Abstract

Previous work showed that histamine (HA) infused into hippocampi excited CA1 pyramidal neurons and lengthened hibernation bouts by 50%. However, HA effectiveness in increasing CA1 pyramidal neuron excitability at low levels of synaptic stimulation (mirroring that when entering torpor) is unknown. We tested the hypotheses that HA modulation of Syrian hamster CA1 pyramidal neurons: increased evoked response amplitude (ERA) to threshold level voltages, persisted at temperatures below 37°C, and involved H2 receptors. We measured CA1 ERAs in response to Schaffer collateral stimulation ranging from near‐maximal saturation (“max”) to below threshold levels at 30°C (n=14) and 20°C (n=17). Addition of 10µM HA to the perfusate increased near‐threshold stimulation ERAs [Taking the max response before HA as 100%, near‐threshold ERAs increased from 2.7% to 12.9% at 30°C (P<0.01), and from 2.5% to 20.7% at 20°C (P<0.001)]. These HA‐mediated increases in ERAs decreased as stimulation intensity approached max. Cimetidine (H2 antagonist; 20 µM) blocked the HA‐mediated ERA increase in 8 of 8 slices stimulated at 50‐75% of saturation. Data support our hypotheses, showing HA enhanced responses near threshold at both 30°C and 20°C, and that HA enhancement was mediated via H2 receptors. Data are consistent with the proposal that HA may modulate a low‐level hippocampal signal to the ascending arousal system to prolong torpor.Grant Funding Source: Supported by UC Davis Provost's Undergraduate Fellowship to KJM

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