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Related Concept Videos

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...
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.
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...

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Related Experiment Video

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Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

Dopamine modulates an mGluR5-mediated depolarization underlying prefrontal persistent activity.

Kyriaki Sidiropoulou1, Fang-Min Lu, Melissa A Fowler

  • 1Department of Neuroscience, Rosalind Franklin University of Health and Science/Chicago Medical School, 3333 Green Bay Road, North Chicago, Illinois 60064, USA.

Nature Neuroscience
|January 27, 2009
PubMed
Summary

Neurons possess intrinsic properties for sustained activity, crucial for short-term memory. Dopamine and cocaine alter this cellular memory in prefrontal cortex neurons.

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Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry (CIS-FSCV) to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine
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Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry (CIS-FSCV) to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine

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Last Updated: Jun 26, 2026

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry
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Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry

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Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry (CIS-FSCV) to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine
06:40

Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry (CIS-FSCV) to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine

Published on: April 23, 2020

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Neuropharmacology

Background:

  • Prefrontal cortex (PFC) neurons exhibit persistent activity vital for short-term memory.
  • Dopamine and drugs of abuse are known to impact PFC function and working memory.
  • The intrinsic neuronal mechanisms underlying persistent activity remain incompletely understood.

Purpose of the Study:

  • To investigate the intrinsic postsynaptic depolarization evoked by action potential bursts in layer 5 PFC pyramidal neurons.
  • To determine the role of metabotropic glutamate receptor 5 (mGluR5) in this depolarization.
  • To examine the modulatory effects of dopamine D1 receptor (D1R) signaling and cocaine sensitization on this cellular mechanism.

Main Methods:

  • Utilized patch-clamp recordings in layer 5 PFC pyramidal neurons.
  • Investigated postsynaptic potentials evoked by action potential bursts.
  • Examined the influence of dopamine D1 receptor (D1R) activation and protein kinase A (PKA) pathway.
  • Assessed changes in depolarization following behavioral sensitization to cocaine.

Main Results:

  • Identified a burst-evoked postsynaptic depolarization mediated by mGluR5, independent of recurrent synaptic activity.
  • Demonstrated that a dopamine D1 receptor (D1R) and protein kinase A (PKA) pathway reduced this depolarization.
  • Observed a significant reduction in burst-evoked depolarization and loss of D1R modulation after cocaine sensitization.

Conclusions:

  • Burst-evoked intrinsic depolarization represents a form of short-term cellular memory in PFC neurons.
  • Dopamine, via D1R signaling, modulates this cellular memory.
  • Cocaine experience, through sensitization, disrupts this dopamine modulation, potentially impacting working memory.