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Ünal, Betül, Cumhur İbrahim Başsorgun, Meryem İlkay Eren Karanis, and Gülsüm Özlem Elpek. "Perianal Median Raphe Cyst: A Rare Lesion with Unusual Histology and Localization." Case Reports in Dermatological Medicine 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/487814.
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Median raphe cysts present anywhere between the external urethral meatus and the anus. The cysts can occur at parameatus, glans penis, penile shaft, scrotum, or perineum. Perianal region is an extremely rare location for these lesions. Here we present a 50-year-old male patient who presented with a cystic, fluctuant lesion, located at 12 o’clock in perianal region. Microscopic examination revealed a cystic lesion with keratinized and nonkeratinized stratified squamous epithelium, pseudostratified ciliated epithelium, and scattered goblet cells. The final diagnosis of the lesion was median raphe cyst. Ciliated cells and perianal localization in median raphe cysts are extremely rare characteristics.
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Chaves, Tiago, Bibiána Török, Csilla Lea Fazekas, Pedro Correia, Eszter Sipos, Dorottya Várkonyi, Ákos Hellinger, Dogu Erk, and Dóra Zelena. "Median raphe region GABAergic neurons contribute to social interest in mouse." Life Sciences 289 (January 2022): 120223. http://dx.doi.org/10.1016/j.lfs.2021.120223.
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Nitz, Douglas A., and Bruce L. McNaughton. "Hippocampal EEG and Unit Activity Responses to Modulation of Serotonergic Median Raphe Neurons in the Freely Behaving Rat." Learning & Memory 6, no. 2 (March 1, 1999): 153–67. http://dx.doi.org/10.1101/lm.6.2.153.
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Hippocampal EEG, GABAergic interneurons, and principal cells were recorded simultaneously as rats foraged within one of three environments both before and after modulation of serotonergic inputs to the hippocampus. Median raphe microinjections of the 5-HT1a receptor agonist 8-OH-DPAT were made to produce inhibition of serotonergic neurons in this region. Such microinjections produced behavioral arousal and increases in the amplitude of hippocampal EEG theta. Consistent with the pattern of serotonergic innervation of the hippocampus, the GABAergic interneuron population was affected differentially by the microinjections. Principal cells were generally unaffected by the manipulation and maintained robust spatial firing correlates within the foraging environment. The results provide basic data on the relationship between serotonergic median raphe neurons and hippocampal activity in a behaving animal. The data suggest that behavioral responses to manipulation of the serotonergic system are mediated by brain regions other than the hippocampus or are mediated through changes in the activity of hippocampal interneurons.
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Balázsfi, Diána G., Dóra Zelena, Lívia Farkas, Kornél Demeter, István Barna, Csaba Cserép, Virág T. Takács, et al. "Median raphe region stimulation alone generates remote, but not recent fear memory traces." PLOS ONE 12, no. 7 (July 14, 2017): e0181264. http://dx.doi.org/10.1371/journal.pone.0181264.
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Sos, Katalin E., Márton I. Mayer, Csaba Cserép, Flóra S. Takács, András Szőnyi, Tamás F. Freund, and Gábor Nyiri. "Cellular architecture and transmitter phenotypes of neurons of the mouse median raphe region." Brain Structure and Function 222, no. 1 (April 4, 2016): 287–99. http://dx.doi.org/10.1007/s00429-016-1217-x.
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Park, Min-Young, Jeong-Min Kim, Gun-Wook Kim, Hoon-Soo Kim, Byung-Soo Kim, Moon-Bum Kim, and Hyun-Chang Ko. "Pigmented Median Raphe Cysts on the Scrotum and Perianal Region: A Case Report." Annals of Dermatology 30, no. 5 (2018): 622. http://dx.doi.org/10.5021/ad.2018.30.5.622.
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Szőnyi, András, Krisztián Zichó, Albert M. Barth, Roland T. Gönczi, Dániel Schlingloff, Bibiána Török, Eszter Sipos, et al. "Median raphe controls acquisition of negative experience in the mouse." Science 366, no. 6469 (November 28, 2019): eaay8746. http://dx.doi.org/10.1126/science.aay8746.
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Adverse events need to be quickly evaluated and memorized, yet how these processes are coordinated is poorly understood. We discovered a large population of excitatory neurons in mouse median raphe region (MRR) expressing vesicular glutamate transporter 2 (vGluT2) that received inputs from several negative experience–related brain centers, projected to the main aversion centers, and activated the septohippocampal system pivotal for learning of adverse events. These neurons were selectively activated by aversive but not rewarding stimuli. Their stimulation induced place aversion, aggression, depression-related anhedonia, and suppression of reward-seeking behavior and memory acquisition–promoting hippocampal theta oscillations. By contrast, their suppression impaired both contextual and cued fear memory formation. These results suggest that MRR vGluT2 neurons are crucial for the acquisition of negative experiences and may play a central role in depression-related mood disorders.
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Cudennec, Annie, Danielle Duverger, Eric T. MacKenzie, Bernard Scatton, and André Serrano. "Serotonergic Neuron Stimulation Modulates Thalamocortical Glucose Use in the Conscious Rat." Journal of Cerebral Blood Flow & Metabolism 7, no. 4 (August 1987): 502–6. http://dx.doi.org/10.1038/jcbfm.1987.94.
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We have studied the effects, in the conscious rat, of electrical stimulation of the dorsal or median raphe nuclei on integrated functional activity, as assessed by the quantitative 2-deoxyglucose autoradiographic technique, Stimulation of serotonergic neurons elicits metabolic changes in cortical and thalamic regions that are not limited to those structures known to receive the densest serotonergic innervation. The thalamic nuclei that are activated by raphe stimulation include those that subserve the processing of somesthetic, accessory visual, and limbic information, Raphe stimulation increased cortical glucose use in a laminar and columnar pattern, but only in a highly circumscribed region that corresponds to the somatotopic representation of the rat's face and head. These findings indicate that ascending serotonergic neurons play an important modulatory role in the regulation of thalamocortical glucose use, observations that may be of value in the understanding of the etiology and expression of classic migraine.
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Domonkos, Andor, Litsa Nikitidou Ledri, Tamás Laszlovszky, Csaba Cserép, Zsolt Borhegyi, Edit Papp, Gábor Nyiri, Tamás F. Freund, and Viktor Varga. "Divergent in vivo activity of non‐serotonergic and serotonergic VGluT3–neurones in the median raphe region." Journal of Physiology 594, no. 13 (April 28, 2016): 3775–90. http://dx.doi.org/10.1113/jp272036.
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Le Bars, Pierre, Gaston Niagha, Ayepa Alain Kouadio, Julien Demoersman, Elisabeth Roy, Valérie Armengol, and Assem Soueidan. "Pilot Study of Laser Doppler Measurement of Flow Variability in the Microcirculation of the Palatal Mucosa." BioMed Research International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/5749150.
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Background.Histopathological alterations can arise when the denture-supporting mucosa experiences microbial and mechanical stress through the denture base and diagnosis of these diseases usually follows microvascular changes. Microcirculation measurement could allow for detection of such dysfunction and aid in the early diagnosis of palatal mucosa pathologies.Materials and Methods. We tested the sensitivity of laser Doppler for measuring the microcirculation of the palatal mucosa, assessing the median raphe (MR), Schroeder area (SA), and retroincisive papilla (RP). A Doppler PeriFlux 5000 System, containing a laser diode, was used. 54 healthy participants were recruited. We compare the measurements of PU (perfusion unit) using ANOVA test.Results.The numerical values for palatal mucosa blood flow differed significantly among the anatomical areas (p=0.0167). The mean value of Schroeder area was 92.6 (SD: 38.4) and was significantly higher than the retroincisive papilla (51.9) (SD: 20.2) (p<0.05), which in turn was higher than that of median raphe (31.9) (SD: 24.2) (p<0.0001).Conclusion.Schroeder area appeared to have the greatest sensitivity, and vascular flow variability among individuals was also greatest in this region. We suggest that analysis of blood stream modification with laser Doppler of the palatal mucosa can help to detect onset signs of pathological alterations.
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Fazekas, Csilla Lea, Manon Bellardie, Bibiána Török, Eszter Sipos, Blanka Tóth, Mária Baranyi, Beáta Sperlágh, Mihály Dobos-Kovács, Elodie Chaillou, and Dóra Zelena. "Pharmacogenetic excitation of the median raphe region affects social and depressive-like behavior and core body temperature in male mice." Life Sciences 286 (December 2021): 120037. http://dx.doi.org/10.1016/j.lfs.2021.120037.
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McNamara, Dennis, Denise M. Larson, Stanley I. Rapoport, and Timothy T. Soncrant. "Preferential Metabolic Activation of Subcortical Brain Areas by Acute Administration of Nicotine to Rats." Journal of Cerebral Blood Flow & Metabolism 10, no. 1 (January 1990): 48–56. http://dx.doi.org/10.1038/jcbfm.1990.7.
