Contribution of CaMKIV to injury and fear- induced ultrasonic vocalizations in adult mice

Calcium-calmodulin dependent protein kinase IV (CaMKIV) is a protein kinase that activates the transcription factor CREB. Our previous work demonstrated that mice lacking CaMKIV had a defect in fear memory while behavioral responses to noxious stimuli were unchanged. Here, we measured ultrasonic vocalizations (USVs) before and after fear conditioning and in response to a noxious injection of capsaicin to measure behavioral responses to emotional stimuli. Consistent with previous findings, behavioral nociceptive responses to capsaicin were undistinguishable between wild-type and CaMKIV(-/- )mice. Wild-type animals showed a selective increase in 50 kHz USVs in response to capsaicin while such an increase was absent in CaMKIV(-/- )mice. The foot shock given during fear conditioning caused an increase in 30 kHz USVs in both wild-type and CaMKIV(-/- )mice. When returned to the context one hour later, USVs from the wild-type were significantly decreased. Additionally, the onset of a tone, which had previously been paired with the foot shock, caused a significant decrease in USVs during auditory conditioning. CaMKIV(-/- )mice showed significantly less reduction in USVs when placed in the same context three days after receiving the shock, consistent with the decrease in freezing reported previously. Our results provide a new approach for investigating the molecular mechanism for emotional vocalization in mice and suggest that CaMKIV dependent signaling pathways play an important role in the emotional response to pain and fear

Z factor: a new index for measuring academic research output

With rapid progress in scientific research activities and growing competition for funding resources, it becomes critical to effectively evaluate an individual researcher's annual academic performance, or their cumulative performance within the last 3–5 years. It is particularly important for young independent investigators, and is also useful for funding agencies when determining the productivity and quality of grant awardees. As the funding becomes increasingly limited, having an unbiased method of measuring recent performance of an individual scientist is clearly needed. Here I propose the Z factor, a new and useful way to measure recent academic performance

Plasticity of NMDA receptor NR2B subunit in memory and chronic pain

Glutamatergic synapses play critical roles in brain functions and diseases. Long-term potentiation (LTP) is a most effective cellular model for investigating the synaptic changes that underlie learning as well as brain disease – although different molecular mechanisms are likely involved in LTP in physiological and pathological conditions. In the case of learning, N-methyl-D-aspartate (NMDA) receptor is known to be important for triggering learning-related plasticity; alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA) receptors are thought to be important for the expression of synaptic changes. In this review, I will examine recent evidence on the novel roles of NMDA receptors, in particular NR2B subunit-containing NMDA receptors in learning and chronic pain. A positive feedback control of NR2B receptor subunit is proposed to explain cortical sensitization involved in chronic pain, but not learning and memory

Quantum dense coding scheme via cavity decay

We investigate a secure scheme for implementing quantum dense coding via cavity decay and liner optics devices. Our scheme combines two distinct advantages: atomic qubit sevres as stationary bit and photonic qubit as flying bit, thus it is suitable for long distant quantum communication.Comment: 5 pages, 2 figure. A revised version, accept for publication in Journal of Modern Optc

Activation of Erk in the anterior cingulate cortex during the induction and expression of chronic pain

The extracellular signal-regulated kinase (Erk) activity contributes to synaptic plasticity, a key mechanism for learning, memory and chronic pain. Although the anterior cingulate cortex (ACC) has been reported as an important cortical region for neuronal mechanisms underlying the induction and expression of chronic pain, it has yet to be investigated whether or not Erk activity in the ACC may be affected by peripheral injury or in chronic pain state. In the present study, we use adult rat animal models of inflammatory and neuropathic pain and demonstrate that Erk signaling pathway in the ACC is potently activated after peripheral tissue or nerve injury. Furthermore, we demonstrate that mechanical allodynia significantly activated Erk activity at synaptic sites at two weeks after the injury. We propose a synaptic model for explaining the roles of Erk activity during different phases of chronic pain. Our findings suggest that cortical activation of Erk may contribute to both induction and expression of chronic pain

Progress and future of molecular pain

Since its launch at the beginning of 2005, Molecular Pain has published pain research articles that cover broad areas including: genetics, molecular and cellular biology, synaptic and neuronal mechanisms, novel animal models and human functional imaging studies. One important feature of Molecular Pain is its high speed in manuscript processing and publication, making the journal one of the best places for pain researchers to publish their novel findings