Understanding mental disorders worksheet,older ladies shops,make an easy presentation - PDF Review

Published 31.08.2014 | Author : admin | Category : What Do Guys Really Want In A Woman

In a world where anyone can fix their nose if they'd like it smaller or plump up their lips if they want them fuller, we expect perfection, especially in Hollywood. We tend to think all leading men should be tall and chiseled and all leading ladies long and lean. While it’s not necessarily an essential quality for public office, the people who run for it tend to have some sort of desire to be in the limelight.
Narcissistic Personality Disorder is a type of personality disorder that makes them self-important, boastful and conceited. Narcissism has a lot of different personality attributions associated with it, such as entitled, self-centered, and greedy. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Understanding the Causes of Reduced Startle Reactivity in Stress-Related Mental DisordersKevin D.
If you are reading this message, Please click this link to reload this page.(Do not use your browser's "Refresh" button). If you see this message, your web browser doesn't support JavaScript or JavaScript is disabled. Through the Newegg EggXpert Review Program, Newegg invites its best reviewers, known as EggXperts, to post opinions about new and pre-release products to help their fellow customers make informed buying decisions.Click here for more details. Why can’t we show you details of this product?Some manufacturers place restrictions on how details of their products may be communicated. Yes, there are some politicians who get into the business because they want to help their constituents, but many more seem to crave the spotlight that comes when they are in the midst of an election run.
In order to increase binding at the glucocorticoid receptors, the synthetic glucocorticoid analog, dexamethasone, was administered s.c. LEW rats exposed to the stressor differed from both their same-strain controls and the WKY groups on the measure of startle magnitude (responsivity). The normal synthesis of serotonin (5-HT) involves the metabolism of tryptophan to 5-hydroxytryophan by tryptophan hydroxylase; however, in the presence of interferon-?, another, competing enzyme, indolamine1,3-dioxygenase is upregulated.
The initiation of an inflammatory response begins with the non-specific macrophage pro-inflammatory response (Th0), which then diverges into either a Th1 (cell-based) or Th2 (humoral-mediated) response. Startle sensitivity and responsivity were assessed 30 and 90 min following an acute systemic injection of IFN-? (n = 16).
Based on the literature and the collected data from our laboratory, concerning the modulation of the ASR, we propose the following cascade of events may occur as a result of stressor exposure in our female rat model. With great prices, fast shipping, and top-rated customer service - once you know, you Newegg. Enabling JavaScript in your browser will allow you to experience all the features of our site.
We've picked out some of the most shockingly short celebs to put in a lineup and see how they measure up against other Hollywood elites, and the average American (5-foot-10 for males, 5-foot-4 for females). Dashed red lines represent cholinergic inhibitory influences from the laterodorsal tegmental nuclei (LDT) and pedunculopontine tegmentum (PPT). Startle sensitivity was equally effected 1 and 3 h following administration and is shown collapsed over Session Time.
The result of this shift in the metabolism of tryptophan towards the formation of kynurenine is a reduction in the amount available for metabolism towards the formation of serotonin (i.e. There is evidence that suggests ovarian hormones may influence the path of the subsequent immune cascade from the Th0 response. First, the acute-phase (pro-inflammatory) response causes a transient reduction in startle responsivity (magnitude) that appears to last as long as IL-1 continues to be elevated above the levels of circulating IL-1ra.
Dashed black lines represent inhibitory GABAergic projections from the substantial nigra pars reticulata (SNR).
Startle responsivity was only effected 1 h following administration; therefore, the 3 h time-point is not shown.
Hence, the pretreatment with LPS, which should have increased the glucocorticoid response to the inescapable tailshocks, blocked the suppression of startle responsivity following shock exposure.
Differences in startles elicited (sensitivity) and the magnitudes of those elicited startle responses (responsivity) each were assessed via a 5 (Condition) x 3 (Stimulus Intensity) repeated measures ANOVA.
IL-1? treatment to oil-treated controls was associated with significantly lower NE levels than oil-treated saline-controls (*).