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Cerebral metabolic and behavioral effects of acutely administered nicotine were measured in rats in relation to dose. Nicotine 0.1, 1, or 10 mg/kg or vehicle was administered intraperitoneally to 3-month-old male Fischer-344 rats that had been pretreated with hexamethonium bromide 5 mg/kg i.p. to reduce peripheral autonomic effects. Regional CMRglc (rCMRglc) values were measured, using the quantitative autoradiographic [14C]-2-deoxy-d-glucose method, in 71 brain regions, beginning 3 min after nicotine or vehicle administration. Intensity of body tremor, scored by a blinded rater, was dose related and peaked at 3 min after nicotine injection. rCMRglc rose in a dose-related manner: Nicotine 0.1 mg/kg had no significant effect in any region, whereas 1 mg/kg elevated rCMRglc significantly in 21 regions (mean rise 20%) and 10 mg/kg produced generalized (56 regions) and greater (mean rise 50%) increases in rCMRglc. Nicotine 1 mg/kg activated thalamic nuclei, cerebellum, geniculate nuclei, superior colliculus, median raphe, reticular formation, and the habenulointerpeduncular pathway, but was without effect in the telencephalon. Effects of nicotine in the hindbrain were related anatomically to reported distributions of [3H]nicotine and [3H]acetylcholine but not [125I]α-bungarotoxin binding sites, implying that the former ligands label functional nicotine receptors. The pattern of change in rCMRglc after nicotine administration suggests that its cognitive effects in humans are due to augmented arousal/attention and visual processing rather than to direct neocortical or hippocampal activation.
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Laberge, Frédéric, and Allison Smith. "Efferent Axonal Projections of the Habenular Complex in the Fire-Bellied Toad Bombina orientalis." Brain, Behavior and Evolution 90, no. 4 (2017): 276–88. http://dx.doi.org/10.1159/000481394.
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The habenular complex and its associated axonal pathways are often thought of as phylogenetically conserved features of the brain among vertebrates despite the fact that detailed studies of this brain region are limited to a few species. Here, the gross morphology and axonal projection pattern of the habenular complex of an anuran amphibian, the fire-bellied toad Bombina orientalis, was studied to allow comparison with the situation in other vertebrates. Axonal pathways were traced using biocytin applications in dissected brain preparations. The results show that the rostral part of the left dorsal nucleus is enlarged in this species, while the rostral ventral nucleus and caudal parts do not show left-right size differences. Biocytin applications revealed widespread axonal projections of the habenular complex to the posterior tuberculum/dorsal hypothalamic region, ventral tegmentum, interpeduncular nucleus (IPN), and raphe median. Additionally, axons targeting the lateral hypothalamus originated from the ventral habenular nuclei. The results also suggest an asymmetrical pattern of projection to the IPN in the rostral part of the habenular complex, where the left habenula preferentially targeted the dorsal IPN while the right habenula preferentially targeted the ventral IPN. The caudal habenular nuclei showed no asymmetry of projections as both sides targeted the ventral IPN. Comparison of the habenular complex axonal connectivity across vertebrates argues against strong phylogenetic conservation of the axonal projection patterns of different habenular nuclei.
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Baraniuk, James N., Alison Amar, Haris Pepermitwala, and Stuart D. Washington. "Differential Effects of Exercise on fMRI of the Midbrain Ascending Arousal Network Nuclei in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) in a Model of Postexertional Malaise (PEM)." Brain Sciences 12, no. 1 (January 5, 2022): 78. http://dx.doi.org/10.3390/brainsci12010078.
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Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Gulf War Illness (GWI) and control subjects underwent fMRI during difficult cognitive tests performed before and after submaximal exercise provocation (Washington 2020). Exercise caused increased activation in ME/CFS but decreased activation for GWI in the dorsal midbrain, left Rolandic operculum and right middle insula. Midbrain and isthmus nuclei participate in threat assessment, attention, cognition, mood, pain, sleep, and autonomic dysfunction. Methods: Activated midbrain nuclei were inferred by a re-analysis of data from 31 control, 36 ME/CFS and 78 GWI subjects using a seed region approach and the Harvard Ascending Arousal Network. Results: Before exercise, control and GWI subjects showed greater activation during cognition than ME/CFS in the left pedunculotegmental nucleus. Post exercise, ME/CFS subjects showed greater activation than GWI ones for midline periaqueductal gray, dorsal and median raphe, and right midbrain reticular formation, parabrachial complex and locus coeruleus. The change between days (delta) was positive for ME/CFS but negative for GWI, indicating reciprocal patterns of activation. The controls had no changes. Conclusions: Exercise caused the opposite effects with increased activation in ME/CFS but decreased activation in GWI, indicating different pathophysiological responses to exertion and mechanisms of disease. Midbrain and isthmus nuclei contribute to postexertional malaise in ME/CFS and GWI.
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McMahon, Lori L., and Julie A. Kauer. "Hippocampal Interneurons Are Excited Via Serotonin-Gated Ion Channels." Journal of Neurophysiology 78, no. 5 (November 1, 1997): 2493–502. http://dx.doi.org/10.1152/jn.1997.78.5.2493.
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McMahon, Lori L. and Julie A. Kauer. Hippocampal interneurons are excited via serotonin-gated ion channels. J. Neurophysiol. 78: 2493–2502, 1997. Serotonergic neurons of the median raphe nucleus heavily innervate hippocampal GABAergic interneurons located in stratum radiatum of area CA1, suggesting that this strong subcortical projection may modulate interneuron excitability. Using whole cell patch-clamp recording from interneurons in brain slices, we tested the effects of serotonin (5-HT) on the physiological properties of these interneurons. Serotonin produces a rapid inward current that persists when synaptic transmission is blocked by tetrodotoxin and cobalt, and is unaffected by ionotropic glutamate and γ-aminobutyric acid (GABA) receptor antagonists. The 5-HT–induced current was independent of G-protein activation. Pharmacological evidence indicates that 5-HT directly excites these interneurons through activation of 5-HT3 receptors. At membrane potentials negative to −55 mV, the current-voltage ( I-V) relationship of the 5-HT current displays a region of negative slope conductance. Therefore the response of interneurons to 5-HT strongly depends on membrane potential and increases greatly as cells are depolarized. Removal of extracellular calcium, but not magnesium, increases the amplitude of 5-HT–induced currents and removes the region of negative slope conductance, thereby linearizing the I-V relationship. The axons of 5-HT–responsive interneurons ramify widely within CA1; some of these interneurons also project to and arborize extensively in the dentate gyrus. The organization of these inhibitory connections strongly suggests that these cells regulate excitability of both CA1 pyramidal cells and dentate granule cells. As our results indicate that 5-HT may mediate fast excitatory synaptic transmission onto these interneurons, serotonergic inputs can simultaneously modulate the output of both hippocampus and dentate gyrus.
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Bonvento, G., P. Lacombe, and J. Seylaz. "Effects of Electrical Stimulation of the Dorsal Raphe Nucleus on Local Cerebral Blood Flow in the Rat." Journal of Cerebral Blood Flow & Metabolism 9, no. 3 (June 1989): 251–55. http://dx.doi.org/10.1038/jcbfm.1989.41.
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We have studied the effects of electrical stimulation of the dorsal raphe nucleus on local cerebral blood flow (LCBF), as assessed by the quantitative [14C]-iodoantipyrine autoradiographic technique. Stimulation of the dorsal raphe nucleus in the α-chloralose anesthetized rat caused a significant decrease in LCBF, ranging from – 13 to – 26% in 24 brain structures out of 33 investigated. The most pronounced decreases (– 23 to – 26%) were observed in the accumbens, amygdaloid, interpeduncular nuclei and in the median raphe nucleus, limbic system relays. The decreases also concerned cortical regions and the extrapyramidal system. These results indicate that activation of ascending serotonergic system produces a vasoconstriction and that the dorsal raphe nucleus has a widespread modulatory influence on the cerebral circulation.
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Roberts, Claire, Ana Belenguer, Derek N. Middlemiss, and Carol Routledge. "Differential effects of 5-HT1B/1D receptor antagonists in dorsal and median raphe innervated brain regions." European Journal of Pharmacology 346, no. 2-3 (April 1998): 175–80. http://dx.doi.org/10.1016/s0014-2999(98)00061-2.
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Bernard, D. G., A. Li, and E. E. Nattie. "Evidence for central chemoreception in the midline raphe." Journal of Applied Physiology 80, no. 1 (January 1, 1996): 108–15. http://dx.doi.org/10.1152/jappl.1996.80.1.108.
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We injected acetazolamide (AZ; 5 x 10(-6) M; 1 nl; n = 14), its inactive analogue 2-acetylamino-1,3,4-thiadiazole-5-sulfon-t-butylamide (5 x 10(-5) M; n = 6), or mock cerebrospinal fluid (n = 5) into the caudal raphe in the midline brain stem of anesthetized paralyzed ventilated rats. These AZ injections have been shown to produce a focal region of tissue acidosis with a radius < 350 microns and are used as a probe for sites of central chemosensitivity. Compared with control injections, AZ injection into the raphe, as demonstrated by anatomic analysis of injection location, significantly increased the amplitude of the integrated phrenic neurogram over 10-40 min. Not all raphe injections produced such a response. AZ injections identified as responders (n = 8 of 14) increased integrated phrenic amplitude 43.3 +/- 10.7% (SE) of baseline 20 min after the injection. We conclude that the midline caudal raphe contains sites of ventilatory chemoreception.
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Yates, B. J., M. S. Siniaia, and A. D. Miller. "Descending pathways necessary for vestibular influences on sympathetic and inspiratory outflow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 6 (June 1, 1995): R1381—R1385. http://dx.doi.org/10.1152/ajpregu.1995.268.6.r1381.
