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Temperature Dependence of Hippocampal Short‐term Facilitation (STF) in Syrian Hamsters, a Hibernating Species
Author(s) -
Horwitz Barbara,
Horowitz John M.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09840
Subject(s) - neuroscience , inhibitory postsynaptic potential , excitatory postsynaptic potential , hippocampal formation , gabaergic , hippocampus , neuron , hamster , biology , biological neural network , neural facilitation , chemistry , endocrinology
Studies on non‐hibernating mammals have identified short‐term facilitation (STF) as a form of cellular neural plasticity that modulates information processing over a hippocampal neural network of CA3 and CA1 pyramidal neurons. The circuit has two branches: (1) a monosynaptic excitatory (E) feedforward pathway wherein CA3 axons directly excite CA1 neurons, and (2) a bi‐synaptic inhibitory (I) feed‐forward pathway. Pathway I includes a GABAergic inhibitory neuron such that CA3 axons excite GABAergic interneurons that in turn inhibit CA1 neurons. The present study evaluated the possibility that such a dual feedforward circuit supported STF in hibernating as well as in non‐hibernating Syrian hamsters ( Mesocricetus auratus ). We tested the hypotheses that: (1) at temperatures at (or above) 25° C, the hamster’s circuits support STF as in non‐hibernating species, and (2) as temperature declines from 25° to 20° (simulating brain temperatures encountered during entry into torpor), STF is attenuated. For this, we evaluated responses in 400μ hamster hippocampal slices, using tungsten stimulating electrodes placed to excite CA3 axons (Schaffer collaterals/commissural fibers) and a glass electrode positioned to record CA1 neuron evoked responses (fEPSPs). Paired‐pulse stimulation (with an interpulse interval of 30 msec and an interval between pairs of 60 sec) evoked a pair of responses – i.e., fEPSP1 followed fEPSP2. With bath temperature at (or above) 25° C, the initial slope of fEPSP2 was greater than that of fEPSP1. This finding supports the presence of a hamster facilitating circuit with at least an E feedforward pathway linking CA3 and CA1 neurons. To determine if the hamster circuit also has a bi‐synaptic inhibitory branch, paired‐pulse experiments were repeated in the presence and absence of picrotoxin, a non‐competitive GABA receptor antagonist. Picrotoxin altered fEPSP1 and fEPSP2 slopes (e.g., when GABAergic interneurons were blocked, fEPSP1 slope increased), indicating the hamster circuit also had an inhibitory feedforward branch. Additionally, paired‐pulse experiments with bath temperature lowered to 20° C resulted in a decreased ratio of fEPSP2/fEPSP1, marking a decline in STF. Nonetheless, at 20° C (and even at 15° C), single‐shock CA3 stimulation still evoked action potentials (population spikes) in CA1 neurons, showing that, despite a loss in facilitation, the circuit continued to relay signals from CA3 to CA1 neurons. Taken together, our data are consistent with the proposal that awake and behaving hamsters have a dual feed‐forward neural circuit supporting STF, as in non‐hibernating mammalian species, but when the hamsters are hibernating, STF is muted.