Input to the NTS via either the from the vagus nerve (X n.) or diffusion of IL-1? across the blood-brain barrier in the nearby area postrema is necessary for the noradrenergic changes in the brain in response to peripheral pro-inflammatory cytokine signaling. To date, the Th1 response has been more intently studied for its possible role in effecting behavior (i.e. IL-1ra serves to normalize the response; thus, when the levels of IL-1ra are elevated to a sufficient degree, it causes an increase in ASR sensitivity (a rebound effect). IntroductionMany questions have plagued the study of the etiology and subsequent treatment of mental illness. An asterisk (*) represents a significant difference from saline-treated controls at the same stimulus intensity. This suggests that prior experiences likely cause a more robust anti-inflammatory glucocorticoid response that actually reduces the influence of the peripheral immune pro-inflammatory immune response upon the areas of the brain capable of suppressing startle responsivity. As above, red lines denote cholinergic pathways, and dashed lines represent inhibitory circuits.
An asterisk (*) represents a significant between-group difference from the vehicle-treated controls at the same intensity. An asterisk represents a significant difference in the low-dose group at the 90 min test as compared to the same time high-dose and the 30-min low-dose test. In part, it is simply because, as far as we know, some mental illnesses are somewhat unique to the human condition. In addition, the 2 hormone treated saline control conditions also differed from each other, with the estradiol-treated saline-controls exhibiting higher levels of NE than those pretreated with progesterone prior to saline administration (‡).
Moreover, clinical studies have produced many different results concerning potential biomarkers for conditions such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD). Immune influences on serotonin synthesis: A possible central mechanism of continued suppression?
This could cause a chronic condition where ASRs are “blunted” in people with conditions ranging from PTSD to MDD to BPD.7.
In this chapter, we review how we approached modeling a specific behavioral condition, suppression of the startle reflex, by examining whether one of two commonly associated peripheral biomarkers of anxiety and depression could potentially cause this rather specific symptom. The two peripheral systems under investigation were the hypothalamic-pituitary-adrenal (HPA) axis and the peripheral pro-inflammatory immune response, both of which have been implicated as a vulnerability factor, causal factor, or resultant (perpetuating) effect of PTSD and MDD.Our general theory is that peripheral endocrine and immune signals, measured to be abnormal in patients with either PTSD or MDD (as well as other mental disorders), are actually perpetuating the behavioral features of these disorders. A double cross (‡) represents a significant difference from both estradiol-treatment groups. This may then lead the brain to compensate for those peripheral abnormalities, but, at the same time, cause other imbalances, which lead to the experience of a decline into mental illness. Thus, treating these peripheral markers as part of the “mental” disorder may be quite beneficial in normalizing certain aspects of the diagnosed abnormal behavior.
The startle reflex as an assessment tool One of the major impediments to the mechanistic study of mental illness is establishing analogs of the abnormal behaviors expressed in humans in animal models, especially in sub-primate species.
This has led some to adopt reflex-based measures such that the face and construct validity of the behavior change can be readily translated between the model and patient populations. Consequently, a popular measures for the study of anxiety disorders has been the potentiation of the startle reflex; however, there is growing evidence that a dampening of the startle response may be indicative of changes in physiology that underlie different mental disorders. The startle reflex comprises a 3-synaptic sensory-motor neuronal pathway that serves as a defensive behavioral response to abrupt, usually intense, stimuli. The acoustic startle response (ASR) is the most commonly used form for studying this reflex.
As shown in Figure 1, the primary ASR circuit begins with neurons in the cochlear nerve, transmitting the representation of the acoustic stimulus from the cochlea of the inner ear to the cochlear nucleus (in the brainstem). Efferent pathways from the cochlear nucleus project to the nucleus reticularis pontis caudalis (PnC), in the pons, forming the second synapse in this reflex arc. The third synapse forms from the efferent projections from the PnC to various motor nuclei, through the recticulospinal spinal tracts to the muscles of the torso [1] and the muscles enervated by the facial nerve. These muscle enervations create a rapid cascade of near-immediate behavioral responses to abrupt acoustic stimuli, ranging from less than 10 ms to approximately 50 ms.The ASR is modulated by several afferent connections originating from higher brain areas (midbrain, limbic, and cortical nuclei). At the level of the PnC, there are several inputs that can either enhance or inhibit the magnitude of an elicited ASR.