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The objective of this study was to determine which brain stem regions that have projections to sympathetic preganglionic neurons or phrenic motoneurons ae necessary for vestibulosympathetic or vestibulorespiratory responses in decerebrate cats. Bilateral kainic acid injections into the rostral ventrolateral medulla abolished splanchnic nerve responses to electrical stimulation of the vestibular nerve, suggesting that this region is critical for the production of vestibulosympathetic responses. In contrast, injections into the caudal medullary raphe nuclei had no apparent effect on the responses. Neither the dorsal nor the ventral respiratory group appears to be necessary for mediating vestibular influences on the phrenic nerve, suggesting that nonrespiratory neurons (such as vestibulospinal neurons) may be important for producing vestibulorespiratory responses.
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Fitzgibbon, T., and W. Burke. "Representation of the temporal raphe within the optic tract of the cat." Visual Neuroscience 2, no. 3 (March 1989): 255–67. http://dx.doi.org/10.1017/s0952523800001176.
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AbstractThe retinal topography of the cat's optic tract was determined by means of injections of the enzyme horseradish peroxidase (HRP) into the tract. This analysis was accomplished by the subtraction of all HRP injection sites not labeling a defined retinal area from those injection sites which resulted in ganglion cell labeling (Venn diagram analysis). Using this method, the following correspondences were demonstrated for the ipsilateral and contralateral projections: superior retina represented in medial optic tract; inferior retina in lateral tract; and area centralis in a dorsocentral location (which was part of a larger area representing the visual streak). The temporal raphe was represented in the ipsilateral tract as a band curving from the area centralis region toward the dorsomedial border of the tract. Contralateral fibers from a region superior to the optic disc were found to be displaced with respect to the general retinal representation in the optic tract and this appeared to be related to retinal development. The ratio of contralateral to ipsilateral fibers was determined and found to be nonuniform within the tract.Injection of HRP into the optic tract of the cat also allowed the axons from labeled retinal ganglion cells to be traced within the retina and optic disc. Axons from ganglion cells lying temporal to the raphe curve around the area centralis enter the optic disc on the lateral and inferior aspects. Ganglion cells lying nasal to the raphe send their axons more directly to enter the optic disc on its superior aspect. A schema is proposed whereby the retina is mapped onto the optic tract.
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Coleman, M. J., and R. A. Dampney. "Powerful depressor and sympathoinhibitory effects evoked from neurons in the caudal raphe pallidus and obscurus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 5 (May 1, 1995): R1295—R1302. http://dx.doi.org/10.1152/ajpregu.1995.268.5.r1295.
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Microinjection of glutamate into sites within the medullary raphe nuclei (pallidus and obscurus) at levels caudal to the obex resulted in a dose-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate in anesthetized rabbits. The depressor and sympathoinhibitory responses were similar in magnitude to those elicited from the previously described depressor region in the caudal ventrolateral medulla (CVLM) but had a shorter duration, in both intact and barodenervated animals. The bradycardia was not altered by barodenervation but was reduced after administration of propranolol or atropine and abolished after administration of both drugs. The neuroinhibitory compounds gamma-aminobutyric acid or muscimol had no effect on MAP or RSNA when injected into the caudal medullary raphe nuclei but evoked a pressor and sympathoexcitatory response when injected into the CVLM. The results indicate that neurons within the caudal raphe pallidus and obscurus can powerfully inhibit sympathetic activity, but unlike sympathoinhibitory neurons in the CVLM, they are not tonically active and are not capable of producing sustained changes in arterial pressure and sympathetic activity.
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Webb, Sierra M., Fiori R. Vollrath-Smith, Rick Shin, Thomas C. Jhou, Shengping Xu, and Satoshi Ikemoto. "Rewarding and incentive motivational effects of excitatory amino acid receptor antagonists into the median raphe and adjacent regions of the rat." Psychopharmacology 224, no. 3 (June 30, 2012): 401–12. http://dx.doi.org/10.1007/s00213-012-2759-0.
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Hinckel, P., and W. T. Perschel. "Influence of cold and warm acclimation on neuronal responses in the lower brain stem." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1281–89. http://dx.doi.org/10.1139/y87-204.
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Neurons in two lower brain stem areas, the nucleus raphe magnus and the subcoeruleus region, have been shown to be part of the thermoafferent system. It is concluded from microcut experiments in unanaesthetized guinea pigs that inhibition of shivering caused by nucleus raphe magnus stimulation is mediated partly by ascending and partly by descending efferents of the nucleus raphe magnus. Electrical stimulation of the subcoeruleus area caused excitatory metabolic responses. Interruption of the ascending efferents of the subcoeruleus area did not prevent the metabolic activation. It is concluded that the excitatory responses are partly mediated by descending efferents of the subcoeruleus area. The descending pathways project mainly to motoneurone pools and to dorsal horn cells. In cold-acclimated guinea pigs, the average maximum activity of bell-shaped subcoeruleus cold-responsive units was reduced significantly in comparison with cold-responsive neurons in animals acclimated to normal room temperature. Furthermore, peak activity of warm-responsive units in the nucleus raphe magnus was larger in cold-acclimated animals than in animals acclimated to normal room termperature. These neuronal changes may contribute via descending lower loops and via ascending upper loops to long-term slope reduction of metabolic cold defence and shivering threshold displacements.
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de Oliveira, Rodolpho Pereira, José Simões de Andrade, Marianna Spina, João Vítor Chamon, Paulo Henrique Dias Silva, Ana Keyla Werder, Daniela Ortolani, et al. "Clozapine prevented social interaction deficits and reduced c-Fos immunoreactivity expression in several brain areas of rats exposed to acute restraint stress." PLOS ONE 17, no. 3 (March 3, 2022): e0262728. http://dx.doi.org/10.1371/journal.pone.0262728.
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In the present study, we evaluate the effect of acute restraint stress (15 min) of male Wistar rats on social interaction measurements and c-Fos immunoreactivity (c-Fos-ir) expression, a marker of neuronal activity, in areas involved with the modulation of acute physical restraint in rats, i.e., the paraventricular nucleus of the hypothalamus (PVN), median raphe nucleus (MnR), medial prefrontal cortex (mPFC), cingulate prefrontal cortex (cPFC), nucleus accumbens (NaC), hippocampus (CA3), lateral septum (LS) and medial amygdala (MeA). We considered the hypothesis that restraint stress exposure could promote social withdrawal induced by the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis, and increase c-Fos expression in these limbic forebrain areas investigated. In addition, we investigated whether pretreatment with the atypical antipsychotic clozapine (5 mg/kg; I.P.) could attenuate or block the effects of restraint on these responses. We found that restraint stress induced social withdrawal, and increased c-Fos-ir in these areas, demonstrating that a single 15 min session of physical restraint of rats effectively activated the HPA axis, representing an effective tool for the investigation of neuronal activity in brain regions sensitive to stress. Conversely, pretreatment with clozapine, prevented social withdrawal and reduced c-Fos expression. We suggest that treatment with clozapine exerted a preventive effect in the social interaction deficit, at least in part, by blocking the effect of restraint stress in brain regions that are known to regulate the HPA-axis, including the cerebral cortex, hippocampus, hypothalamus, septum and amygdala. Further experiments will be done to confirm this hypothesis.
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Brusin, Victor, Maria Camila Ceballos, Pedro Henrique Esteves Trindade, Karen Camille Rocha Góis, Gabriel Conde, Virginia Tessarine Barbosa, Gustavo dos Santos Rosa, and Mateus Jose Rodrigues Paranhos da Costa. "Flunixin Meglumine Is Superior to Meloxicam for Providing Analgesia after Surgical Castration in 2-Month-Old Goats." Animals 12, no. 23 (December 6, 2022): 3437. http://dx.doi.org/10.3390/ani12233437.
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Farm animals are exposed to various painful procedures during their productive lives, making it necessary to implement anesthetic and analgesic protocols. However, there are few studies evaluating the effectiveness of these drugs. Our objective was to compare the analgesic effects of two nonsteroidal anti-inflammatory drugs (NSAIDs): meloxicam (MEL) and flunixin meglumine (FLU), in goat kids subjected to surgical castration under local anesthesia. Anglo-Nubian goat kids (60 days old) were allocated into two groups: MEL (n = 9), and FLU (n = 8), each administered 5 min before starting castration. All had been previously subjected to local anesthesia with lidocaine, injected bilaterally into the testes, plus subcutaneous in the scrotal raphe. Pain sensitivity was evaluated using the von Frey monofilaments test. Reactions were recorded before castration (M0), immediately after castration (M1), and once-daily for three consecutive days post-castration (M2, M3, and M4, respectively). Pain assessments were conducted in three body regions: at four points of the scrotum (dorsal and ventral; left and right lateral; R1); medial region of the pelvic limb, gracilis muscle (R2); and hypogastric region of the abdomen (R3). MEL goats had considerably greater pain reaction in R1 and R2 over time, mainly in M2; therefore, FLU was a more effective analgesic than MEL, resulting in less pain reaction.
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van Baardwijk, Charles, Sharon E. Barwick, and Margot R. Roach. "Organization of medial elastin at aortic junctions in sheep and lambs." Canadian Journal of Physiology and Pharmacology 63, no. 7 (July 1, 1985): 855–62. http://dx.doi.org/10.1139/y85-140.
