scholarly journals Serotonergic development of active sensing

2019 ◽  
Author(s):  
Alireza Azarfar ◽  
Yiping Zhang ◽  
Artoghrul Alishbayli ◽  
Dirk Schubert ◽  
Judith R. Homberg ◽  
...  
Keyword(s):  
Motor Control ◽  
Postnatal Development ◽  
Network Formation ◽  
Sensory Information ◽  
Network Connectivity ◽  
Object Localization ◽  
Active Sensing ◽  
Early Postnatal Development ◽  
Sensorimotor Network ◽  
Intracortical Circuits

AbstractActive sensing requires adaptive motor (positional) control of sensory organs based on contextual, sensory and task requirements, and develops postnatally after the maturation of intracortical circuits. Alterations in sensorimotor network connectivity during this period are likely to impact sensorimotor computation also in adulthood. Serotonin is among the cardinal developmental regulators of network formation, thus changing the serotonergic drive might have consequences for the emergence and maturation of sensorimotor control. Here we tested this hypothesis on an object localization task by quantifying the motor control dynamics of whiskers during tactile navigation. The results showed that sustained alterations in serotonergic signaling in serotonin transporter knockout rats, or the transient pharmacological inactivation of the transporter during early postnatal development, impairs the emergence of adaptive motor control of whisker position based on recent sensory information. A direct outcome of this altered motor control is that the mechanical force transmitted to whisker follicles upon contact is reduced, suggesting that increased excitability observed upon altered serotonergic signaling is not due to increased synaptic drive originating from the periphery upon whisker contact. These results argue that postnatal development of adaptive motor control requires intact serotonergic signaling and that even its transient dysregulation during early postnatal development causes lasting sensorimotor impairments in adulthood.

scholarly journals Development of adaptive motor control for tactile navigation

2019 ◽  
Author(s):  
Alireza Azarfar ◽  
Tansu Celikel
Keyword(s):  
Motor Control ◽  
Closed Loop ◽  
Sensory Information ◽  
Sensorimotor Control ◽  
Object Localization ◽  
Closed Loop Control ◽  
Active Sensing ◽  
Stationary Target ◽  
Loop Control ◽  
Tactile Navigation

Navigation is a result of complex sensorimotor computation which requires integration of sensory information in allocentric and egocentric coordinates as the brain computes a motor plan to drive navigation. In this active sensing process, motor commands are adaptively regulated based on prior sensory information. In the darkness, rodents commonly rely on their tactile senses, in particular to their whiskers, to gather the necessary sensory information and instruct navigation. Previous research has shown that rodents can process whisker input to guide mobility even prior to whisking onset by the end of the second postnatal week, however, when and how adaptive sensorimotor control of whisker position matures is still not known. Here, we addressed this question in rats longitudinally as animals searched for a stationary target in darkness. The results showed that juvenile rats perform object localization by controlling their body, but not whisker position, based on the expected location of the target. Adaptive, closed-loop, control of whisker position matures only after the third postnatal week. Computational modeling of the active whisking showed the emergence of the closed-loop control of whisker position and reactive retraction, i.e. whisker retraction that ensures the constancy of duration of tactile sampling, facilitate the maturation of sensorimotor exploration strategies during active sensing. These results argue that adaptive motor control of body and whiskers develop sequentially, and sensorimotor control of whisker position emerges later in postnatal development upon the maturation of intracortical sensorimotor circuits.

scholarly journals Sensory over-responsivity is related to GABAergic inhibition in thalamocortical circuits

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emily T. Wood ◽  
Kaitlin K. Cummings ◽  
Jiwon Jung ◽  
Genevieve Patterson ◽  
Nana Okada ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Sensory Information ◽  
Network Connectivity ◽  
Sensory Stimulation ◽  
Autism Spectrum ◽  
Future Research ◽  
Resonance Spectroscopy ◽  
Gamma Aminobutyric Acid ◽  
Sensory Stimuli ◽  
Brain Responses

AbstractSensory over-responsivity (SOR), extreme sensitivity to or avoidance of sensory stimuli (e.g., scratchy fabrics, loud sounds), is a highly prevalent and impairing feature of neurodevelopmental disorders such as autism spectrum disorders (ASD), anxiety, and ADHD. Previous studies have found overactive brain responses and reduced modulation of thalamocortical connectivity in response to mildly aversive sensory stimulation in ASD. These findings suggest altered thalamic sensory gating which could be associated with an excitatory/inhibitory neurochemical imbalance, but such thalamic neurochemistry has never been examined in relation to SOR. Here we utilized magnetic resonance spectroscopy and resting-state functional magnetic resonance imaging to examine the relationship between thalamic and somatosensory cortex inhibitory (gamma-aminobutyric acid, GABA) and excitatory (glutamate) neurochemicals with the intrinsic functional connectivity of those regions in 35 ASD and 35 typically developing pediatric subjects. Although there were no diagnostic group differences in neurochemical concentrations in either region, within the ASD group, SOR severity correlated negatively with thalamic GABA (r = −0.48, p < 0.05) and positively with somatosensory glutamate (r = 0.68, p < 0.01). Further, in the ASD group, thalamic GABA concentration predicted altered connectivity with regions previously implicated in SOR. These variations in GABA and associated network connectivity in the ASD group highlight the potential role of GABA as a mechanism underlying individual differences in SOR, a major source of phenotypic heterogeneity in ASD. In ASD, abnormalities of the thalamic neurochemical balance could interfere with the thalamic role in integrating, relaying, and inhibiting attention to sensory information. These results have implications for future research and GABA-modulating pharmacologic interventions.