In the area of fear and anxiety, the central amygdala and bed nucleus of the stria terminalis (BNST) are considered the 2 major excitatory modulation structures on this reflex [2].

Some have proposed that the BNST is the origin of anxiety-like behaviors whereas the nuclei of the amygdala are the origin of acute fear responses and explicit fear-learning [3, 4]. The amygdala is predominately associated with causing classically conditioned fear-potentiated ASRs [5], and, in fact, has been specifically shown not to have a role in startle inhibition, at least via a learned conditioned inhibitor [6]. On the other hand, the process known as pre-pulse inhibition of the startle reflex (PPI) has elucidated neural pathways that can inhibit the expression of the ASR. For instance, the substantial nigra pars retriculata (SNR), pedunculopontine tegmentum (PPT) and laterodorsal tegmental nuclei (LDT) have inhibitory influence upon the PnC, thus reducing the measured ASR [7-10]. These three mid-brain nuclei (inhibitory) receive projections from various forebrain areas, including the amygdala, BNST, and medial prefrontal cortex (mPFC). Thus, limbic system modulation of the ASR can occur through direct enervation of the PnC (excitatory) or indirect enervation through mid-brain nuclei. Abnormalities in the expression of the startle reflex in mental disordersOver all other mental disorders, PTSD is associated with changes in the startle reflex. Commonly associated with exaggerated startle responses [11-14], higher or exaggerated startle reflex responses are a criteria symptom for the diagnosis of PTSD [15]. In fact, others have reviewed the literature and found there are a significant number of reports where the startle responses in PTSD patients are not exaggerated [16]. More extreme, there are reports, albeit limited, where patients diagnosed with PTSD appeared to have blunted motor reflex responses to an acoustic stimulus [17, 18]. These populations had distinctive qualities that were different than those studies that had found enhanced startle reactivity in their PTSD patients. First, the one study was exclusively female [18] and the other had a majority of female subjects [17], suggesting there may be a sex difference in the presentation of ASR in females as a result of experiencing trauma. However, others have reported enhanced startle responses in a different population of women diagnosed with PTSD following automobile accidents [19]. Thus, a second distinction between the two studies that observed suppressed startle reactions, which should be considered, is that the trauma was specifically associated with being the target of violence [17, 18]. A third quality of at least one of these two reports is that the subjects also exhibited symptoms associated with major depressive disorder [18]. This suggests stressful experiences may not cause a uniform change in sensory reactivity, and the expression of the coping response to the trauma may have psychophysiological ramifications that are quite different, both in terms of effects upon sensory-motor responding to acoustic stimuli as well as the full expression of symptoms.There is evidence that symptoms associated with depression may also include a blunted reaction to acoustic stimuli. Patients designated as “depressed”, having either a diagnosis of MDD or a significantly higher score on the Beck Depression Inventory (with or without additional neurological conditions), have been reported to exhibit blunted reactivity to acoustic stimuli, either with or without manipulations of affect [22-26].
Similarly, there is also evidence that bipolar disorder (BPD), the occurrence of at least one manic or mixed manic episode over the course of a patient’s lifetime, is characterized by blunted startle reactions as well, even during periods of remission [27]. A study by Carroll and colleagues found patients suffering from BPD exhibit attenuated baseline startle, most notably in those having experienced mixed episodes, not pure mania [28]. Animal models utilizing stress to dampen startle reactivityAcross the studies that have documented reductions in the expression of the startle reflex in rodents, the common-most feature is that the magnitude of the response is dampened following exposure to a stressor manipulation. Interestingly, despite some differences in methodology, inescapable tailshock [30], inescapable footshock [36], and predator exposure with injection [33], all showed reduction in ASR measurements that could not be attributable to enhanced habituation to the acoustic stimuli. Yet, studies utilizing inescapable tailshock (in females) have established that exposure to the stressor condition causes a change in startle responsivity (the magnitude of the measured startle responses), not startle sensitivity (the threshold to elicit a certain percentage of startle responses). Thresholds for eliciting ASRs are not increased in the shocked females; instead, the magnitudes of the elicited startle responses are lower [31, 32].