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Aortas from four sheep and three fetal lambs were fixed at physiological pressure in 10% neutral buffered formalin. The regions with branches were serially sectioned in either cross or longitudinal section at 7-μm intervals and stained for elastin with Gomori–aldehyde–fuchsin. A large model of one aortointercostal junction was made from Plexiglas to show that bundles of elastin appeared to be continuous from the aorta into the branch. These bundles were then studied from large photomicrographs of the other junctions. At the intercostals and lumbars, the elastin lamellae ran continuously from the outer third of the media into the branch. There was often an added "pad" of elastin and other acellular material on the flow divider (distal lip). The large muscular branches which arose from the abdominal aorta have much less elastin than the intercostals. In them the aortic elastin appears to merge into a raphe on the proximal and lateral sides of the junction, with a very abrupt transition. A "tongue" of muscle from the branch often penetrated into the media of the aorta distally. Occasionally a small acellular cap was seen on the apex of the flow divider. There were few significant differences between the lambs and the sheep, probably because embryologically the arteries develop very early. The proximal and distal lips of all junctions were easily distinguished from each other, and the small and large branches were also different. We suspect these regions may respond differently to pressure, but we did not test this hypothesis.
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Kung, Ling-Hsuan, Jaimee Glasgow, Anna Ruszaj, Thackery Gray, and Karie E. Scrogin. "Serotonin neurons of the caudal raphe nuclei contribute to sympathetic recovery following hypotensive hemorrhage." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R939—R953. http://dx.doi.org/10.1152/ajpregu.00738.2009.
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Serotonin is thought to contribute to the syncopal-like response that develops during severe blood loss by inhibiting presympathetic neurons of the rostroventrolateral medulla (RVLM). Here, we tested whether serotonin cells activated during hypotensive hemorrhage, i.e., express the protein product of the immediate early gene c-Fos, are critical for the normal sympathetic response to blood loss in unanesthetized rats. Serotonin-immunoreactive cells of the raphe obscurus and raphe magnus, parapyramidal cells of the B3 region, subependymal cells of the ventral parapyramidal region, and cells of the ventrolateral periaqueductal gray region were activated by hypotensive hemorrhage, but not by hypotension alone. In contrast to findings in anesthetized animals, lesion of hindbrain serotonergic cells sufficient to produce >80% loss of serotonin nerve terminal immunoreactivity in the RVLM accelerated the sympatholytic response to blood loss, attenuated recovery of sympathetic activity after termination of hemorrhage, and exaggerated metabolic acidosis. Hindbrain serotonin lesion also attenuated ventilatory and sympathetic responses to stimulation of central chemoreceptors but increased spontaneous arterial baroreflex sensitivity and decreased blood pressure variability. A more global neurotoxic lesion that also eliminated tryptophan hydroxylase-immunoreactive cells of the ventrolateral periaqueductal gray region had no further effect on the sympatholytic response to blood loss. Together, the data indicate that serotonin cells of the caudal hindbrain contribute to compensatory responses following blood loss that help maintain oxygenation of peripheral tissue in the unanesthetized rat. This effect may be related to facilitation of chemoreflex responses to acidosis.
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Arthur, J. M., A. C. Bonham, D. D. Gutterman, G. F. Gebhart, M. L. Marcus, and M. J. Brody. "Coronary vasoconstriction during stimulation in hypothalamic defense region." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 2 (February 1, 1991): R335—R345. http://dx.doi.org/10.1152/ajpregu.1991.260.2.r335.
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Previous studies have identified a site in lateral hypothalamus (LH) in which electrical stimulation elicits coronary vasoconstriction. We injected the retrogradely transported tracer Fast Blue to determine which brain regions project to LH. Projections to or through LH were found from the paraventricular nucleus (PVN) of the hypothalamus, bed nucleus of the stria terminalis (BNST), and dorsal raphe nucleus (DRN). In chloralose-anesthetized cats, electrical stimulation in DRN and BNST failed to increase coronary vascular resistance (CVR). However, stimulation lateral to PVN in the anterior hypothalamic area (AHA), a region not labeled by the tracer, caused a transient decrease in coronary blood flow similar to that elicited from LH. The increase in CVR was accompanied by hemodynamic changes that are characteristic of the defense reaction including a cholinergically mediated decrease in hindquarter vascular resistance. This response is likely due to activation of fibers of passage and not cell bodies, since cell bodies in the region were not retrogradely labeled and coronary vasoconstriction was not seen following microinjection of several excitatory amino acids into AHA. These data suggest that coronary vasoconstriction may be a component of the defense reaction elicited by electrical activation of AHA.
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Hornby, P. J., C. D. Rossiter, R. L. White, W. P. Norman, D. H. Kuhn, and R. A. Gillis. "Medullary raphe: a new site for vagally mediated stimulation of gastric motility in cats." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 4 (April 1, 1990): G637—G647. http://dx.doi.org/10.1152/ajpgi.1990.258.4.g637.
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Thyrotropin-releasing hormone (TRH) is clearly implicated in the control of gastric function via interactions in the dorsal motor nucleus of the vagus (DMV) of the cat. The source of the TRH innervation of the DMV is important to determine because this region could be of importance in control of gastric function. TRH-immunoreactive (ir) neurons are located in the raphe obscurus (Ro), raphe pallidus (Rp), and raphe magnus (Rm). Retrograde tracer applied to the DMV resulted in the most numerous labeled neurons in the caudal Ro and Rp in the same region where TRH-ir neurons are located. To address the question whether DMV-projecting neurons in the raphe subnuclei play a role in control of gastric motility, the following experiments were performed in alpha-chloralose-anesthetized cats while recording pyloric motility and blood pressure. Microinjection of a cell body excitant L-glutamate (44-200 nl, 0.5 M) into the caudal Ro and Rp in 15 experiments produced significant increases in pyloric minute motility index (MMI) of 4.9 +/- 1.5 (from 1.6 +/- 0.7 preinjection to 6.5 +/- 1.8 postinjection, P less than 0.05). Mean blood pressure (MBP) decreased significantly in these animals by 12 +/- 7 mmHg (from 100 +/- 6 to 88 +/- 8 mmHg, P less than 0.05). Saline microinjection in the same sites in seven cases resulted in no significant change in pyloric MMI (-1.0 +/- 0.8) or MBP (-4 +/- 11 mmHg). In five of these experiments, a second microinjection of L-glutamate (132-240 nl) was performed into the caudal Ro and Rp after spinal cord transection. This resulted in a significant increase in pyloric MMI of 3.3 +/- 0.9 (from 1.0 +/- 0.5 preinjection to 4.3 +/- 1.1 postinjection, P less than 0.05) but no change in MBP (+1 +/- 1 mmHg). Bilateral vagotomy resulted in the abrupt cessation of the pyloric response to caudal Ro and Rp stimulation. Microinjection of L-glutamate into the rostral Rp and caudal Rm in nine experiments resulted in no significant changes in pyloric MMI (-0.4 +/- 0.8) or MBP (-10 +/- 11 mmHg). These data indicate that a population of neurons in the caudal raphe nuclei, which may contain TRH, project to the DMV. In addition, excitation of these neurons causes an increase in gastric motility that is not caused by inhibition of sympathetic outflow to the gut but rather by excitation of vagal neurons in the DMV.
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Höflich, A. S., C. Philippe, M. Savli, P. Baldinger, G. S. Kranz, S. Müller, D. Häusler, et al. "Prediction of steady-state occupancy of the serotonin transporter based on single-dose occupancy: A [11C]DASB pet study." European Psychiatry 26, S2 (March 2011): 929. http://dx.doi.org/10.1016/s0924-9338(11)72634-7.
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IntroductionClinical studies point toward a potential role of the serotonin transporter (SERT) binding as a predictor of clinical outcome in the treatment of depression. After long-term treatment with clinical doses of SSRIs the expected SERT occupancy is about 80%. Here, we were interested to investigate the relationship of SERT occupancy values between short- and longterm treatment.ObjectivesTo test if the SERT occupancy at steady-state can be predicted based on the single dose occupancy by escitalopram (S-citalopram) or citalopram (racemate of S-citalopram and R-citalopram).Methods18 patients with major depressive disorder received either escitalpram (10 mg/d) or citalopram (20 mg/d) in a double-blind, randomized, longitudinal study. They underwent three PET scans using the radioligand [11C]DASB: PET1 baseline, PET2 6 hours after first drug intake and PET3 after three weeks of daily oral treatment. Occupancy of SERT was quantified in six subcortical regions: thalamus, N. caudatus, putamen, mibrain, dorsal raphe and median raphe nuclei. Data was analyzed by means of multiple linear regression models corrected for baseline SERT availability values using SPSS 15.0.ResultsSingle dose occupancy of the SERT significantly predicted steady-state occupancy after three weeks in three regions: thalamus (r2 = 0.45, p = 0.009), N. caudatus (r2 = 0.4, p = 0.006) and putamen (r2 = 0.43, p = 0.005). Other regions did not show significant relationships.ConclusionsIn this study we demonstrated that single-dose occupancy in SERT rich regions such as thalamus, N. caudatus and the putamen could serve as reliable predictors for steady-state occupancy. However, a linear model failed to explain the relationship in regions known for serotonergic cell origin.
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McCall, R. B., and L. T. Harris. "Sympathetic alterations after midline medullary raphe lesions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 1 (July 1, 1987): R91—R100. http://dx.doi.org/10.1152/ajpregu.1987.253.1.r91.
