Petrin D, Gagolewicz PJ, Mehder R, Bennett B, Jin AY, Andrew RD. Spreading depolarization and neuronal damage or survival in mouse neocortical brain slices immediately and 12 hours following middle cerebral artery occlusion. Accepted with revisions Oct 30, 2018.
Ventura, NM, Li TY Tse, MY, Richard L, Tayade C, Jin AY, Andrew RD, Pang SC. (2018) Developmental origins of pregnancy-induced cardiac changes: Establishment of a novel model using the atrial natriuretic peptide gene-disrupted mice. Molecular and Cellular Biochemistry. Accepted: April 13, 2018.
Andrew RD, Hsieh YT, Brisson CD. (2016) Spreading depolarization triggered by elevated potassium is weak or absent in the rodent lower brain., 7-2016 (e-pub), J. Neurophysiology
Spong KE, Andrew RD, Robertson RM, (2016) Mechanisms of spreading depolarization in vertebrate and insect central nervous systems., 10-2016, J. Neurophysiology, Vol. 116(3):1117-27
Hartings JA, Shuttleworth CW, Kirov SA, Ayata C, Hinzman JM, Foreman B, Andrew RD, et al. (2016) The continuum of spreading depolarizations in acute cortical lesion development: Examining Leao's legacy., 7-2016 (e-pub), J Cereb Blood Flow Metab.
Dreier JP, Fabricius M, Ayata C, ...Andrew RD et al. (2016) Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group., 7-2016 (e-pub), J Cereb Blood Flow Metab.
Hubel N, Andrew RD, Ullah G, (2016) Large extracellular space leads to neuronal susceptibility to ischemic injury in a Na+/K+ pumps-dependent manner., 5-2016, J. Neurophysiology, Vol. 40(2):177-92
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
Ventura NM, Jin AY, Tse MY, Peterson NT, Andrew RD, Pang SC. (2015). Onset and Regression of Pregnancy-Induced Cardiovascular Alterations in Gestationally-Hypertensive Mice: The Role of the Natriuretic Peptide System. Biol. Reprod. Dec; 93(6):142. doi: 10.1095/biolreprod.115.132696.
Ventura NM, Jin AY, Tse MY, Peterson NT, Andrew RD, Mewburn JD, Pang SC. (2015). Maternal hypertension programs increased cerebral tissue damage following stroke in adult offspring. Molecular and Cellular Biochemistry 408(1): 223-233.
D'Souza Y, Elharram A, Soon-Shiong R, Andrew RD, Bennett BM. (2015). Characterization of Aldh2-/- mice as an age-related model of cognitive impairment and Alzheimer's Disease. Molecular Brain 8:27. doi: 10.1186/s13041-015-0117-y.
Brisson CD, Jin AY, Andrew RD. (2014) Brainstem neurons resist the same acute ischemia that injures higher neurons: Insight to the persistent vegetative state. PLoS ONE. 9(5): e96585. doi:10.1371/journal.pone.0096585
Ventura NM, Jin AY, Peterson NT, Tse MY, Andrew RD, Pang SC. (2014) Molecular adaptations in vasoactive systems during acute stroke in salt-induced hypertension. Molecular and Cellular Biochemistry: 399(1-2):39-47.
Gagolewicz PJ and Andrew RD (2017) The elusive channel driving ischemic spreading depolarization. Society for Neuroscience, United States
Mehder RH, Petrin D, Gagolewicz PJ, Bennett BM, Jin AY, Andrew RD (2017) Survival of pyramidal neurons within the ischemic core of 12-hour post-MCAo mice. Society for Neuroscience, United States
Lowry C, Golod M, Bennett BM, Andrew RD (2017) Neuroprotection and differential Na+/K+ pump isoform expression in higher and lower brain regions. Canadian Assoc Neuroscience. Montreal PQ
Andrew RD, Hsieh Y-T and Brisson.CD (2016) Spreading depression is weak or absent in the rodent lower brain. Canadian Association for Neuroscience 2016, Toronto, Canada
Gagolewicz PJ and Andrew RD. (2016) Still unidentified: The channel driving spreading depolarization during ischemia. Canadian Association for Neuroscience 2016, Toronto, Canada
El-Kerdawy H, Carr J and Andrew RD. (2016) Mechanisms underlying neuronal swelling during acute osmotic or acute ischemic stress. Canadian Association for Neuroscience 2016, Toronto, Canada
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 during 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 tenaciously maintain their volume. However, these same neurons then swell dramatically upon oxygen/glucose deprivation or [K+]o elevation. We proposed 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 the neuronal membrane.