This suggests, at least for the female stress model, that the presumed increased inhibition upon the activity in the intrinsic ASR circuit is occurring through the motor response aspect of the reflex arc. This model condition has been termed by some stress-induced startle suppression [32, 34].There are significant differences in the temporal characteristics of these different startle-suppression models in rodents. Inescapable tailshock causes a reduction in startle magnitude in female rats that is evident hours within exposure [31, 32], possibly lasting up to a day later, when the bouts of shock are expanded to a few consecutive days [30].
The footshock-induced suppression of startle reactivity is evident 4 h following stressor exposure [36]. The immune-challenge models parallel these stressor manipulations by causing reductions in startle reactivity within a couple hours of administration of the challenge [34, 35]. Thus, one interpretation of these data is that painful stressors are causing changes in the peripheral immune system, which, in turn, dampen startle reactivity during the time of their activity [34], on the range of hours. Following this logic, when females were tracked 4 and 8 days following tailshock, reductions in startle reactivity in the stressor-exposed rats did not reach statistical significance [30].
In contrast, the predator-exposure + injection model shows immediate suppression following the stressor exposure, which continues to be present 1 week later [33]. In addition, it is evident both under dark and light conditions [33], suggesting the change in the startle response is not occurring due to a change in reactivity to other stimuli that are known to modulate startle reactivity, such as light-enhanced startle [37]. Thus, this observance suggests that changes in ASR magnitude may be extended beyond the acute effects of stressor exposure that could be attributed to the short-term effects of immune signaling that would be in response to the injection (or possibly even shock). Hypothalamic-Pituitary Adrenal (HPA)–axis Two interrelated mechanisms have been proposed as potential causes of startle suppression, the first being glucocorticoid hormone reception. Adamec and colleagues showed the reduction of startle magnitudes following combined cat exposure and saline injection could be blocked by substituting the saline injection with the glucocorticoid receptor antagonists RU-486 [33]. We subsequently tried to induce the effect in our female rats by administering the synthetic glucocorticoid agonist, dexamethasone. As shown in Figure 2, the dexamethasone did not appreciably change the magnitude of the elicited ASRs, nor did it affect the number of ASRs elicited (data not shown).
These findings suggest that the reception of corticosterone at the glucorticoid receptor is not sufficient to reduce ASR magnitudes.
One possibility is that RU-486 blocked the suppressed startle, in that model system, via a non-glucocorticoid mechanism, for example via progesterone receptor antagonism. A connection to progesterone will be discussed further below as it pertains to a pro-inflammatory response mechanism, in contrast to an anti-inflammatory glucocorticoid response, but this finding is supported by previous work that shows elevations in circulating corticosterone are not necessary for corticotrophin releasing hormone to increase ASR magnitudes, despite stimulating increased activity in the HPA-axis [38]. Likewise, the suppression of ASR magnitudes in Occidental low saccharine consuming rats is not recapitulated by substituting corticosterone administration for the shock exposure [36].
Pro-inflammatory cytokinesThe second mechanism, which is intertwined with the HPA-axis, is the peripheral pro-inflammatory immune response.
We first showed that a ovarian hormone-dependent suppression of startle magnitudes could be induced by a single injection of the pro-inflammatory cytokine interleukin (IL)-1? [34], an effect that appears to parallel that observed following tailshock [31].
Still, peripherally released IL-1? elicits the release of glucocorticoids from the adrenal through stimulation of the vagus nerve, paraventricular nucleus of the hypothalamus, and pituitary gland, which provides an anti-inflammatory response to the pro-inflammatory signal [39-44].
In order to further delineate that pro-inflammatory cytokines, and not anti-inflammatory glucocorticoids, are necessary for stress-induced startle suppression, we compared the effect of inescapable tailshock upon the induction of ASRs in two strains of rats, specifically chosen because of their pro-inflammatory and glucocorticoid responsiveness to stressors.
Females of each of these strains were exposed to inescapable tailshock and subsequently tested for startle reactivity 1 and 3 h later.