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The present study was designed to determine the functional importance of the midline medullary raphe nuclei in the autonomic regulation of the cardiovascular system in the anesthetized cat. Baroreceptor and somatosympathetic reflexes as well as the effects of electrical stimulation of vagal afferents and pressor and depressor sites in the hypothalamus and spinal trigeminal tract were determined before and after midline medullary lesions that extended from 2 to 7 mm rostral to the obex. Midline medullary lesions failed to affect baroreceptor reflexes as judged by the lack of effect on the sympathoinhibition associated with the pressor response to phenylephrine and the degree of slow-wave locking of sympathetic activity to the cardiac cycle. However, the lesion did significantly increase spontaneous sympathetic activity recorded from the inferior cardiac nerve. Blood pressure and heart rate were not altered by midline lesions. In addition, the computer-summed sympathoexcitatory response to electrical stimulation of somatic afferents in the sciatic nerve and the sympathoinhibitory response to stimulation of vagal afferent fibers were not affected by midline lesions. In contrast, the decrease in blood pressure and inhibition of sympathetic nerve activity elicited by electrical stimulation of the spinal trigeminal tract were completely abolished by the lesion. Depressor responses evoked from the anteroventral third ventricle region of the hypothalamus but not pressor responses elicited from the posterior hypothalamus were eliminated following midline medullary lesions. Finally, the sympathoinhibitory actions of the serotonin antagonist methysergide were blocked by medullary raphe lesions. These data indicate that neural elements in the medial medullary area function to provide a tonic inhibition of sympathetic nerve activity that is of nonbaroreceptor origin. Depressor responses evoked from the anterior hypothalamus and the spinal trigeminal tract also are mediated through this area of the medulla. Finally, the data support our contention that medullary serotonergic neurons have a sympathoexcitatory function.
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Tanaka, Mutsumi, and Robin M. McAllen. "A subsidiary fever center in the medullary raphé?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 6 (December 2005): R1592—R1598. http://dx.doi.org/10.1152/ajpregu.00141.2005.
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In fever, as in normal thermoregulation, signals from the preoptic area drive both cutaneous vasoconstriction and thermogenesis by brown adipose tissue (BAT). Both of these responses are mediated by sympathetic nerves whose premotor neurons are located in the medullary raphé. EP3 receptors, key prostaglandin E2 (PGE2) receptors responsible for fever induction, are expressed in this same medullary raphé region. To investigate whether PGE2 in the medullary raphé might contribute to the febrile response, we tested whether direct injections of PGE2 into the medullary raphé could drive sympathetic nerve activity (SNA) to BAT and cutaneous (tail) vessels in anesthetized rats. Microinjections of glutamate (50 mM, 60–180 nl) into the medullary raphé activated both tail and BAT SNA, as did cooling the trunk skin. PGE2 injections (150–500 ng in 300–1,000 nl) into the medullary raphé had no effect on tail SNA, BAT SNA, body temperature, or heart rate. By contrast, 150 ng PGE2 injected into the preoptic area caused large increases in both tail and BAT SNA (+60 ± 17 spikes/15 s and 1,591 ± 150% of control, respectively), increased body temperature (+1.8 ± 0.2°C), blood pressure (+17 ± 2 mmHg), and heart rate (+124 ± 19 beats/min). These results suggest that despite expression of EP3 receptors, neurons in the medullary raphé are unable to drive febrile responses of tail and BAT SNA independently of the preoptic area. Rather, they appear merely to transmit signals for heat production and heat conservation originating from the preoptic area.
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Taylor, Natalie C., Aihua Li, Adam Green, Hannah C. Kinney, and Eugene E. Nattie. "Chronic fluoxetine microdialysis into the medullary raphe nuclei of the rat, but not systemic administration, increases the ventilatory response to CO2." Journal of Applied Physiology 97, no. 5 (November 2004): 1763–73. http://dx.doi.org/10.1152/japplphysiol.00496.2004.
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In conscious rats, focal CO2 stimulation of the medullary raphe increases ventilation, whereas interference with serotonergic function here decreases the ventilatory response to systemic hypercapnia. We sought to determine whether repeated administration of a selective serotonin reuptake inhibitor in this region would increase the ventilatory response to hypercapnia in unanesthetized rats. In rats instrumented with electroencephalogram-electromyogram electrodes, 250 or 500 μM fluoxetine or artificial cerebrospinal fluid (aCSF) was microdialyzed into the medullary raphe for 30 min daily over 15 days. To compare focal and systemic treatment, two additional groups of rats received 10 mg·kg−1·day−1 fluoxetine or vehicle systemically. Ventilation was measured in normocapnia and in 7% CO2 before treatment ( day 0), acutely ( days 1 or 3), on day 7, and on day 15. There was no change in normocapnic ventilation in any treatment group. Rats that received 250 μM fluoxetine microdialysis showed a significant 13% increase in ventilation in wakefulness during hypercapnia on day 7, due to an increase in tidal volume. In rats microdialyzed with 500 μM fluoxetine, there were 16 and 32% increases in minute ventilation during hypercapnia in wakefulness and sleep on day 7, and 20 and 28% increases on day 15, respectively, again due to increased tidal volume. There was no change in the ventilatory response to CO2 in rats microdialyzed with aCSF or in systemically treated rats. Chronic fluoxetine treatment in the medullary raphe increases the ventilatory response to hypercapnia in an unanesthetized rat model, an effect that may be due to facilitation of chemosensitive serotonergic neurons.
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Brown, J. W., E. A. Sirlin, A. M. Benoit, J. M. Hoffman, and R. A. Darnall. "Activation of 5-HT1A receptors in medullary raphé disrupts sleep and decreases shivering during cooling in the conscious piglet." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 3 (March 2008): R884—R894. http://dx.doi.org/10.1152/ajpregu.00655.2007.
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Activation of 5-HT1A receptors in the medullary raphé decreases sympathetically mediated brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction when previously activated with leptin, LPS, prostaglandins, or cooling. It is not known whether shivering is also modulated by medullary raphé 5-HT1A receptors. We previously showed in conscious piglets that activation of 5-HT1A receptors with (±)-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT) in the paragigantocellularis lateralis (PGCL), a medullary region lateral to the raphé that contains substantial numbers of 5-HT neurons, eliminates rapid eye movement (REM) sleep and decreases shivering in a cold environment, but does not attenuate peripheral vasoconstriction. Hoffman JM, Brown JW, Sirlin EA, Benoit AM, Gill WH, Harris MB, Darnall RA. Am J Physiol Regul Integr Comp Physiol 293: R518–R527, 2007. We hypothesized that, during cooling, activation of 5-HT1A receptors in the medullary raphé would also eliminate REM sleep and, in contrast to activation of 5-HT1A receptors in the PGCL, would attenuate both shivering and peripheral vasoconstriction. In a continuously cool environment, dialysis of 8-OH-DPAT into the medullary raphé resulted in alternating brief periods of non-REM sleep and wakefulness and eliminated REM sleep, as observed when 8-OH-DPAT is dialyzed into the PGCL. Moreover, both shivering and peripheral vasoconstriction were significantly attenuated after 8-OH-DPAT dialysis into the medullary raphé. The effects of 8-OH-DPAT were prevented after dialysis of the selective 5-HT1A receptor antagonist WAY-100635. We conclude that, during cooling, exogenous activation of 5-HT1A receptors in the medullary raphé decreases both shivering and peripheral vasoconstriction. Our data are consistent with the hypothesis that neurons expressing 5-HT1A receptors in the medullary raphé facilitate spinal motor circuits involved in shivering, as well as sympathetic stimulation of other thermoregulatory effector mechanisms.
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Passerin, Alicia M., and William N. Henley. "Activation of spinal cord serotonergic neurons accompanies cold-induced sympathoexcitation." Canadian Journal of Physiology and Pharmacology 72, no. 8 (August 1, 1994): 884–92. http://dx.doi.org/10.1139/y94-125.
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These studies examined the hypothesis that serotonergic neurons located in central sites known to be involved with autonomic regulation are activated by cold exposure, a potent stimulator of the sympathetic nervous system. In all experiments, rats were exposed to either 3 °C or 22 °C for 24 h. Significant increases (p < 0.05) in urinary norepinephrine excretion, depletions of myocardial norepinephrine, and enhanced myocardial L-DOPA accumulation following decarboxylase inhibition provided evidence of sympathoexcitation at 3 °C. Accumulations of the serotonin metabolite 5-hydroxyindoleacetic acid, in saline-injected rats, and 5-hydroxytryptophan in decarboxylase-inhibited rats were increased in spinal cord and brainstem regions of cold-exposed rats. Two hours after injection of the serotonin synthesis inhibitor p-chlorophenylalanine, significantly greater depletions of serotonin in spinal cord and 5-hydroxyindoleacetic acid in spinal cord and brainstem of cold-exposed rats were noted; synthesis inhibition also caused a larger drop in body temperature in cold-exposed rats. Microdissections of raphe nuclei and thoracic spinal cord sites indicated that the principal sites of serotonergic activation were the dorsal and intermediate spinal regions, and the raphe magnus. Thus, cold-induced sympathoexcitation was accompanied by activation of serotonergic neurons in spinal cord and brainstem regions known to be involved in autonomic regulation.Key words: serotonin, cold, stress, sympathetic nervous system, spinal cord.
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Ngampramuan, Sukonthar, Mathias Baumert, Mirza Irfan Beig, Naiphinich Kotchabhakdi, and Eugene Nalivaiko. "Activation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 1 (January 2008): R132—R141. http://dx.doi.org/10.1152/ajpregu.00464.2007.
