China
Africa
Explore chapters and articles related to this topic
Neuropeptides: Evidence for Central Pathways and Role in Cardiovascular Regulation
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Giora Feuerstein, Anna Leena Siren, Stefan Vonhof, Robert Willette
The tripeptide thyrotropin-releasing hormone (TRH, pyro-Glu-His-Pro-NH2) is abundantly distributed throughout the central nervous system (Palkovits, 1984). Immunoreactive THR, TRH precursor protein (pro-TRH), its messenger RNA (mRNA), as well as TRH receptors are found in brain areas involved in the cardiovascular control (Palkovits, 1984; Merchenthaler et al., 1988; Sergerson et al., 1987; Lechan and Jackson, 1986; Mantyh and Hunt, 1985; Sharif and Burt, 1985). Most of the TRH-containing perikarya are located in the parvocellular part of the hypothalamic paraventricular nucleus (PVN), the suprachiasmatic portion of the medial preoptic nucleus (POM), the dorsomedial nucleus (DMH), the lateral basal hypothalamus (LH), and the periaqueductal grey (PAG) and the raphe nuclei (Merchenthaler et al., 1988). TRH-immunoreactive cell bodies are also present in the diagonal band of Broca, lateral septum, the bed nucleus of stria terminālis (BNST), reticular thalamus, the amygdaloid complex, subfornical organ (SFO), the supraoptic nucleus (SON), the parabrachial nucleus, the lateral reticular nucleus, nucleus paragigantocellularis, nucleus of the solitary tract (NTS), and the dorsal vagal complex (DMV) (Merchenthaler et al., 1988; Tsuruo et al., 1987; Hokfelt et al., 1989). Dense TRH-positive fiber networks are found in the lateral septum, the hypothalamus, and the subiculum-amygdalohippocampal area (Hokfelt et al., 1989). Fibers and nerve terminals with TRH-positive immunoreactivity have also been described in the intermediolateral cell column (IML) of the spinal cord (Appel et al., 1987; Hirsch and Helke, 1988; Helke et al., 1986; Merchenthaler et al., 1988; Hokfelt et al., 1989; Harkness and Brownfeld, 1986). The distribution of pro-TRH in several of these brain regions is identical to that of TRH (Lechan et al., 1986). The same was also shown by in situ hybridization of pro-TRH mRNA in the rat brain (Segerson et al., 1987). Likewise, the regional distribution of TRH receptors corresponds well with the immunoreactive TRH content in many CNS areas, including the hypothalamus, septum amygdala, NTS, DMV, and the spinal cord (Sharif and Burt, 1983; Mantyh and Hunt, 1985). It was recently shown that in the SHR the development of hypertension paralleled with increased TRH receptors in the hypothalamus and striatum (Bhargava et al., 1987). Increased amount of TRH binding in SHR compared to normotensive WKY rats was also detected in the spinal cord (Bhargava and Gulati, 1988).
A different view on the link between tinnitus and cognition; is there a reciprocal link?
Published in International Journal of Neuroscience, 2018
Elham Tavanai, Ghassem Mohammadkhani
Cuny et al. (2003) suggest fixation of this phantom auditory perception in the central auditory system may be influenced by attending to that. Based on the findings, tinnitus disturbs the automatic system responsible for automatic attention switching. Tinnitus subjects seem to have trouble in redirecting attention to something other than the tinnitus ear [22]. As a result, disabling tinnitus could lead to a higher level of selective attention directed toward the tinnitus signal that may increase the tinnitus-induced distress and prevent habituation. Several authors have argued that an attentional process may be involved in delaying or preventing habituation mechanisms in tinnitus [22]. Ridder et al. (2006) suggested that amygdala suppression can distract the center of attention. They performed selective amobarbital injections in the anterior choroidal artery that resulted in a nonfunctional amygdalohippocampal area for 10 min to evaluate the function of hippocampus and amygdala in tinnitus patients. Amytal injection ipsilateral to the tinnitus side leaded to a maximum of 30% tinnitus suppression, whereas amytal injection contralateral to the tinnitus side yielded 60–70% tinnitus suppression. They concluded that the amygdalohippocampal involvement in tinnitus perception might be crossed. As mentioned earlier, hippocampus and amygdala are involved in both cognitive function and tinnitus. It has been suggested that the essential function of the amygdalohippocampal structures is the forming of a paradoxical auditory memory for tinnitus. Therefore, it seems that the role of hippocampus and amygdala in tinnitus is persistence of tinnitus by updating auditory memory for tinnitus. As a result, suppressing the hippocampus causes the brain not to able to update the memory for the tinnitus and in turn disappearance of the tinnitus sounds [65].