study:

  • To explore the mechanisms of eCB-mediated synaptic depression.
  • To investigate the role of this synaptic plasticity in striatal function.
  • To examine the link between dopamine depletion, corticostriatal alterations, and Parkinson's disease (PD).

Main Methods:

  • Electrophysiological recordings to assess synaptic transmission.
  • Pharmacological manipulation of endocannabinoid and dopamine systems.
  • Analysis of synaptic plasticity in animal models of dopamine depletion.

Main Results:

  • Dopamine and its receptors enhance eCB-mediated depression of glutamatergic synapses.
  • Dopamine depletion in animal models leads to alterations in corticostriatal synapses.
  • Evidence suggests altered eCB signaling in Parkinson's disease patients.

Conclusions:

  • eCB-mediated synaptic plasticity is a key regulator of striatal function.
  • Disruptions in dopamine signaling impact corticostriatal pathways relevant to PD.
  • Targeting the endocannabinoid system presents a potential therapeutic strategy for Parkinson's disease.