Caveolin proteins physically interact with and compartmentalize membrane-localized signaling proteins to facilitate high-fidelity intracellular signaling. Though primarily studied outside the nervous system, recent investigations have revealed that caveolin proteins are key modulators of a variety of neuronal intracellular signaling pathways. Through both protein aggregation and segregation, caveolin proteins can exert positive and negative influences on intracellular signaling. This review will detail recent findings regarding caveolin function in the brain.
Both hemispheric bias and sex differences exist in striatal-mediated behaviors and pathologies. The extent to which these dimorphisms can be attributed to an underlying neuroanatomical difference is unclear. We therefore quantified neuron soma size and density in the dorsal striatum (CPu) as well as the core (AcbC) and shell (AcbS) subregions of the nucleus accumbens to determine whether these anatomical measurements differ by region, hemisphere, or sex in adult Sprague-Dawley rats. Neuron soma size was larger in the CPu than the AcbC or AcbS. Neuron density was greatest in the AcbS, intermediate in the AcbC, and least dense in the CPu. CPu neuron density was greater in the left in comparison to the right hemisphere. No attribute was sexually dimorphic. These results provide the first evidence that hemispheric bias in the striatum and striatal-mediated behaviors can be attributed to a lateralization in neuronal density within the CPu. In contrast, sexual dimorphisms appear mediated by factors other than gross anatomical differences. KeywordsStriatum, sexual dimorphism; rat; nucleus accumbens, lateralization; morphometry Lateralizations and sex differences in neural circuitry and behavior occur across animal taxa and brain region. These brain dimorphisms can take many forms, including but not limited to differences in neuroanatomy, neurochemistry, and electrophysiology [1,2]. In some model systems, these differences are dramatic and have a fairly straightforward connection to behavior [3,4]. In other areas, these differences may be more subtle, although no less important. One of these regions is the mammalian striatum, including the dorsal striatum (CPu) and the core and shell subregions of the nucleus accumbens (AcbC and AcbS, respectively). Though clear lateralizations [5][6][7][8][9][10][11][12] and sex differences [13][14][15] exist in the striatum and striatal-related behaviors and pathologies, whether this is reflected in striatal neuron morphology remains largely unknown.Corresponding Author: John Meitzen, Ph.D., Dept. of Neuroscience, University of Minnesota, 321 Church St SE, Minneapolis, MN, 55455, meitz010@umn.edu,. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Given that differences in neuronal soma size and density have previously been found between hemispheres and sexes in other brain regions, we decided to quantify these neuronal attributes in the CPu, AcbC and AcbS of adult gonadectomized male and female rats. Gonadectomized rats were used to avoid any potential confounds induced by steroid sex hormones, which exert activational effects on striat...
Despite this recognition, the intracellular signaling mechanisms by which NE modulates striatal neurons are not well understood. While over 30 years ago activation of striatal b-adrenergic receptors was demonstrated to increase cAMP concentrations (Forn et al. 1974;Harris 1976), since that time there have been few follow-up studies examining NE-mediated signaling in striatal neurons. This is particularly true regarding b-adrenergic receptors (Hara et al. 2010). Thus, many questions remain regarding striatal NE signaling. Our work has focused on answering three of those questions.
Progesterone is being utilized as a therapeutic means to ameliorate neuron loss and cognitive dysfunction following traumatic brain injury Although there have been numerous attempts to determine the means by which progesterone exerts neuroprotective effects, studies describing the underlying molecular mechanisms are lacking What has become clear, however, is the notion that progesterone can thwart several physiological processes that are detrimental to neuron function and survival, including inflammation, edema, demyelination and excitotoxicity One clue regarding the means by which progesterone has restorative value comes from the notion that these aforementioned biological processes all share the common theme of eliciting pronounced increases in intracellular calcium. Thus, we propose the hypothesis that progesterone regulation of calcium signaling underlies its ability to mitigate these cellular insults, ultimately leading to neuroprotection. Further, we describe recent findings that indicate neuroprotection is achieved via progesterone block of voltage-gated calcium channels, although additional outcomes may arise from blockade of various other ion channels and neurotransmitter receptors.
The peptide corticotropin-releasing factor (CRF) was initially identified as a critical component of the stress response. CRF exerts its cellular effects by binding to one of two cognate G-protein coupled receptors (GPCRs), CRF receptor 1 (CRFR1) or 2 (CRFR2). While these GPCRs were originally characterized as being coupled to Gαs, leading to downstream activation of adenylyl cyclase (AC) and subsequent increases in cAMP, it has since become clear that CRFRs couple to and activate numerous other downstream signaling cascades. In addition, CRF signaling influences the activity of many diverse brain regions, affecting a variety of behaviors. One of these regions is the striatum, including the nucleus accumbens (NAc). CRF exerts profound effects on striatal-dependent behaviors such as drug addiction, pair-bonding, and natural reward. Recent data indicate that at least some of these behaviors regulated by CRF are mediated through CRF activation of the transcription factor CREB. Thus, we aimed to elucidate the signaling pathway by which CRF activates CREB in striatal neurons. Here we describe a novel neuronal signaling pathway whereby CRF leads to a rapid Gβγ- and MEK-dependent increase in CREB phosphorylation. These data are the first descriptions of CRF leading to activation of a Gβγ-dependent signaling pathway in neurons, as well as the first description of Gβγ activation leading to downstream CREB phosphorylation in any cellular system. Additionally, these data provide additional insight into the mechanisms by which CRF can regulate neuronal function.
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