Selected Publications

Some Recent Publications

Andrew RD. (2016). Spreading depression is weak or absent in the rodent lower brain. J Cerebral Blood Flow and Metabolism. In press. 

Spong KE, Andrew RD, Robertson RM (2016). Mechanisms of spreading depolarization in vertebrate and insect central nervous systems. J Neurophysiol; published ahead of print June 22, 2016, doi:10.1152/jn.00352.2016 

Dreier JP…Andrew RD…et al. (2016). Recommendations of the COSBID study group on recording and analysis of spreading depolarizations in neurointensive care. J Cerebral Blood Flow and Metabolism DOI:10.1177/0271678X16654496. 

Hartings JA…Andrew RD et al. (2016). The continuum of spreading mass depolarizations in acute cortical lesion development: redefining Leao`s legacy. J Cerebral Blood Flow and Metabolism. In press. 

Hubel N, Andrew RD, Ullah G. (2016). Large extracellular space leads to neuronal susceptibility to ischemic injury in Na+/K+ pumps-dependent manner. J Computational Neuroscience. In press. 

Andrew RD. (2015).The Persistent Vegetative State: Evidence That the Lower Brain Survives Because Its Neurons Intrinsically Resist Ischemia. M.M. Monti, W.G. Sannita (eds.), Brain Function and Responsiveness in Disorders of Consciousness,© Springer International Publishing Switzerland 2016 DOI 10.1007/978-3-319-21425-2_10



Significant Contributions

1. Andrew, R.D. el al. (1981) in Science 211, 1187-1189  and

    Andrew, R.D. and F.E. Dudek (1983) in Science 221, 1050-1052.

The first study demonstrated extensive dye-coupling in the hypothalamus between neuroendocrine neurons and in the cortex between hippocampal pyramidal neurons. The experiments were among the first showing that electrical coupling is probably an important synchronizing mechanism among certain neuronal populations, even in adult animals. The second study first reported that mammalian neuroendocrine cells possess intrinsic bursting properties that are powerful enough to drive phasic bursting. This patterned firing causes vasopressin release, a process that has been studied for twenty years in intact rats. This paper set the stage for numerous intracellular studies describing the electrophysiological properties of these mammalian secretory neurons.
 

2. Andrew, R.D. (1991) in J. Neurological Sciences 101, 7-18.

This article tied together clinical and electrophysiological evidence showing that acute but clinically relevant decreases or increases in osmolality can affect CNS excitability to the point of inducing or suppressing seizure respectively.

3. Andrew, R.D. et al. (1997) in Experimental Neurology 143, 300-3312.

This study challenged the established concept that mammalian brain neurons can easily regulate their volume during acute osmotic stress. We demonstrated that regulatory volume decreases (RVD) or increases (RVI) do not occur within the osmotic range experienced by the intact animal. We argued that previous studies have detected RVD and RVI only in cultured cells and when osmotic stress was so unphysiological as to be irrelevant to the intact animal. This was followed up in 5 below.

4. Obediat, A.S. and R.D. Andrew (1998) in European J. Neuroscience 10, 3451-3461.

This work showed that spreading depression-like events induced by simulated ischemia can be imaged in real time across brain slices. Its initiation, propagation and damaging effects were mapped across many square millimeters of brain tissue, permitting a detailed assessment of potentially therapeutic drugs to reduce stroke damage.
 

5. Andrew, R.D. et al. (2007) in Cerebral Cortex ;17:787-802.

This study provided direct, real-time imaging that supported our study carried out 10 years earlier (3,above). Two photon microscopy of live neurons showed no cellular volume regulation during acute osmotic or ischemic stress. Pyramidal somata, dendrites and spines steadfastly maintained their volume durind osmotic challenge, as did cerebellar axon terminals. This precluded a need for the neurons to acutely regulate volume, preserved their intrinsic electrophysiological stability, and confirmed that these CNS nerve cells lack functional aquaporins. Thus, whereas water easily permeates the aquaporin-rich endothelia and glia driving osmotic brain swelling, neurons tenatiously maintain their volume. However, these same neurons then swell dramatically upon oxygen/glucose deprivation or [K+]o elevation. We propposed that prolonged depolarization (as during stroke or seizure) swells neurons not by opening water channels, but by either passive influx of water or (more likely) by an inability to pump out metabolic water that then accumulates during energy failure. More recently other labs have shown that ion transporters can also move water across neuronal membrane.