If pro-inflammatory signaling, not anti-inflammatory glucocorticoid release is critical for eliciting startle suppression, then LEW rats would exhibit suppression of the ASR, and the WKY rats would not. The hypothesis that pro-inflammatory cytokines are a necessary component in the suppression of startle responses following stress was further evaluated in the immune-sensitive Lewis rat strain by determining if elevations of peripheral IL-1? is sufficient to suppress startle reactivity in female rats.
As shown in Figure 4, both startle responsivity and sensitivity were reduced in female Lewis rats administered IL-1?. Prior immune challenge effects on stress-induced startle in SD ratsOne consequence of the peripheral immune system having an effect on behavior, in this case sensory reactivity to acoustic stimuli, is that prior immune challenges may influence how future pro-inflammatory signaling or anti-inflammatory glucocorticoid responses influences behavior following stressor exposure.
LPS is a commonly used endotoxin that elicits sickness behaviors due to a release of peripheral and central pro-inflammatory cytokines, followed by an increase in circulating glucocorticoids [53, 54].
Others have shown that immune challenges days prior to shock exposure causes a greater increase in glucocorticoid release in response to shocks [55, 56]; therefore, we used this known method of causing a sensitized glucocorticoid response to determine if a greater glucocorticoid release enhances or reduces the degree by which tailshock suppresses startle responsivity. As expected, the number of startle responses elicited did not differ based on prior treatment but did differ across stimulus intensity (data not shown); however, prior exposure to LPS reduced the effectiveness of inescapable shock to attenuate startle magnitudes (see Figure 5). Although LPS has a short-term suppressing effect upon the startle response [35], it both causes an acute increase in pro-inflammatory cytokines (and sickness behaviors) followed by an increase in anti-inflammatory glucocorticoid signaling. This “priming” effect upon the anti-inflammatory glucocorticoid response to shock is a likely mechanism for “buffering” the behavior from being affected. Again, this suggests the glucocorticoid response may actually counteract the suppressive effects originating from peripheral pro-inflammatory cytokine signaling. Neuroanatomy and endocrine modulation of startle suppression As mentioned above, studies of pre-pulse inhibition of the ASR have elucidated neural circuitry that underlie the suppression of ASRs when they are immediately preceded by a salient auditory stimulus, for a review see [57]. Inputs from the PPT, LDT, and SNR to the PnC cause inhibition of the startle response [7, 9, 59, 60]. More specifically, it appears the magnocellular portion of the PnC has muscarinic receptors to receive the inhibitory cholinergic signal from PPT and LDT [61] and GABAB receptors receive the inhibitory signal from the SNR [62]. The question is whether these areas could provide more tonic inhibition of the ASR, outside of the attentional processes associated with PPI. For instance, it is known that lesions to the medial septum and the fimbra-fornix increase startle reactivity because these areas provide tonic inhibition upon the amygdala [63]; thus, removal of inhibition upon the amygdala increases tonic excitatory activity to the PnC (from the amygdala).

In contrast, lesions to the noradrenergic cell bodies of the LC reduce startle response magnitudes, as these neurons probably serve a tonic excitation function upon the PnC [64]. Thus, there are circuits within the brain that are situated such that they could provide more tonic changes in the ASR. Ovarian hormones can have a significant impact on many of the neural structures associated with startle regulation.
Yet, despite all these areas of influence, rodent studies usually do not find any differences in baseline startle reactivity across the estrus cycle or with hormone replacement [68, 69]; however, see [70] for an example of oral-contraceptive usage effecting baseline startle in women. When significant arousal or stress occurs in the rodents, however, the modulatory actions of ovarian hormones on startle become evident. For example, Toufexis and colleagues have shown the magnitude of CRH-enhanced startle is attenuated when progesterone levels are increased [71]. One possibility is that progesterone, or its metabolite allopregnanolone, may decrease the excitatory signaling from the BNST to the PnC by increasing GABA inhibition in this structure [77]. Thus, it appears that progesterone or allopregnanolone should facilitate the actions of CRH on startle, unless they act through different mechanisms within the BNST or outside of the BNST. On the other hand, progesterone also affects how IL-1? influences sexual receptivity [79], and both glucocorticoid receptor activation [77] and progesterone-induced changes in central neuroadrenergic activity [80] have been suggested to attenuate startle reactivity selectively in female rats.