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To better understand the central mechanisms that mediate increases in heart rate (HR) during psychological stress, we examined the effects of systemic and intramedullary (raphe region) administration of the serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di- n-propylamino)tetraline (8-OH-DPAT) on cardiac changes elicited by restraint in hooded Wistar rats with preimplanted ECG telemetric transmitters. 8-OH-DPAT reduced basal HR from 356 ± 12 to 284 ± 12 beats/min, predominantly via a nonadrenergic, noncholinergic mechanism. Restraint stress caused tachycardia (an initial transient increase from 318 ± 3 to 492 ± 21 beats/min with a sustained component of 379 ± 12 beats/min). β-Adrenoreceptor blockade with atenolol suppressed the sustained component, whereas muscarinic blockade with methylscopolamine (50 μg/kg) abolished the initial transient increase, indicating that sympathetic activation and vagal withdrawal were responsible for the tachycardia. Systemic administration of 8-OH-DPAT (10, 30, and 100 μg/kg) attenuated stress-induced tachycardia in a dose-dependent manner, and this effect was suppressed by the 5-HT1A antagonist WAY-100635 (100 μg/kg). Given alone, the antagonist had no effect. Systemically injected 8-OH-DPAT (100 μg/kg) attenuated the sympathetically mediated sustained component (from +85 ± 19 to +32 ± 9 beats/min) and the vagally mediated transient (from +62 ± 5 to +25 ± 3 beats/min). Activation of 5-HT1A receptors in the medullary raphe by microinjection of 8-OH-DPAT mimicked the antitachycardic effect of the systemically administered drug but did not affect basal HR. We conclude that tachycardia induced by restraint stress is due to a sustained increase in cardiac sympathetic activity associated with a transient vagal withdrawal. Activation of central 5-HT1A receptors attenuates this tachycardia by suppressing autonomic effects. At least some of the relevant receptors are located in the medullary raphe-parapyramidal area.
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Almasabi, Faris, Faisal Alosaimi, Minerva Corrales-Terrón, Anouk Wolters, Dario Strikwerda, Jasper V. Smit, Yasin Temel, Marcus L. F. Janssen, and Ali Jahanshahi. "Post-Mortem Analysis of Neuropathological Changes in Human Tinnitus." Brain Sciences 12, no. 8 (August 1, 2022): 1024. http://dx.doi.org/10.3390/brainsci12081024.
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Tinnitus is the phantom perception of a sound, often accompanied by increased anxiety and depressive symptoms. Degenerative or inflammatory processes, as well as changes in monoaminergic systems, have been suggested as potential underlying mechanisms. Herein, we conducted the first post-mortem histopathological assessment to reveal detailed structural changes in tinnitus patients’ auditory and non-auditory brain regions. Tissue blocks containing the medial geniculate body (MGB), thalamic reticular nucleus (TRN), central part of the inferior colliculus (CIC), and dorsal and obscurus raphe nuclei (DRN and ROb) were obtained from tinnitus patients and matched controls. Cell density and size were assessed in Nissl-stained sections. Astrocytes and microglia were assessed using immunohistochemistry. The DRN was stained using antibodies raised against phenylalanine hydroxylase-8 (PH8) and tyrosine-hydroxylase (TH) to visualize serotonergic and dopaminergic cells, respectively. Cell density in the MGB and CIC of tinnitus patients was reduced, accompanied by a reduction in the number of astrocytes in the CIC only. Quantification of cell surface size did not reveal any significant difference in any of the investigated brain regions between groups. The number of PH8-positive cells was reduced in the DRN and ROb of tinnitus patients compared to controls, while the number of TH-positive cells remained unchanged in the DRN. These findings suggest that both neurodegenerative and inflammatory processes in the MGB and CIC underlie the neuropathology of tinnitus. Moreover, the reduced number of serotonergic cell bodies in tinnitus cases points toward a potential role of the raphe serotonergic system in tinnitus.
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Salo, Lauren M., Eugene Nalivaiko, Colin R. Anderson, and Robin M. McAllen. "Control of cardiac rate, contractility, and atrioventricular conduction by medullary raphé neurons in anesthetized rats." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 2 (February 2009): H318—H324. http://dx.doi.org/10.1152/ajpheart.00951.2008.
Full textAbstract:
The sympathetic actions of medullary raphé neurons on heart rate (HR), atrioventricular conduction, ventricular contractility, and rate of relaxation were examined in nine urethane-anesthetized (1–1.5 g/kg iv), artificially ventilated rats that had been adrenalectomized and given atropine methylnitrate (1 mg/kg iv). Mean arterial pressure (MAP), ECG, and left ventricular pressure were recorded. The peak rates of rise and fall in the first derivative of left ventricular (LV) pressure (dP/d tmax and dP/d tmin, respectively) and the stimulus-R ($-R) interval were measured during brief periods of atrial pacing at 8.5 Hz before and after ventral medullary raphé neurons were activated by dl-homocysteic acid (DLH, 0.1 M) or inhibited by GABA (0.3 M) in local microinjections (90 nl). LV dP/d tmax values were corrected for the confounding effect of MAP, determined at the end of the experiments after giving propranolol (1 mg/kg iv) to block sympathetic actions on the heart. DLH microinjections into the ventral medullary raphé region increased HR by 44 ± 2 beats/min, LV dP/d tmax by 1,055 ± 156 mmHg/s, and the negative value of LV dP/d tmin by 729 ± 204 mmHg/s (all, P < 0.001) while shortening the $-R interval by 2.8 ± 0.8 ms ( P < 0.01). GABA microinjections caused no significant change in HR, LV dP/d tmax, or $-R interval but reduced LV dP/d tmin from −5,974 ± 93 to −5,548 ± 171 mmHg/s and MAP from 115 ± 4 to 105 ± 5 mmHg (both, P < 0.01). Rises in tail skin temperature confirmed that GABA injections effectively inhibited raphé neurons. When activated, the neurons in the ventral medullary raphé region thus enhance atrioventricular conduction, ventricular contractility, and relaxation in parallel with HR, but they provide little or no tonic sympathetic drive to the heart.
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Kirouac, Gilbert J., and Quentin J. Pittman. "A projection from the ventral tegmental area to the periaqueductal gray involved in cardiovascular regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 6 (June 1, 2000): R1643—R1650. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1643.
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Experiments were done in α-chloralose-anesthetized rats to determine a pathway mediating the cardiovascular depressor responses elicited from stimulation of the ventral tegmental area (VTA). The magnitude of the depressor responses elicited by glutamate stimulation (0.1 M/30 nl) of the VTA was examined after neuronal block produced by microinjections of lidocaine into ascending fiber bundles leaving the VTA to innervate the forebrain and thalamus. Bilateral microinjections of 1 μl of 4% lidocaine in the medial forebrain bundle ( n = 6) and in the periventricular fibers of the midbrain ( n = 5) did not attenuate the depressor response from stimulation of the VTA. Experiments were done using the anterograde tracer biotinylated dextran amine to identify descending projections from the VTA to cardiovascular centers in the brain stem. Examination of the nucleus of the solitary tract, ventrolateral medulla, and A5 catecholaminergic cell group revealed few or no fibers or terminals. Occasional fibers and some terminals were observed in the nucleus of raphe magnus, parabrachial nucleus, and locus ceruleus. A very dense bilateral projection was found to the ventrolateral periaqueductal gray (PAGvl) and dorsal raphe nucleus adjacent to the PAGvl. Bilateral injections of 4% lidocaine ( n = 4) or 10 mM cobalt chloride ( n = 5) into the PAGvl region attenuated the depressor responses elicited by stimulation of the VTA by ∼50%. These experiments indicate that the depressor responses elicited from activation of the VTA are mediated in part by a pathway to a cardiovascular depressor area located in the PAGvl.
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Zhang, Zhenxiong, Fadi Xu, Cancan Zhang, and Xiaomin Liang. "Activation of opioid μ-receptors in medullary raphe depresses sighs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 5 (May 2009): R1528—R1537. http://dx.doi.org/10.1152/ajpregu.90748.2008.
Full textAbstract:
Sighs, a well-known phenomenon in mammals, are substantially augmented by hypoxia and hypercapnia. Because (d-Ala2,N-Me-Phe4,Gly-ol)-enkephalin (DAMGO), a μ-receptor agonist, injected intravenously and locally in the caudal medullary raphe region (cMRR) decreased the ventilatory response to hypoxia and hypercapnia, we hypothesized that these treatments could inhibit sigh responses to these chemical stimuli. The number and amplitude of sighs were recorded during three levels of isocapnic hypoxia (15%, 10%, and 5% O2 for 1.5 min) or hypercapnia (3%, 7%, and 10% CO2 for 4 min) to test the dependence of sigh responses on the intensity of chemical drive in anesthetized and spontaneously breathing rats. The role of μ-receptors in modulating sigh responses to 10% O2 or 7% CO2 was subsequently evaluated by comparing the sighs before and after 1) intravenous administration of DAMGO (100 μg/kg), 2) microinjection of DAMGO (35 ng/100 nl) into the cMRR, and 3) intravenous administration of DAMGO after microinjection of d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 100 ng/100 nl), a μ-receptor antagonist, into the cMRR. Hypoxia and hypercapnia increased the number, but not amplitude, of sighs in a concentration-dependent manner, and the responses to hypoxia were significantly greater than those to hypercapnia. Systemic and local injection of DAMGO into the cMRR predominantly decreased the number of sighs, while microinjection into the rostral and middle MRR had no or limited effects. Microinjecting CTAP into the cMRR significantly diminished the systemic DAMGO-induced reduction of the number of sighs in response to hypoxia, but not to hypercapnia. Thus we conclude that hypoxia and hypercapnia elevate the number of sighs in a concentration-dependent manner in anesthetized rats, and this response is significantly depressed by activating systemic μ-receptors, especially those within the cMRR.
