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2.  N-Methyl-D-aspartate and TrkB Receptor Activation in Cerebellar Granule Cells 
Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as neuroprotectants against the causes of acute neurodegeneration. We have employed cultured rat cerebellar granule cells as a model for determining the mechanisms of these intraneuronal survival pathways. Glutamate has long been known to kill neurons by an N-methyl-d-aspartate (NMDA) receptor-mediated mechanism. Paradoxically, subtoxic concentrations of NMDA protect neurons against glutamate-mediated excitotoxicity. Because NMDA protects neurons in physiologic concentrations of glucose and oxygen, we refer to this phenomenon as physiologic preconditioning. One of the major mechanisms of NMDA neuroprotection involves the activation of NMDA receptors leading to the rapid release of brain-derived neurotrophic factor (BDNF). BDNF then binds to and activates its cognate receptor, receptor tyrosine kinase B (TrkB). The efficient utilization of these two receptors confers remarkable resistance against millimolar concentrations of glutamate that kill more than eighty percent of the neurons in the absence of preconditioning the neurons with a subtoxic concentration of NMDA. Exactly how the neurons mediate neuroprotection by activation of both receptors is just beginning to be understood. Both NMDA and TrkB receptors activate nuclear factor kappaB (NF-kB), a transcription factor known to be involved in protecting neurons against many different kinds of toxic insults. By converging on survival transcription factors, such as NF-kB, NMDA and TrkB receptors protect neurons. Thus, crosstalk between these very different receptors provides a rapid means of neuronal communication to upregulate survival proteins through release and transcriptional activation of messenger RNA.
PMCID: PMC2597300  PMID: 12853306
N-methyl-d-aspartate; TrkB; receptor activation; cerebellar granular cells; survival pathways; neurons
3.  Personality Traits and Sex Differences in Emotions Recognition Among African Americans and Caucasians 
PMCID: PMC2580736  PMID: 14766644
emotion recognition; personality traits; openness; sex differences; cross; cultural
4.  Developing a Sense of Safety: The Neurobiology of Neonatal Attachment 
Clinical data suggests a strong negative impact of traumatic attachments on adult mental illness, presumably through organizing brain development. To further explore this clinical issue, a mammalian model of imprinting was developed to characterize the neural basis of attachment in both healthy and traumatic attachments. The altricial neonatal rat must learn the mother’s odor for nipple attachment, huddling, and orienting to the mother, all of which are required for pup survival. While it appears maladaptive to depend upon learning for attachment, the unique learning system of neonatal pups greatly enhances odor-preference learning and attachment while pups are confined to the nest. This heightened learning is expressed behaviorally as an enhanced ability to acquire learned odor preferences and a decreased ability to acquire learned odor aversions. Specifically, both odor-milk and odor-shock (0.5 mA) conditioning result in odor-preference acquisition. It appears as though there are at least three brain structures underlying the neonatal rat’s sensitive period for heightened odor learning: (1) odor learning is encoded in the olfactory bulb; (2) the hyperfunctioning noradrenergic locus coeruleus (LC) appears to support preference conditioning through release of NE; and (3) the hypofunctioning amygdala appears to underlie pups’ difficulty in learning odor aversions. Overall, this suggests that the CNS of altricial infants is specialized for optimizing attachments to their caregiver.
PMCID: PMC1868534  PMID: 14998878
mother-infant interactions; olfactory bulb; classical conditioning; norepinephrine; attachment; imprinting; locus coeruleus; amygdala; learning; abuse; stress; corticosterone; fear conditioning
5.  Analysis of CD4+CD25+ Cell Population in the Thymus from Myasthenia Gravis Patients 
The present study is aimed at exploring the regulatory CD4+CD25+ T cells in the thymus from myasthenia gravis (MG) patients. In early-onset MG, the thymus is hyperplastic and contains autoreactive activated T cells. Preliminary studies indicate that these CD4+CD25+ cells include activated autoreactive T cells. Studies to characterize the phenotype and suppressive capacity of these cells will be discussed.
PMCID: PMC1847366  PMID: 14592885
CD4+CD25+ T cells; myasthenia gravis; thymus; thymocyte population

Results 1-5 (5)