As shown in Figure 6, the administration of progesterone to ovariectomized rats appears to be necessary for IL-1? to suppress startle magnitudes. Thus, ovarian hormones are not sufficient to cause changes in startle reactivity in female rats. Therefore, stress-induced startle suppression in female rats appears to necessitate a combination of the two factors, a peripheral pro-inflammatory immune response and the presence of progesterone. Figure 6.Startle sensitivity and responsiveness were assessed 2 h following IL-1? administration.
Evidence for limbic regulation of startle suppressionPeripheral IL-1? is known to have a significant impact on brain activity.
Systemic IL-1 administration activates key afferent pathways in brainstem (lateral parabrachial nucleus and dorsomedial and ventrolateral medulla) and limbic system nuclei (BNST and central nucleus of the amygdala) [81].
Still, increasing peripheral IL-1? signaling increases NE and serotonin levels in these brain areas [83] and noradrenergic metabolism in the paraventricular nucleus of the hypothalamus (PVN), locus coeruleus (LC), and amygdala [83].
In fact, as the IL-1? dose is increased, the amount of NE metabolism increases linearly in the amygdala, lasting as much as an hour [83].
Yet, stimulation of ?-adrenergic receptors also attenuate startle responses and facilitate non-associative habituation of the startle response [84-88]. IL-1? affects activity in the LC in a dose dependent manner as well, with low doses inhibiting activity and higher doses causing excitation; a process mediated by CRH at the time of IL-1? release [89]. Further, when the exposure to painful stimuli is prolonged or LPS is used to cause a significant pro-inflammatory response, additional release of central IL-1? occurs, especially in the hypothalamus [90, 91]. These data suggest that activity in the limbic system, monoamine activity in particular, is significantly affected by peripheral immune signaling.Based on the above logic, we hypothesized that the reduction in ASR magnitude occurring as a result of IL-1? administration to progesterone-pretreated female rats could be associated with changes in the central noradrenergic activity in one of the known modulatory nuclei of the acoustic startle response.
Therefore, we measured norepinephrine levels in brain tissue-punches from 4 brain areas: BNST, amygdala, medial prefrontal cortex (mPFC), and dorsal hippocampus. As stated above, both the BNST and cAMG have direct excitatory projections to the PnC and indirect inhibitory connections via the PPT. The medial prefrontal cortex projects to the primary startle circuit via the LDT, whereas the dorsal hippocampus was included as an area that is both reactive to stress and ovarian hormone manipulation, but it is actually several synapses removed from the PPT.
As shown in Figure 7, differences due to hormone pretreatment and subsequent IL-1? administration were found in the BNST, not in any of the other 3 areas. For example, an endotoxin-induced suppression of social interactions is both associated with increased activity in the BNST as well as reduced activity in the BNST when the suppressed behavior is blocked by IL-1ra [92]. Similarly, the behavioral depression exhibited in the forced-swim test can be reduced by stimulating the vagus nerve, leading to changes in brainstem nuclei activation (including the NTS) and also activation of the BNST [93].
Others have shown NE release is elevated with stressor exposure in the BNST, which is necessary for some stress-induced behaviors [94, 95].
With particular attention to the startle reflex, the BNST is commonly associated with enhancing startle reactivity [2, 96]. However, as shown in Figure 8), there is an inhibitory pathway from the BNST to the PnC via the PPT that has been examined as a cholinergic mechanism for eliciting PPI [97, 98]. Further, PPI has been shown to fluctuate over the estrus cycle, while not being sensitive to apomorphine disruption, implicating a non-dopaminergic mechanism for these hormone-induced changes in female pre-pulse inhibition, which could rule-out a role of the substantia nigra in this process [68].