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Samuels, B. C., D. V. Zaretsky, and J. A. DiMicco. "Dorsomedial hypothalamic sites where disinhibition evokes tachycardia correlate with location of raphe-projecting neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 2 (August 2004): R472—R478. http://dx.doi.org/10.1152/ajpregu.00667.2003.
Full textAbstract:
Disinhibition of neurons in the region of the dorsomedial hypothalamus (DMH) elicits sympathetically mediated tachycardia in rats through activation of the brain stem raphe pallidus (RP), and this same mechanism appears to be largely responsible for the increases in heart rate (HR) seen in air jet stress in this species. Neurons projecting to the RP from the DMH are said to be concentrated in a specific subregion, the dorsal hypothalamic area (DA). Here, we examined the hypothesis that the location of RP-projecting neurons in the DA correspond to the sites at which microinjection of bicuculline methiodide (BMI) evokes the greatest increases in HR. To determine the distribution of RP-projecting neurons in the DA, cholera toxin B was injected in the RP in four rats. A consistent pattern of retrograde labeling was seen in every rat. In the hypothalamus, RP-projecting neurons were most heavily concentrated midway between the mammillothalamic tract and the dorsal tip of the third ventricle dorsal to the dorsomedial hypothalamic nucleus ∼3.30 mm caudal to bregma. In a second series of experiments, the HR response to microinjections of BMI (2 pmol/5 nl; n = 76) was mapped at sites in the DA and surrounding areas in 22 urethane-anesthetized rats. All injection sites were located from 2.56 to 4.16 mm posterior to bregma, and the microinjections that evoked the largest increase in HR (i.e., >100 beats/min in some instances) were located in a region where RP-projecting neurons were most densely concentrated. Thus RP-projecting neurons in the DA may mediate DMH-induced tachycardia and thus play a role in stress-induced cardiac stimulation.
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Zhang, Zhenxiong, Fadi Xu, Cancan Zhang, and Xiaomin Liang. "Activation of Opioid μ Receptors in Caudal Medullary Raphe Region Inhibits the Ventilatory Response to Hypercapnia in Anesthetized Rats." Anesthesiology 107, no. 2 (August 1, 2007): 288–97. http://dx.doi.org/10.1097/01.anes.0000270760.46821.67.
Full textAbstract:
Background : Opioids, extensively used as analgesics, markedly depress ventilation, particularly the ventilatory responsiveness to hypercapnia in humans and animals predominantly via acting on mu receptors. The medullary raphe region (MRR) contains abundant mu receptors responsible for analgesia and is also an important central area involving carbon dioxide chemoreception and contributing to the ventilatory responsiveness to hypercapnia. Therefore, the authors asked whether activation of mu receptors in the caudal, medial, or rostral MRR depressed ventilation and the response to hypercapnia, respectively. Methods : Experiments were conducted in 32 anesthetized and spontaneously breathing rats. Ventilation and it response to progressive hypercapnia were recorded. The slopes obtained from plotting minute ventilation, respiratory frequency, and tidal volume against the corresponding levels of end-tidal pressure of carbon dioxide were used as the indices of the respiratory responsiveness to carbon dioxide. DAMGO ([d-Ala2, N-Me-Phe4, Gly-ol]-enkephalin), a mu-receptor agonist, was systemically administered (100 mug/kg) before and/or after local injection of CTAP (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2) (100 ng/100 nl), a mu-receptor antagonist, into the caudal MRR, or locally administered (35 ng/100 nl) into the MRR subnuclei. Results : The authors found that systemic DAMGO significantly inhibited ventilation and the response to carbon dioxide by 20% and 31%, respectively, and these responses were significantly diminished to 11% and 14% after pretreatment of the caudal MRR with CTAP. Local administration of DAMGO into the caudal MRR also reduced ventilation and the response to carbon dioxide by 22% and 28%, respectively. In sharp contrast, these responses were not observed when the DAMGO microinjection was made in the middle MRR or rostral MRR. Conclusions : These results lead to the conclusion that mu receptors in the caudal MRR rather than the middle MRR or rostral MRR are important but not exclusive for attenuating the hypercapnic ventilatory response.
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Vissing, John, Martin Andersen, and Nils H. Diemer. "Exercise-Induced Changes in Local Cerebral Glucose Utilization in the Rat." Journal of Cerebral Blood Flow & Metabolism 16, no. 4 (July 1996): 729–36. http://dx.doi.org/10.1097/00004647-199607000-00025.
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In exercise, little is known about local cerebral glucose utilization (LCGU), which is an index of functional neurogenic activity. We measured LCGU in resting and running (≈85% of maximum O2 uptake) rats (n = 7 in both groups) previously equipped with a tail artery catheter. LCGU was measured quantitatively from 2-deoxy-D-[1-14C]glucose autoradiographs. During exercise, total cerebral glucose utilization (TCGU) increased by 38% (p < 0.005). LCGU increased (p < 0.05) in areas involved in motor function (motor cortex 39%, cerebellum ≈110%, basal ganglia ≈30%, substantia nigra ≈37%, and in the following nuclei: subthalamic 47%, posterior hypothalamic 74%, red 61%, ambiguus 43%, pontine 61%), areas involved in sensory function (somatosensory 27%, auditory 32%, and visual cortex 42%, thalamus ≈75%, and in the following nuclei: Darkschewitsch 22%, cochlear 51%, vestibular 30%, superior olive 23%, cuneate 115%), areas involved in autonomic function (dorsal raphe nucleus 30%, and areas in the hypothalamus ≈35%, amygdala ≈35%, and hippocampus 29%), and in white matter of the corpus callosum (36%) and cerebellum (52%). LCGU did not change with exercise in prefrontal and frontal cortex, cingulum, inferior olive, nucleus of solitary tract and median raphe, lateral septal and interpenduncular nuclei, or in areas of the hippocampus, amygdala, and hypothalamus. Glucose utilization did not decrease during exercise in any of the studied cerebral regions. In summary, heavy dynamic exercise increases TCGU and evokes marked differential changes in LCGU. The findings provide clues to the cerebral areas that participate in the large motor, sensory, and autonomic adaptation occurring in exercise.
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Ootsuka, Youichirou, William W. Blessing, Alexandre A. Steiner, and Andrej A. Romanovsky. "Fever response to intravenous prostaglandin E2 is mediated by the brain but does not require afferent vagal signaling." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 4 (April 2008): R1294—R1303. http://dx.doi.org/10.1152/ajpregu.00709.2007.
Full textAbstract:
PGE2 produced in the periphery triggers the early phase of the febrile response to infection and may contribute to later phases. It can be hypothesized that peripherally synthesized PGE2 transmits febrigenic signals to the brain via vagal afferent nerves. Before testing this hypothesis, we investigated whether the febrigenic effect of intravenously administered PGE2 is mediated by the brain and is not the result of a direct action of PGE2 on thermoeffectors. In anesthetized rats, intravenously injected PGE2 (100 μg/kg) caused an increase in sympathetic discharge to interscapular brown adipose tissue (iBAT), as well as increases in iBAT thermogenesis, end-expired CO2, and colonic temperature (Tc). All these effects were prevented by inhibition of neuronal function in the raphe region of the medulla oblongata using an intra-raphe microinjection of muscimol. We then asked whether the brain-mediated PGE2 fever requires vagal signaling and answered this question by conducting two independent studies in rats. In a study in anesthetized rats, acute bilateral cervical vagotomy did not affect the effects of intravenously injected PGE2 (100 μg/kg) on iBAT sympathetic discharge and Tc. In a study in conscious rats, administration of PGE2 (280 μg/kg) via an indwelling jugular catheter caused tail skin vasoconstriction, tended to increase oxygen consumption, and increased Tc; none of these responses was affected by total truncal subdiaphragmatic vagotomy performed 2 wk before the experiment. We conclude that the febrile response to circulating PGE2 is mediated by the brain, but that it does not require vagal afferent signaling.
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Kung, Ling-Hsuan, and Karie E. Scrogin. "Serotonin nerve terminals in the dorsomedial medulla facilitate sympathetic and ventilatory responses to hemorrhage and peripheral chemoreflex activation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1367—R1379. http://dx.doi.org/10.1152/ajpregu.00576.2010.
Full textAbstract:
Serotonin neurons of the caudal raphe facilitate ventilatory and sympathetic responses that develop following blood loss in conscious rats. Here, we tested whether serotonin projections to the caudal portion of the dorsomedial brain stem (including regions of the nucleus tractus solitarius that receive cardiovascular and chemosensory afferents) contribute to cardiorespiratory compensation following hemorrhage. Injections of the serotonin neurotoxin 5,7-dihydroxytryptamine produced >90% depletion of serotonin nerve terminals in the region of injection. Withdrawal of ∼21% of blood volume over 10 min produced a characteristic three-phase response that included 1) a normotensive compensatory phase, 2) rapid sympathetic withdrawal and hypotension, and 3) rapid blood pressure recovery accompanied by slower recovery of heart rate and sympathetic activity. A gradual tachypnea developed throughout hemorrhage, which quickly reversed with the advent of sympathetic withdrawal. Subsequently, breathing frequency and neural minute volume (determined by diaphragmatic electromyography) declined below baseline following termination of hemorrhage but gradually recovered over time. Lesioned rats showed attenuated sympathetic and ventilatory responses during early compensation and later recovery from hemorrhage. Both ventilatory and sympathetic responses to chemoreceptor activation with potassium cyanide injection were attenuated by the lesion. In contrast, the gain of sympathetic and heart rate baroreflex responses was greater, and low-frequency oscillations in blood pressure were reduced after lesion. Together, the data are consistent with the view that serotonin innervation of the caudal dorsomedial brain stem contributes to sympathetic compensation during hypovolemia, possibly through facilitation of peripheral chemoreflex responses.
