Syrian hamster neuroplasticity mechanisms fail as temperature declines to 15 °C, but histaminergic neuromodulation persists

Jock S. Hamilton, Sat M. Chau, Kevin J. Malins, Giancarlo G. Ibanez, John M. Horowitz, Barbara A Horwitz

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Previous research suggests that hippocampal neurons in mammalian hibernators shift their major function from memory formation at euthermic brain temperatures (Tb = ~37 °C) to modulation of hibernation bout duration as Tb decreases. This role of hippocampal neurons during torpor is based in part on in vivo studies showing that histamine (HA) infused into ground squirrel hippocampi lengthened torpor bouts by ~50%. However, it was unclear if HA acted directly on hippocampal neurons or on downstream brain regions via HA spillover into lateral ventricles. To clarify this, we used hippocampal slices to determine if HA would modulate pyramidal neurons at low levels of synaptic activity (as occurs in torpor). We tested the hypotheses that although LTP (a neuroplasticity mechanism) could not be generated at low temperatures, HA (via H2 receptors) would increase population spike amplitudes (PSAs) of Syrian hamster CA1 pyramidal neurons at low stimulation voltages and low temperatures. PSAs were recorded following Schaffer collateral stimulation from subthreshold levels to a maximum response plateau. We found that tetanus evoked LTP at 35 °C but not 15 °C; and at temperatures from 30 to 15 °C, HA significantly enhanced PSA at near threshold levels in slices from non-hibernating hamsters housed in “summer-like” or “winter-like” conditions and from hibernating hamsters. Cimetidine (H2 antagonist) blocked HA-mediated PSA increases in 8 of 8 slices; pyrilamine (H1 antagonist) had no effect in 7 of 8 slices. These results support our hypotheses and show that HA can directly enhance pyramidal neuron excitability via H2 receptors and thus may prolong torpor bouts.

Original languageEnglish (US)
Pages (from-to)1-13
Number of pages13
JournalJournal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology
DOIs
StateAccepted/In press - Apr 9 2017

Fingerprint

torpor
Neuronal Plasticity
Mesocricetus
histamine
Torpor
Histamine
Neurons
resting periods
neurons
Temperature
Pyramidal Cells
brain
Histamine H2 Receptors
temperature
tetanus
Cricetinae
Population
hibernation
Hippocampus
hamsters

Keywords

  • Ascending arousal system
  • CA1 pyramidal cells
  • Hibernation
  • Histamine
  • Torpor

ASJC Scopus subject areas

  • Physiology
  • Ecology, Evolution, Behavior and Systematics
  • Biochemistry
  • Animal Science and Zoology
  • Endocrinology

Cite this

Syrian hamster neuroplasticity mechanisms fail as temperature declines to 15 °C, but histaminergic neuromodulation persists. / Hamilton, Jock S.; Chau, Sat M.; Malins, Kevin J.; Ibanez, Giancarlo G.; Horowitz, John M.; Horwitz, Barbara A.

In: Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology, 09.04.2017, p. 1-13.

Research output: Contribution to journalArticle

Hamilton, Jock S. ; Chau, Sat M. ; Malins, Kevin J. ; Ibanez, Giancarlo G. ; Horowitz, John M. ; Horwitz, Barbara A. / Syrian hamster neuroplasticity mechanisms fail as temperature declines to 15 °C, but histaminergic neuromodulation persists. In: Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology. 2017 ; pp. 1-13.
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