M Bruce MacIver

Administrative Appointments

• Faculty Senate, Stanford Medical School (2008 - 2011)
• Committee on Graduate Studies, Stanford University (2008 - 2011)
• Environmental Health & Safety, Stanford University (2006 - 2009)
• Neuroscience Subcommittee, Amer Soc Anesthesiology (2006 - 2011)
• NIH Study Section - Adjunct, NIH (2004 - 2012)
View All 7administrative appointments of M MacIver

Honors and Awards

• Top 100 Photographs, Google Earth (2007 to Present)
• Top 10 % of Reviews, Faculty of 1000 (Medicine) (2009)
• Top 100 Citations, Anesthesia & Analgesia (2005)
• Allen V. Cox Medal, Stanford University (2004)

Professional Education

Graduate & Fellowship Program Affiliations

• Anesthesia
• Neurosciences
• Bioengineering

Community & International Work

• Sierra Club since 1987 
• Amnesty International since 1996 
• Wilderness Foundation since 1991 

Web Site Links

• 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.

Publications

• Anesthetics discriminate between tonic and phasic gamma-aminobutyric acid receptors on hippocampal CA1 neurons. Bieda MC, Su H, Maciver MB. Anesth Analg. 2009; 108 (2): 484-90
• Slow GABA(A) mediated synaptic transmission in rat visual cortex. Sceniak MP, Maciver MB. BMC Neurosci. 2008: 9 8
• Cellular actions of urethane on rat visual cortical neurons in vitro. Sceniak MP, Maciver MB. J Neurophysiol. 2006; 95 (6): 3865-74
• Isoflurane depresses hippocampal CA1 glutamate nerve terminals without inhibiting fiber volleys. Winegar BD, MacIver MB. BMC Neurosci. 2006: 7 5
• Anesthesia in silico. Sceniak MP, MacIver MB. Anesthesiology. 2006; 104 (3): 400-2