scholarly journals Impact of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behaviors and BDNF mRNA expression in the adult Sprague–Dawley rats exposed to glutathione deficit during early postnatal development of the brain

2021 ◽  
Author(s):  
Marta A. Lech ◽  
Kinga Kamińska ◽  
Monika Leśkiewicz ◽  
Elżbieta Lorenc-Koci ◽  
Zofia Rogóż
Keyword(s):  
Mrna Expression ◽  
Postnatal Development ◽  
Repeated Treatment ◽  
Sprague Dawley ◽  
Biochemical Tests ◽  
Bdnf Mrna ◽  
Adult Rats ◽  
Behavioral Deficits ◽  
Glutathione Synthesis ◽  
Early Postnatal Development

Abstract Background Preclinical and clinical studies have indicated that impaired endogenous synthesis of glutathione during early postnatal development plays a significant role in the pathophysiology of schizophrenia. Moreover, some studies have suggested that antidepressants are able to increase the activity of atypical antipsychotics which may efficiently improve the treatment of negative and cognitive symptoms of schizophrenia. Methods In the present study, we investigated the influence of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behavior and BDNF mRNA expression in adult rats exposed to glutathione deficit during early postnatal development. Male pups between the postnatal days p5–p16 were treated with the inhibitor of glutathione synthesis, BSO (L-buthionine-(S,R)-sulfoximine) and the dopamine uptake inhibitor, GBR 12,909 alone or in combination. Escitalopram and aripiprazole were given repeatedly for 21 days before the tests. On p90–92 rats were evaluated in the behavioral and biochemical tests. Results BSO given alone and together with GBR 12,909 induced deficits in the studied behavioral tests and decreased the expression of BDNF mRNA. Repeated aripiprazole administration at a higher dose reversed these behavioral deficits. Co-treatment with aripiprazole and an ineffective dose of escitalopram also abolished the behavioral deficits in the studied tests. Conclusion The obtained data indicated that the inhibition of glutathione synthesis in early postnatal development induced long-term deficits corresponding to schizophrenia-like behavior and decreased the BDNF mRNA expression in adult rats, and these behavioral deficits were reversed by repeated treatment with a higher dose of aripiprazole and also by co-treatment with aripiprazole and ineffective dose of escitalopram.

scholarly journals Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6171
Author(s):  
Marta Anna Lech ◽  
Monika Leśkiewicz ◽  
Kinga Kamińska ◽  
Zofia Rogóż ◽  
Elżbieta Lorenc-Koci
Keyword(s):  
Postnatal Development ◽  
Time Course ◽  
Postnatal Life ◽  
Positive Symptoms ◽  
Gbr 12909 ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Synthesis Inhibitor ◽  
Early Postnatal Development ◽  
Middle Adolescence

Growing body of evidence points to dysregulation of redox status in the brain as an important factor in the pathogenesis of schizophrenia. The aim of our study was to evaluate the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and 1-[2-Bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR 12909), a dopamine reuptake inhibitor, given alone or in combination, to Sprague–Dawley pups during early postnatal development (p5–p16), on the time course of the onset of schizophrenia-like behaviors, and on the expression of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the prefrontal cortex (PFC) and hippocampus (HIP) during adulthood. BSO administered alone decreased the levels of BDNF mRNA and its protein both in the PFC and HIP. Treatment with the combination of BSO + GBR 12909 also decreased BDNF mRNA and its protein in the PFC, but in the HIP, only the level of BDNF protein was decreased. Schizophrenia-like behaviors in rats were assessed at three time points of adolescence (p30, p42–p44, p60–p62) and in early adulthood (p90–p92) using the social interaction test, novel object recognition test, and open field test. Social and cognitive deficits first appeared in the middle adolescence stage and continued to occur into adulthood, both in rats treated with BSO alone or with the BSO + GBR 12909 combination. Behavior corresponding to positive symptoms in humans occurred in the middle adolescence period, only in rats treated with BSO + GBR 12909. Only in the latter group, amphetamine exacerbated the existing positive symptoms in adulthood. Our data show that rats receiving the BSO + GBR 12909 combination in the early postnatal life reproduced virtually all symptoms observed in patients with schizophrenia and, therefore, can be considered a valuable neurodevelopmental model of this disease.

Early postnatal development of the mandibular permanent first molar in infants with isolated cleft palate

2011 ◽  
Vol 22 (4) ◽  
pp. 280-285 ◽  
Author(s):  
NUNO V. HERMANN ◽  
MOSTAFA ZARGHAM ◽  
TRON A. DARVANN ◽  
IB J. CHRISTENSEN ◽  
SVEN KREIBORG
Keyword(s):  
Cleft Palate ◽  
Postnatal Development ◽  
Early Postnatal Development ◽  
Isolated Cleft Palate

EFFECTS OF COBALT SULFATE ON PRENATAL DEVELOPMENT OF MICE, RATS, AND RABBITS, AND ON EARLY POSTNATAL DEVELOPMENT OF RATS

2001 ◽  
Vol 62 (5) ◽  
pp. 367-386 ◽  
Author(s):  
Éva Szakmáry ◽  
György Ungváry ◽  
Aranka Hudák ◽  
Erzsébet Tátrai ◽  
Miklós Náray ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Prenatal Development ◽  
Cobalt Sulfate ◽  
Early Postnatal Development
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