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M Bruce MacIverAcademic Appointments
Appointment
Organization
Associate Professor (Research)
Member
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NIH Biosketch DocHonors & Awards
Title
Organization
Date(s)
Top 100 Citations
Anesthesia & Analgesia
2005
Allen V. Cox Medal
Stanford University
2004
Administrative Appointments
Title
Organization
Start Year
End Year
Neuroscience Subcommittee
Amer Soc Anesthesiology
2006
2009
Environmental Health & Safety
Stanford
2006
2009
NIH Study Section - Adjunct
NIH
2004
2008
Neuroscience Admissions Panel
Stanford Medical School
2000
2005
Neuroscience Program Executive
Stanford Medical School
1997
2005
Professional Education
Degree
Awarding Institution
Field of Study
Year of Graduation
MSc PhD
University of Calgary
Neuroscience and Pharmacology
1987
Postdoctoral Advisees
Stephen Towers
Web Site Links
Research/Lab website:
MacIver Lab Home Page
Research Interests
Neuropharmacology
Cellular, synaptic and molecular mechanisms of action of central nervous system drugs; especially barbiturates, opiates, anesthetics and other CNS depressants. We use electrophysiological recording techniques and selective pharmacological probes, in hippocampal and cortical brain slices, to investigate the sites and mechanisms of action for CNS active agents. The long-term goal of our studies is to provide physiological background information required for the rational design of safer and more effective anesthetics and analgesics. Our recent studies have focussed on anesthetic effects at glutamate and GABA-mediated synapses as important targets for the CNS depressant effects of these agents. Depressed glutamate-mediated excitatory neurotransmission appears to be a common effect produced by most general anesthetics. We are currently studying agent specific actions at AMPA and NMDA glutamate receptor subtypes. Enhanced GABA-mediated inhibitory neurotransmission also appears to play an important role for many anesthetics. Anesthetics appear to act at both pre- and post-synaptic sites to alter neurotransmission in higher brain centers. Thus, discrete synaptic targets could provide fruitful avenues for the development of safer and more effective therapeutic agents for analgesia and anesthesia.
Cellular, synaptic and molecular mechanisms of action of central nervous system drugs; especially barbiturates, opiates, anesthetics and other CNS depressants. We use electrophysiological recording techniques and selective pharmacological probes, in hippocampal and cortical brain slices, to investigate the sites and mechanisms of action for CNS active agents. The long-term goal of our studies is to provide physiological background information required for the rational design of safer and more effective anesthetics and analgesics. Our recent studies have focussed on anesthetic effects at glutamate and GABA-mediated synapses as important targets for the CNS depressant effects of these agents. Depressed glutamate-mediated excitatory neurotransmission appears to be a common effect produced by most general anesthetics. We are currently studying agent specific actions at AMPA and NMDA glutamate receptor subtypes. Enhanced GABA-mediated inhibitory neurotransmission also appears to play an important role for many anesthetics. Anesthetics appear to act at both pre- and post-synaptic sites to alter neurotransmission in higher brain centers. Thus, discrete synaptic targets could provide fruitful avenues for the development of safer and more effective therapeutic agents for analgesia and anesthesia.
Community and International Work
- Sierra Club since 1987 More »
- Amnesty International since 1996 More »
- Wilderness Foundation since 1991 More »
Publications
- Sceniak MP, Maciver MB "Cellular actions of urethane on rat visual cortical neurons in vitro." J Neurophysiol 2006; More »
- Sceniak MP, Maciver MB "Anesthesia in silico." Anesthesiology 2006; 104: 3: 400-2 More »
- Winegar BD, MacIver MB "Isoflurane depresses hippocampal CA1 glutamate nerve terminals without inhibiting fiber volleys." BMC Neurosci 2006; 7: 5 More »
- Lukatch HS, Kiddoo CE, Maciver MB "Anesthetic-induced Burst Suppression EEG Activity Requires Glutamate-mediated Excitatory Synaptic Transmission." Cereb Cortex 2005; More »
- Bieda MC, MacIver MB "Major role for tonic GABAA conductances in anesthetic suppression of intrinsic neuronal excitability." J Neurophysiol 2004; 92: 3: 1658-67 More »
9 publications: view full list
