Data from: Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous response of experimental epilepsy to focal brain cooling

Experiments with drug-induced epilepsy in rat brains and epileptic human
brain region reveal that focal cooling can suppress epileptic discharges
without affecting the brain’s normal neurological function. Findings
suggest a viable treatment for intractable epilepsy cases via an
implantable cooling device. However, precise mechanisms by which cooling
suppresses epileptic discharges are still not clearly understood. Cooling
experiments in vitro presented evidence of reduction in neurotransmitter
release from presynaptic terminals and loss of dendritic spines at
post-synaptic terminals offering a possible synaptic mechanism. We show
that termination of epileptic discharges is possible by introducing a
homogeneous temperature factor in a neural mass model which attenuates the
post-synaptic impulse responses of the neuronal populations. This result
however may be expected since such attenuation leads to reduced
post-synaptic potential and when the effect on inhibitory interneurons is
less than on excitatory interneurons, frequency of firing of pyramidal
cells is consequently reduced. While this is observed in cooling
experiments in vitro, experiments in vivo exhibit persistent discharges
during cooling but suppressed in magnitude. This leads us to conjecture
that reduction in the frequency of discharges may be compensated through
intrinsic excitability mechanisms. Such compensatory mechanism is modelled
using a reciprocal temperature factor in the firing response function in
the neural mass model. We demonstrate that the complete model can
reproduce attenuation of both magnitude and frequency of epileptic
discharges during cooling. The compensatory mechanism suggests that
cooling lowers the average and the variance of the distribution of
threshold potential of firing across the population. Bifurcation study
with respect to the temperature parameters of the model reveals how
heterogeneous response of epileptic discharges to cooling (termination or
suppression only) is exhibited. Possibility of differential temperature
effects on post-synaptic potential generation of different populations is
also explored.

对大鼠脑内药物诱导癫痫（drug-induced epilepsy）及人类癫痫脑区的实验表明，局部冷却（focal cooling）可抑制癫痫放电（epileptic discharges），且不影响大脑正常神经功能。研究结果提示，通过植入式冷却装置（implantable cooling device）可为难治性癫痫（intractable epilepsy）病例提供一种可行的治疗方案。然而，冷却抑制癫痫放电的精确机制仍未明确。体外冷却实验提供了证据，表明突触前末梢（presynaptic terminals）神经递质释放减少，且突触后末梢（post-synaptic terminals）树突棘（dendritic spines）丢失，这为可能的突触机制提供了线索。我们发现，在神经团模型（neural mass model）中引入均匀温度因子可减弱神经元群体的突触后冲动响应，从而终止癫痫放电。然而，这一结果在意料之中，因为这种减弱会导致突触后电位降低；且当对抑制性中间神经元的影响小于兴奋性中间神经元时，锥体细胞（pyramidal cells）的放电频率会随之降低。虽然在体外冷却实验中观察到这一现象，但体内实验显示冷却期间放电持续存在，只是幅度受到抑制。这使我们推测，放电频率的降低可能通过内在兴奋性机制（intrinsic excitability mechanisms）得到补偿。这种补偿机制通过在神经团模型（neural mass model）的放电响应函数（firing response function）中引入倒数温度因子来建模。我们证明，完整模型可再现冷却期间癫痫放电幅度和频率的衰减。该补偿机制表明，冷却降低了群体中放电阈值电位分布的均值和方差。针对模型温度参数的分岔研究（bifurcation study）揭示了癫痫放电对冷却的异质性响应（heterogeneous response）（终止或仅抑制）是如何表现的。还探讨了温度对不同群体突触后电位生成的差异效应的可能性。