In addition, the changes in measured NE levels in the BNST are consistent with previous studies citing peripheral IL-1? administration as a trigger for central noradrenergic activity [82, 99]. See text for further details.There is evidence that could suggest a connection between the known effects of peripheral cytokine activity upon brain noradrenergic activity (most reported males) and an ovarian hormone influence upon these processes. For one, there is growing information pertaining to ovarian hormone influences on noradrenergic activity initiated from the NTS. Many of the brainstem noradrenergic nuclei, including the NTS, exhibit cyclic changes in estrogen and progesterone receptors [100]. Removal of ovarian hormones with or without hormone replacement particularly has a significant impact on NTS physiology. Specifically, the mRNA for prolactin-releasing peptide (PrRP) in noradrenergic neurons is decreased by ovariectomy and increased with subsequent replacement of either estradiol or progesterone [101].
Although the PrRP mRNA levels are reported to not change significantly across the estrus cycle in the NTS, an inspection of the data suggests the levels are a bit higher during proestrus [102]. PrRP labeling in the NTS is also preferentially sensitive to painful stressors, such as tailshock [103]. These data suggest ovarian hormone influences on NE NTS physiology could occur through changes in the regulation of a co-expressing neuropeptide.
This could serve a filtering function for the vagal activity representing immune activity changes in the periphery, as the NTS projects its NE efferent connections to key areas involved in arousal and sensory reactivity, such as the BNST, AMG, hypothalamus, and parabrachial nucleus [105]. For example, core body temperature increases from peripheral IL-1? occur for a longer period of time during proestrus (compared to diestrus) apparently do to the actions of progesterone [106]. Although it is clear hypothalamic cyclooxygenase is the necessary mechanism for this effect [107] the noradrenergic input to the hypothalamus is required and may be changed as well [108]. Therefore, there are anatomical and pharmacological reasons to link NTS noradrenergic projections to the BNST as the primary pathway by which changes in vagal activity could influence startle responsivity through known inhibitory circuitry.Other possible mechanism for startle suppression could occur as a cascade of effects that begin with the hormone-specific effects upon NE in the brain, but end with non-specific hormonal influences upon 5-HT. NE was shown above to be changed in the BNST following systemic increases in IL-1?, confirming the results of others showing noradrenergic activity increases within 30 minutes of a peripheral injection of IL-1? and may last 2 hours [109, 110]. Importantly, as proposed above, the effect of systemic IL-1? injections on brain NE in rodents is dependent upon transmission in the vagus nerve [111]. The effects of peripheral IL-1? on 5-HT are quite different in terms of timing, route, and influence of ovarian hormones. First the increases observed in brain serotonin metabolism are evident 2-4 h following IL-1? administration and, at least in male rats, are reported to be less region specific (compared to NE activity changes) [110]. In addition, the effects of peripheral IL-1? on brain 5-HT are not dependent upon the vagus nerve in male mice but neither are the effects upon brain NE activity [112]. Thus, it is not known if 5-HT requires the same pathway as IL-1? to effect central 5-HT activity, but the difference in the temporal cascade would suggest such a difference is logical. Further, as shown in Figure 9, the same peripheral IL-1? injections that elicited a hormone-dependent change in BNST NE levels caused an increase in 5-HT activity in both estradiol and progesterone-treated female rats. Recovery of startle responsivityThe peripheral immune system also has counter-inflammation mechanisms that could also be potential mechanisms for what appears to be a pro-inflammatory cytokine-mediated effect. Thus, another response to pro-inflammatory cytokine release, is the increase in the endogenous IL-1 receptor antagonist (IL-1ra), which has been shown to attenuate the reductions in food-intake elicited by systemic administration of LPS or IL-1? [113]. Our hypothesis was that elevations in IL-1ra, from systemic administration, would counteract the effects of IL-1?.
Thus, IL-1ra was administered systemically, followed by an assessment of startle reactivity 1 and 3 h later. As shown in Figure 10, the peripheral immune mechanism for stifling the pro-inflammatory response of IL-1? is sufficient to increase startle sensitivity.
This suggests the nervous system is responsive to elevated acute pro-inflammatory signaling, suppressing startle, and elevations in the counter-active IL-1ra, increasing sensitivity to acoustic stimuli. These interactions illustrate the constant inter-relationship between the peripheral immune system and the nervous system regulation of sensory-motor activity.

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