• Publications
  • Influence
Cellular and synaptic adaptations mediating opioid dependence.
Although opioids are highly effective for the treatment of pain, they are also known to be intensely addictive. There has been a massive research investment in the development of opioid analgesics,Expand
  • 800
  • 60
  • PDF
Properties and Opioid Inhibition of Mesolimbic Dopamine Neurons Vary according to Target Location
The mesolimbic dopamine system, which mediates the rewarding properties of nearly all drugs of abuse, originates in the ventral tegmental area (VTA) and sends major projections to both the nucleusExpand
  • 299
  • 50
  • PDF
Regulation of µ-Opioid Receptors: Desensitization, Phosphorylation, Internalization, and Tolerance
Morphine and related µ-opioid receptor (MOR) agonists remain among the most effective drugs known for acute relief of severe pain. A major problem in treating painful conditions is that toleranceExpand
  • 479
  • 35
  • PDF
Nicotine activates and desensitizes midbrain dopamine neurons
Tobacco use in developed countries is estimated to be the single largest cause of premature death. Nicotine is the primary component of tobacco that drives use, and like other addictive drugs,Expand
  • 702
  • 33
Vesicular Dopamine Release Elicits an Inhibitory Postsynaptic Current in Midbrain Dopamine Neurons
Synchronous activation of dopamine neurons, for instance upon presentation of an unexpected rewarding stimulus, results in the release of dopamine from both terminals in projection areas andExpand
  • 262
  • 31
  • PDF
A Common Mechanism Mediates Long-Term Changes in Synaptic Transmission after Chronic Cocaine and Morphine
The mesolimbic system is known to play a role in self-administration of opioids and psychostimulants. Although morphine and cocaine act by separate cellular mechanisms initially, the present studyExpand
  • 216
  • 24
Increased Probability of GABA Release during Withdrawal from Morphine
Opioid receptors located on interneurons in the ventral tegmental area (VTA) inhibit GABAA-mediated synaptic transmission to dopamine projection neurons. The resulting disinhibition of dopamine cellsExpand
  • 259
  • 21
  • PDF
Opioid-Sensitive GABA Inputs from Rostromedial Tegmental Nucleus Synapse onto Midbrain Dopamine Neurons
Opioids increase dopamine release in the brain through inhibition of GABA-A IPSCs onto dopamine cells. Immunolabeling indicates that GABA neurons in the rostromedial tegmental nucleus (RMTg), alsoExpand
  • 133
  • 20
  • PDF
Noradrenaline Triggers GABAA Inhibition of Bed Nucleus of the Stria Terminalis Neurons Projecting to the Ventral Tegmental Area
The lateral part of the ventral bed nucleus of the stria terminalis (vlBNST) is a critical site for the antiaversive effects of noradrenergic drugs during opioid withdrawal. The objective of theExpand
  • 140
  • 20
  • PDF
Dopamine D1 receptors facilitate transmitter release
A PHYSIOLOGICAL role for the dopamine D1 receptor has been difficult to define, particularly because of its complex pre- and postsynaptic localization in brain areas such as the striatum1. In theExpand
  • 268
  • 19