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Many regulatory elements are perfect or approximate palindromes because many tran- scription factors bind DNA as dimers cheap isoniazid 300mg medicine 5325, with each member of the dimer recognizing one of the half-sites. CREB binds to a CRE as a homodimer, with a higher affinity for palindromic than for asymmetric CREs. When bound to a CRE, CREB activates transcription only when it is phosphorylated on its critical ser133. It does so, as described earlier, because phosphorylated CREB, but not dephosphorylated CREB, can recruit the adapter pro- tein, CBP, into the transcription complex. CBP, in turn, interacts with the basal transcription complex. Scheme of the regulation of CREBphosphoryla- tion by several signaling pathways. The figure illustrates how sev- 2 eralsignaling pathwaysconvergeon thephosphorylation ofCREB Regulation by cAMP, Ca , and Growth Factors at a single serine residue, ser133. Neurotransmitters that stimu- late adenylyl cyclase would increase CREBphosphorylation by the As discussed in previous sections, the regulation of CREB activation of protein kinase A (PKA). On activation, free PKA cata- activation by phosphorylation illustrates the requirement lytic subunits would translocate to the nucleus, where they would for nuclear translocation of protein kinases or second mes- phosphorylate ser133 of CREB. Neurotransmitters that inhibit ad- enylyl cyclase would cause the opposite cascade and inhibit CREB sengers when transcription factors are already found in the phosphorylation. Any of several signalsthat increase cellular Ca2 nucleus under basal conditions and the role of phosphoryla- levels (e. An addi- voltage-gated Ca2 channels) would also increase CREBphos- phorylation. Here, it appears that awave of increased Ca2 would tional important principle illustrated by CREB is the con- permeate the nucleus, where it would activate certain Ca2 /cal- vergence of signaling pathways. CREB is activated in modulin–dependent protein kinases (CaM kinases), particularly response to activation of the cAMP or Ca2 pathways. In addition, growth factor regulated pathways lead to CREBphosphorylation, occurs because the same serine residue (ser133)is phosphor- ylated both by protein kinase A and by Ca2 /calmo- although the details are not as well established. One possibility, shown in the figure, is that activation of Ras-Raf-MEK pathways dulin–dependent protein kinases (CaM kinases)(Fig. RSK would then phosphorylate ser133 of the enzyme that mediates this phosphorylation (19,20). MEK, MAP kinase and ERK kinase; ERK, extracellular CREB also appears to be phosphorylated on ser133 by a signal regulated kinase; RSK, ribosomal S6 kinase. Thus, diverse types of signaling pathways converge on CREB Family of Transcription Factors the phosphorylation and activation of CREB. If each indi- CREs were the first second messenger response element to vidual signal is relatively weak, convergence may be a critical be well characterized (12,17,18). As the name suggests, mechanism for achieving significant gene regulation, with CREs confer activation by cAMP on genes to which it is some genes activated only when multiple pathways are stim- linked. Subsequently, it was found that the same element ulated. Furthermore, some genes that contain CREs are confers response to Ca2 and to the Ras pathway as well. In addition 222 Neuropsychopharmacology: The Fifth Generation of Progress to ser133, CREB contains other sites for phosphorylation are transcriptional activators. Thus, CREB-ICER hetero- by a variety of protein kinases, which may fine tune the dimers may occupy CREs, but fail to activate transcription. For example, Like CREB, many of the ATF proteins are constitutively CaM kinase II phosphorylates a distinct serine residue in made in cells, but ATF3 and certain CREM isoforms (e. Activation of CaM kinase II would therefore appear to mediate a dampening of the CREB sig- Leucine Zipper Dimerization Motif nal (19,20). The dimerization domain used by the CREB-ATF proteins and several other families of transcription factors is called Role in Neural Plasticity a leucine zipper (8,9).