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Riley, D., M. Dwinell, B. Qian, K. L. Krause, J. M. Bonis, S. Neumueller, B. D. Marshall, M. R. Hodges, and H. V. Forster. "Differences between three inbred rat strains in number of K+ channel-immunoreactive neurons in the medullary raphé nucleus." Journal of Applied Physiology 108, no. 4 (April 2010): 1003–10. http://dx.doi.org/10.1152/japplphysiol.00625.2009.
Full textAbstract:
Ventilatory sensitivity to hypercapnia is greater in Dahl salt-sensitive (SS) rats than in Fawn Hooded hypertensive (FHH) and Brown Norway (BN) inbred rats. Since pH-sensitive potassium ion (K+) channels are postulated to contribute to the sensing and signaling of changes in CO2-H+ in chemosensitive neurons, we tested the hypothesis that there are more pH-sensitive K+ channel-immunoreactive (ir) neurons within the medullary raphé nuclei of the highly chemosensitive SS rats than in the other two strains. Medullary tissues from male and female BN, FHH, and SS rats were stained with cresyl violet or with antibodies targeting TASK-1, Kv1.4, and Kir2.3 channels. K+ channel-ir neurons were quantified and compared with the total neurons in the region. The total number of neurons in the medullary raphé 1) was greater in male FHH than the other male rats, 2) did not differ among the female rats, and 3) did not differ between sexes. The average number of K+ channel-ir neurons per section was 30–60 neurons higher in the male SS than in the other rat strains. In contrast, for the females, the number of K+ channel-ir neurons was greatest in the BN. We also found significant differences in the number of K+ channel-ir neurons between sexes in SS (males > females) and BN (females > males) rats, but not the FHH strain. Our findings support the hypothesis for males but not for females, suggesting that both genetic background and sex are determinants of K+ channel immunoreactivity of medullary raphé neurons, and that the expression of pH-sensitive K+ channels in the medullary raphé does not correlate with the ventilatory sensitivity to hypercapnia.
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Kumar Ghosh, Saroj, and Padmanabha Chakrabarti. "Histological organization and microarchitecture of various cells lining the olfactory epithelium of Rita rita (Hamilton, 1822) (Siluriformes: Bagridae)." Biological Letters 49, no. 2 (December 1, 2012): 89–96. http://dx.doi.org/10.2478/v10120-012-0005-4.
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Abstract Rita rita is a carnivorous, bottom dwelling catfish inhabits in muddy dirty water and depends on olfactory sensation for procurement of food. The structural organization and function ofvarious cells lining its olfactory epithelium have been investigated by light and scanning electron microscopy. The elongated olfactory organ consists of 64-68 primary lamellae arising from a narrow median raphe. Sensory as well as non-sensory regions are distinctly oriented on each olfactory lamella. The sensory epithelium occupies the apical tongue-shaped area and basal part of the olfactory lamellae, whereas the middle part is covered with non-sensory epithelium. The sensory epithelium is composed of 2 types of dendrites of receptor cells (either ciliated or microvillous), labyrinth cells, and a large number of flagellated supporting cells. The non-sensory epithelium is made up of stratified epithelial cells having a different pattern of microridges and mucous cells. Variations in the cellular orientation of the various cells on the olfactory epithelium have been correlated with the functional views of the fish concerned.
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Nalivaiko, Eugene, Youichirou Ootsuka, and William W. Blessing. "Activation of 5-HT1A receptors in the medullary raphe reduces cardiovascular changes elicited by acute psychological and inflammatory stresses in rabbits." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R596—R604. http://dx.doi.org/10.1152/ajpregu.00845.2004.
Full textAbstract:
The present strategy for the prevention of excessive sympathetic neural traffic to the heart relies on the use of beta-blockers, drugs that act at the heart end of the brain-heart axis. In the present study, we attempted to suppress cardiac sympathetic nerve activity by affecting the relevant cardiomotoneurons in the brain using the selective serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT). In conscious, unrestrained rabbits, instrumented for recordings of heart rate, arterial pressure, or cardiac output, we provoked increases in cardiac sympathetic activity by psychological (loud sound, pinprick, and air jet) or inflammatory (0.5 μg/kg iv lipopolysaccharide) stresses. Pinprick and air-jet stresses elicited transient increases in heart rate (+50 ± 7 and +38 ± 4 beats/min, respectively) and in mean arterial pressure (+16 ± 2 and +15 ± 3 mmHg, respectively). Lipopolysaccharide injection caused sustained increases in heart rate (from 210 ± 3 to 268 ± 10 beats/min) and in arterial pressure (from 74 ± 3 to 92 ± 4 mmHg). Systemically administered 8-OH-DPAT (0.004–0.1 mg/kg) substantially attenuated these responses in a dose-dependent manner. Drug effects were prevented by a selective 5-HT1A receptor antagonist, WAY-100635 (0.1 mg/kg iv). Similarly to systemic administration, microinjection of 8-OH-DPAT (500 nl of 10 mM solution) into the medullary raphe-parapyramidal region caused antitachycardic effects during stressful stimulation and during lipopolysaccharide-elicited tachycardia. This is the first demonstration that activation of 5-HT1A receptors in the medullary raphe-parapyramidal area causes suppression of neurally mediated cardiovascular changes during acute psychological and immune stresses.
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Steele, G. E., and R. E. Weller. "Subcortical connections of subdivisions of inferior temporal cortex in squirrel monkeys." Visual Neuroscience 10, no. 3 (May 1993): 563–83. http://dx.doi.org/10.1017/s0952523800004776.
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AbstractOn the basis of cortical connections and architectonics, inferior temporal (IT) cortex of squirrel monkeys consists of a caudal, prestriate-recipient region, ITC; a rostral region, ITR; and possibly an intermediate region along the border of ITC and ITR, ITI (Weller & Steele, 1992). ITC contains dorsal (ITCd) and ventral (ITCv) areas. The subcortical connections of these subdivisions of IT cortex were determined in the present study from the results of cortical injections of wheat-germ agglutinin conjugated to horseradish peroxidase, [3H]-amino acids and fast blue. ITC and ITR receive afferents from the locus coeruleus, dorsal raphe, nucleus annularis, central superior nucleus, pontine reticular formation, lateral hypothalamus, paracentral nucleus, and central medial nucleus; send efferents to the superior colliculus, reticular nucleus, and striatum; and have both afferent and efferent connections with the pretectum, pulvinar, claustrum, amygdala, and basal nucleus of Meynert. ITC and ITR have different patterns of connections with a number of subcortical structures, including the pulvinar and amygdala. Injections in ITC strongly label multiple nuclei of the inferior pulvinar and the medial division of the lateral pulvinar (PLM), and moderately label the medial pulvinar (PM), whereas injections in ITR strongly label PM and moderately label PLM. Injections in ITC label sparse projections to the lateral nucleus of the amygdala, in contrast to injections in ITR that label strong projections to the lateral and basal nuclei of the amygdala. Injections in “IT” produce a pattern of subcortical label that has some features of that observed from injections in ITC and that observed from injections in ITR. Although most of the connections of ITCd and ITCv appear similar, only injections involving ITCd label the middle nucleus of the inferior pulvinar (PIM).Comparison of the subcortical connections of subdivisions of IT cortex in squirrel monkeys and what is presently known of the subcortical connections of subdivisions of IT cortex in macaque monkeys supports the previous suggestion that ITC of squirrel monkeys may be comparable to area TEO of macaques, IT, may be comparable to posterior area TE, and ITR may be comparable to anterior area TE (Weller & Steele, 1992).
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Ghosh, Saroj Kumar, and Padmanabha Chakrabarti. "Histomorphological and microanatomical characteristics of the olfactory organ of freshwater carp, Cirrhinus reba (Hamilton)." Archives of Polish Fisheries 24, no. 4 (December 1, 2016): 201–8. http://dx.doi.org/10.1515/aopf-2016-0017.
Full textAbstract:
Abstract The morphoanatomy, cellular organization, and surface architecture of the olfactory apparatus in Cirrhinus reba (Hamilton) is described using light and scanning electron microscopy. The oval shaped olfactory rosette contained 32 ± 2 primary lamellae on each side of the median raphe, and was lodged on the floor of the olfactory chamber. The olfactory lamellae were basically flat and compactly arranged in the rosette. The olfactory chamber communicated to the outside aquatic environment through inlet and outlet apertures with a conspicuous nasal flap in between. The mid dorsal portion of the olfactory lamellae was characterized by a linguiform process. Sensory and non-sensory regions were distributed separately on each lamella. The sensory epithelium occupied the apical part including the linguiform process, whereas the resting part of the lamella was covered with non-sensory epithelium. The sensory epithelium comprised both ciliated and microvillous receptor cells distinguished by the architecture on their apical part. The non-sensory epithelium possessed mucous cells, labyrinth cells, and stratified epithelial cells with distinctive microridges. The functional importance of the different cells lining the olfactory mucosa was correlated with the ecological habits of the fish examined.