13
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Nicotinic Cholinergic System in the Hypothalamus Modulates the Activity of the Hypothalamic Neuropeptides during the Stress Response

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The hypothalamus harbors high levels of cholinergic neurons and axon terminals. Nicotinic acetylcholine receptors, which play an important role in cholinergic neurotransmission, are expressed abundantly in the hypothalamus. Accumulating evidence reveals a regulatory role for nicotine in the regulation of the stress responses. The present review will discuss the hypothalamic neuropeptides and their interaction with the nicotinic cholinergic system. The anatomical distribution of the cholinergic neurons, axon terminals and nicotinic receptors in discrete hypothalamic nuclei will be described. The effect of nicotinic cholinergic neurotransmission and nicotine exposure on hypothalamic-pituitaryadrenal (HPA) axis regulation at the hypothalamic level will be analyzed in view of the different neuropeptides involved.

          Methods

          Published research related to nicotinic cholinergic regulation of the HPA axis activity at the hypothalamic level is reviewed.

          Results

          The nicotinic cholinergic system is one of the major modulators of the HPA axis activity. There is substantial evidence supporting the regulation of hypothalamic neuropeptides by nicotinic acetylcholine receptors. However, most of the studies showing the nicotinic regulation of hypothalamic neuropeptides have employed systemic administration of nicotine. Additionally, we know little about the nicotinic receptor distribution on neuropeptide-synthesizing neurons in the hypothalamus and the physiological responses they trigger in these neurons.

          Conclusion

          Disturbed functioning of the HPA axis and hypothalamic neuropeptides results in pathologies such as depression, anxiety disorders and obesity, which are common and significant health problems. A better understanding of the nicotinic regulation of hypothalamic neuropeptides will aid in drug development and provide means to cope with these diseases. Considering that nicotine is also an abused substance, a better understanding of the role of the nicotinic cholinergic system on the HPA axis will aid in developing improved therapeutic strategies for smoking cessation.

          Related collections

          Most cited references 270

          • Record: found
          • Abstract: found
          • Article: not found

          Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior.

          The hypothalamus plays a central role in the integrated control of feeding and energy homeostasis. We have identified two novel neuropeptides, both derived from the same precursor by proteolytic processing, that bind and activate two closely related (previously) orphan G protein-coupled receptors. These peptides, termed orexin-A and -B, have no significant structural similarities to known families of regulatory peptides. prepro-orexin mRNA and immunoreactive orexin-A are localized in neurons within and around the lateral and posterior hypothalamus in the adult rat brain. When administered centrally to rats, these peptides stimulate food consumption. prepro-orexin mRNA level is up-regulated upon fasting, suggesting a physiological role for the peptides as mediators in the central feedback mechanism that regulates feeding behavior.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response.

            The hypothalamo-pituitary-adrenocortical (HPA) axis is required for stress adaptation. Activation of the HPA axis causes secretion of glucocorticoids, which act on multiple organ systems to redirect energy resources to meet real or anticipated demand. The HPA stress response is driven primarily by neural mechanisms, invoking corticotrophin releasing hormone (CRH) release from hypothalamic paraventricular nucleus (PVN) neurons. Pathways activating CRH release are stressor dependent: reactive responses to homeostatic disruption frequently involve direct noradrenergic or peptidergic drive of PVN neurons by sensory relays, whereas anticipatory responses use oligosynaptic pathways originating in upstream limbic structures. Anticipatory responses are driven largely by disinhibition, mediated by trans-synaptic silencing of tonic PVN inhibition via GABAergic neurons in the amygdala. Stress responses are inhibited by negative feedback mechanisms, whereby glucocorticoids act to diminish drive (brainstem) and promote transsynaptic inhibition by limbic structures (e.g., hippocampus). Glucocorticoids also act at the PVN to rapidly inhibit CRH neuronal activity via membrane glucocorticoid receptors. Chronic stress-induced activation of the HPA axis takes many forms (chronic basal hypersecretion, sensitized stress responses, and even adrenal exhaustion), with manifestation dependent upon factors such as stressor chronicity, intensity, frequency, and modality. Neural mechanisms driving chronic stress responses can be distinct from those controlling acute reactions, including recruitment of novel limbic, hypothalamic, and brainstem circuits. Importantly, an individual's response to acute or chronic stress is determined by numerous factors, including genetics, early life experience, environmental conditions, sex, and age. The context in which stressors occur will determine whether an individual's acute or chronic stress responses are adaptive or maladaptive (pathological).
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Differential expression of orexin receptors 1 and 2 in the rat brain.

              Orexins (hypocretins) are neuropeptides synthesized in the central nervous system exclusively by neurons of the lateral hypothalamus. Orexin-containing neurons have widespread projections and have been implicated in complex physiological functions including feeding behavior, sleep states, neuroendocrine function, and autonomic control. Two orexin receptors (OX(1)R and OX(2)R) have been identified, with distinct expression patterns throughout the brain, but a systematic examination of orexin receptor expression in the brain has not appeared. We used in situ hybridization histochemistry to examine the patterns of expression of mRNA for both orexin receptors throughout the brain. OX(1)R mRNA was observed in many brain regions including the prefrontal and infralimbic cortex, hippocampus, paraventricular thalamic nucleus, ventromedial hypothalamic nucleus, dorsal raphe nucleus, and locus coeruleus. OX(2)R mRNA was prominent in a complementary distribution including the cerebral cortex, septal nuclei, hippocampus, medial thalamic groups, raphe nuclei, and many hypothalamic nuclei including the tuberomammillary nucleus, dorsomedial nucleus, paraventricular nucleus, and ventral premammillary nucleus. The differential distribution of orexin receptors is consistent with the proposed multifaceted roles of orexin in regulating homeostasis and may explain the unique role of the OX(2)R receptor in regulating sleep state stability. Copyright 2001 Wiley-Liss, Inc.
                Bookmark

                Author and article information

                Journal
                Curr Neuropharmacol
                Curr Neuropharmacol
                CN
                Current Neuropharmacology
                Bentham Science Publishers
                1570-159X
                1875-6190
                May 2018
                May 2018
                : 16
                : 4
                : 371-387
                Affiliations
                [a ]Center for Brain Research, Ege University, Bornova, Izmir, , Turkey;
                [b ]Department of Physiology, School of Medicine, Ege University, Bornova, Izmir, , Turkey
                Author notes
                [* ]Address correspondence to this author at the Ege University School of Medicine, Physiology Department, Bornova, 35100, Izmir, Turkey; Tel: +90 (232) 390 1808; Fax: +90 (232) 374 6597; E-mail: burcubalkan69@ 123456gmail.com
                Article
                CN-16-371
                10.2174/1570159X15666170720092442
                6018196
                28730966
                © 2018 Bentham Science Publishers

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                Categories
                Article

                Comments

                Comment on this article