Al- cellular hormone-binding protein order isoniazid 300 mg on line treatment algorithm, the estrogen receptor (a though direct isomorphs between basic mechanisms and concept originally proposed by Langley in 1905), and by clinical observations are for the most part absent, our bur- 1966, the estrogen receptor became the first hormone recep- geoning knowledge of the cellular and central nervous sys- tor to be isolated and identified (6). An elegant scheme for tem effects of gonadal steroids is offering new models for the cellular effects of hormones was subsequently elabo- understanding the relevance of gender and gonadal steroids rated. As lipophilic factors, steroid hormones would diffuse in mood regulation. In this chapter, we review some of the into cells, where they would bind the intracytoplasmic re- major findings in reproductive neuroscience, emphasize the ceptor (in contrast to the membrane-bound receptors of context dependency of many of these findings, and suggest neurotransmitters and peptide hormones); the receptor pro- that similar contextual effects underlie the inability to dem- tein would then be phosphorylated to cause dissociation of onstrate uniform effects of gender or gonadal steroids on a heat shock protein and uncapping of the DNA binding mood and behavior. More than 2,000 years (mRNA), and finally translation of the mRNA into proteins ago, Aristotle, in his biological treatise Historia Animalium, in the cell cytoplasm. Because an enormous array of proteins observed that castration of immature male birds prevents relevant to neural transmission (e. One hundred fifty years ago, Berthold (2) teins, signal transduction proteins) were observed to be reg- successfully transplanted testes in castrated roosters and re- ulated by gonadal steroids, this 'genomic' mechanism versed their hypogonadal symptoms, demonstrating that re- promised to explain at a cellular level many of the effects productive organs possess factors that can dramatically alter of reproductive steroids observed at the level of the organ- physiology and behavior. In the past 15 years, the elegant simplicity of this geno- the claims by nineteenth century organotherapists (e. Rubinow: National Institutes of Health, Bethesda, Maryland. Schmidt: Behavioral Endocrinology Branch, National Institute of reproductive steroids and a means for understanding the of Mental Health, Bethesda, Maryland. Roca: Behavioral Endocrinology Branch, National Institute diverse and wide ranging behavioral responses to alterations of Mental Health, Bethesda, Maryland. For example, estradiol increases transcription not as solitary agents but in combination with the firing of neurons in the cerebral cortex and hippocampus other intracellular proteins (7). These protein–protein in- (CA1) (22) and decreases firing in medial preoptic neurons teractions were such that an activated receptor might en- (23). The activity of membrane receptors like the glutamate hance, reduce, initiate, or terminate transcription of a par- and -aminobutyric acid (GABA) receptors is acutely mod- ticular gene solely as a function of the specific proteins with ulated by gonadal steroids (estradiol and the 5- reduced which it interacted (and the ability of these proteins to en- metabolite of progesterone, allopregnanolone, respectively) hance or hinder the recruitment of the general transcription (24,25). Estradiol binds to and modulates the maxi-K potas- factor apparatus). The expression of these proteins—co- sium channel (26), increases cAMP levels (27), activates regulators (co-activators or co-repressors)—proved to be tis- membrane G proteins (G q,G s) (28), inhibits L-type cal- cium channels (via nonclassic receptor) (29), and immedi- sue-specific, and so suggested a means by which a hormone ately activates the mitogen-activated protein kinase (MAPK) receptor modulator (e. Another group diol increases MAPK in neurons but decreases it in astro- of intracellular proteins, the co-integrators, provided a cytes (31) (Zhang et al. The increase means by which classic hormone receptors could bind to in the number of described mechanisms by which gonadal and regulate sites other than hormone response elements steroids can affect cell function has paralleled the rapid [e. Consequently, with each (GR) binding cyclic adenosine monophosphate (cAMP) re- of these newly identified actions (which are usually, but sponse element binding (CREB) protein and, subsequently, sometimes inaccurately, called nongenomic), one needs to the activator protein 1 (AP-1) binding site)] (10), and com- examine multiple factors before inferring the mechanism of petition for co-integrator or other transcriptional regulatory action: (a) the duration required to see the effect, (b) the proteins was demonstrated as a mechanism by which even impact on the effect of inhibitors of transcription and pro- ligand-free hormone receptors could influence (e. Thus, both the intracellular ing (to see if effects are mediated through a classic receptor), hormone receptor environment and the extracellular hor- (e) the effect of hormone receptor blockers, and (f) the abil- mone environment might dictate the response to hormone ity of the ligand to initiate the action from the cell mem- receptor activation. This last Second, the hormone receptors were found to exist in requirement acknowledges the presence on the membrane different forms. For example, isoforms of the progesterone of binding sites for gonadal steroids that appear to be physi- receptor, PR and PR (the latter of which contains a 164- ologically relevant (32). A B amino acid N-terminal extension), have different distribu- Fifth, gonadal steroids regulate cell survival. As another example, two tective effects of estradiol have been described in neurons separate forms of the estrogen receptor, ER and ER , are grown in serum-free media or those exposed to glutamate, amyloid- , hydrogen peroxide, or glucose deprivation (22). Further, a variant of ER ,ER, is expressed diated effect (35). Gonadal steroids may also modulate cell in the brain, where it can form heterodimers with the ER or survival through effects on cell survival proteins (e. This crosstalk is exemplified Allerand (38) has shown that estrogen displays reciprocal by the ability of dopamine to induce lordosis by activating interactions with growth factors and their receptors (e. Additionally, we have demon- the preoptic area (48), and this dimorphism could be altered strated that the ability to modulate serotonin receptor sub- by perinatal steroid manipulation (49). Finally, the effects of gonadal steroids do not occur in In subsequent years, sexual dimorphisms have been iden- isolation, but rather in exquisite interaction with the envi- tified at all levels of the neuraxis and include differences in ronment. Juraska (40), for example, demonstrated that the the following: nuclear volume; neuron number, size, den- rearing environment (enriched vs. Further, the size of the spinal phology, and gene expression; and capacity for certain phys- nucleus of the bulbocavernosus and the degree of adult male iologic (e.
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