4 research outputs found
Combat and Warfare in the Early Paleolithic and Medically Unexplained Musculo-Facial Pain in the 21st Century War Veterns and Active-Duty Military Personnel
In a series of recent articles, we
suggest that family dentists, military
dentists and psychiatrists with expertise
in posttraumatic stress disorder (especially in the Veterans Health Administration) are likely to see an increased
number of patients with symptomatic
jaw-clenching and early stages of tooth-
grinding (Bracha et al., 2005). Returning
warfighters and other returnees from
military deployment may be especially
at risk for high rates of clenching-
induced masticatory muscle disorders
at early stages of incisor grinding. The
literature we have recently reviewed
strongly supports the conclusion that
clenching and grinding may primarily
be a manifestation of experiencing
extreme fear or severe chronic distress
(respectively). We have recently
reviewed the clinical and paleoanthropological literature and have noted that
ancestral warfare and ancestral combat,
in the early Paleolithic Environment of
Evolutionary Adaptedness (EEA) may
be a neglected factor explaining the
conservation of the archaic trait of
bite-muscle strengthening. We have
hypothesized that among ancestral
warriors, jaw clenching may have
rapidly strengthened the two primary
muscles involved in biting, the masseter
muscles and the much larger temporalis muscles. The strengthening of
these muscles may have served the
purpose of enabling a stronger, deeper,
and therefore more lethal, defensive
bite for early Paleolithic humans. The
neuroevolutionary perspective presented here may be novel to many dentists. However, it may be useful in
patient education and in preventing
progression from jaw-clenching to
chronic facial pain
Spike-Timing Precision and Neuronal Synchrony Are Enhanced by an Interaction between Synaptic Inhibition and Membrane Oscillations in the Amygdala
The basolateral complex of the amygdala (BLA) is a critical component of the neural circuit regulating fear learning. During fear learning and recall, the amygdala and other brain regions, including the hippocampus and prefrontal cortex, exhibit phase-locked oscillations in the high delta/low theta frequency band (∼2–6 Hz) that have been shown to contribute to the learning process. Network oscillations are commonly generated by inhibitory synaptic input that coordinates action potentials in groups of neurons. In the rat BLA, principal neurons spontaneously receive synchronized, inhibitory input in the form of compound, rhythmic, inhibitory postsynaptic potentials (IPSPs), likely originating from burst-firing parvalbumin interneurons. Here we investigated the role of compound IPSPs in the rat and rhesus macaque BLA in regulating action potential synchrony and spike-timing precision. Furthermore, because principal neurons exhibit intrinsic oscillatory properties and resonance between 4 and 5 Hz, in the same frequency band observed during fear, we investigated whether compound IPSPs and intrinsic oscillations interact to promote rhythmic activity in the BLA at this frequency. Using whole-cell patch clamp in brain slices, we demonstrate that compound IPSPs, which occur spontaneously and are synchronized across principal neurons in both the rat and primate BLA, significantly improve spike-timing precision in BLA principal neurons for a window of ∼300 ms following each IPSP. We also show that compound IPSPs coordinate the firing of pairs of BLA principal neurons, and significantly improve spike synchrony for a window of ∼130 ms. Compound IPSPs enhance a 5 Hz calcium-dependent membrane potential oscillation (MPO) in these neurons, likely contributing to the improvement in spike-timing precision and synchronization of spiking. Activation of the cAMP-PKA signaling cascade enhanced the MPO, and inhibition of this cascade blocked the MPO. We discuss these results in the context of spike-timing dependent plasticity and modulation by neurotransmitters important for fear learning, such as dopamine