Long-term potentiation in the CAl region of the hippocpus, a model for memory formation in the brain, Is diided into two phases. A transient process (induction) is initiated, which then generates a persistent mechanism (maintenance) for enhancing synaptic strenth. Protein kinase C (PKC), a gene family of multiple isozymes, may play a role in both induction and maintenance. In region CAl from rat hippocampal sices, most of the isozymes of PKC translocated to the partcuate fraction 15 sec after a tetanus. The Increase of PKC in the particulate fraction did not persist into the maintenance phase of long-term potentiation. In contrast, a constitutivey active kinase, PKM, a form specific to a single isozyme (), increased in the cytosol during the maintenance phase. The tramition from trnslocation of PKC to formation of PKM may help to explain the molecular mechanims of induction and maintenance of long-term potentiation.

We describe some of the cultural/religious issues which arose in the treatment of major psychiatric disorders among Orthodox Jewish inpatients at SUNY Health Science Center's University Hospital (SUH) in Brooklyn, New York. The distinct ways in which cultural and religious factors impacted on presentation, therapeutic interventions, and transference-countertransference reactions are noted. Specific reference is made to the use of religion by patients and families as a means of defense, rationalization or power-brokering. Via case vignettes, we explore ways of distinguishing between culturally appropriate vs. maladaptive behaviors in the Orthodox population. Practical solutions are suggested for sensitive ways to surmount culture-based barriers to effective inpatient therapy in this group.

Background: Brain mitochondrial dysfunction is implicated in the pathophysiology of mood disorders. Brain cytochrome-c-oxidase (COX) activity is associated with the mitochondrial function. Near-infrared spectroscopy (NIRS) noninvasively measures oxidized COX (oxCOX) and tissue oxygenation index (TOI) reflecting cerebral blood flow and oxygenation.Methods: oxCOX and TOI were assessed in prefrontal cortex (Fp1/2, Brodmann area 10) in patients in a major depressive episode (N = 13) with major depressive disorder (MDD; N = 7) and bipolar disorder (BD; N = 6) compared with the controls (N = 10).One patient with MDD and all the patients with BD were taking medications.Computational modeling estimated oxCOX and TOI related indices of mitochondrial function and cerebral blood flow, respectively.Results: oxCOX was lower in patients than controls (p = .014) correlating inversely with depression severity (r = −.72; p = .006), driven primarily by lower oxCOX in BD compared with the controls. Computationally modeled mitochondrial parameters of the electron transport chain, such as the nicotinamide adenine dinucleotide ratio (NAD + /NADH; p = .001) and the proton leak rate across the inner mitochondrial membrane (k lk2 ; p = .008), were also lower in patients and correlated inversely with depression severity. No such effects were found for TOI.Conclusions: In this pilot study, oxCOX and related mitochondrial parameters assessed by NIRS indicate an abnormal cerebral metabolic state in mood disorders proportional to depression severity, potentially providing a biomarker of antidepressant effect. Because the effect was driven by the medicated BD group, findings need to be evaluated in a larger, medication-free population.

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