Cultural sensitivity training in mental health: treatment of Orthodox Jewish psychiatric inpatients.

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.

Persistent activation of the zeta isoform of protein kinase C in the maintenance of long-term potentiation.

Long-term potentiation in the CA1 region of the hippocampus, a model for memory formation in the brain, is divided into two phases. A transient process (induction) is initiated, which then generates a persistent mechanism (maintenance) for enhancing synaptic strength. Protein kinase C (PKC), a gene family of multiple isozymes, may play a role in both induction and maintenance. In region CA1 from rat hippocampal slices, most of the isozymes of PKC translocated to the particulate 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 constitutively active kinase, PKM, a form specific to a single isozyme (zeta), increased in the cytosol during the maintenance phase. The transition from translocation of PKC to formation of PKM may help to explain the molecular mechanisms of induction and maintenance of long-term potentiation.

Evidence for a new, high-molecular weight isoform of protein kinase C in rat hippocampus.

We describe a new form of protein kinase C (PKC) with a molecular weight of 97 kDa, higher than the known forms of vertebrate PKC. This putative new high-molecular weight isoform, which we are calling PKC (HMW), is increased in the membrane fraction either upon application of phorbol esters or with afferent synaptic stimulation of Schaffer collaterals in hippocampal slices. The protein cross-reacts on immunoblot with affinity-purified polyclonal antiserum raised against a peptide derived from the carboxy-terminus of PKC eta; it does not cross-react, however, with antiserum against the amino-terminal region of PKC eta. In the tissues examined, PKC(HMW) is localized primarily in brain, in contrast to PKC eta, which is found predominantly in lung and skin.

Stimulus frequency and intensity: critical determinants of opioid enhancement or inhibition of evoked methionine-enkephalin release.

Responses to opioids can be bimodal depending on the concentration of opioid used. For example, low concentrations (nM) enhance whereas higher concentrations (10-100 nM) inhibit the electrically evoked release of enkephalin from the myenteric plexus. The nature of the responsiveness of the enkephalin release process to opioids is also dependent on the intracellular and/or extracellular milieu of enkephalin-containing neurons or other neurons of this plexus. Intracellular levels of cAMP, availability of pertussis toxin- and cholera toxin-sensitive guanine nucleotide binding proteins and intracellular calcium concentration have all been shown to be important determinants of opioid excitatory versus inhibitory actions. The present data indicate that the inhibition of enkephalin release produced by U50,488H or sufentanil is no longer observed when the applied voltage is increased 3- or 2-fold, respectively. Under this condition, a previously inhibitory concentration of opioid produces an enhancement of stimulated enkephalin release. Increasing the frequency of the applied stimulation from 5 to 60 Hz (at a constant voltage) also reverses the sufentanil-induced inhibition to a facilitation of enkephalin release. These data indicate that the intensity (voltage) or frequency of the stimulation that is used to release enkephalin is a critical determinant of the nature of its modulation by opioids. The possible relevance of these findings to known differences in opioid sensitivity between different types of pain is discussed.