Abstract:Adolescence is associated with continued maturation of the cerebral cortex, particularly the medial prefrontal cortex (mPFC). We have previously documented pruning in the number of neurons, dendrites and synapses in the rat mPFC from preadolescence to adulthood, with the period of pubertal onset being particularly important. We hypothesized that dopaminergic innervation of this region, critical for executive functions, would also be influenced by pubertal onset. Here, we measured changes in the volume of tyros… Show more
“…Histological studies have also shown striking late growth of dopaminergic terminals into the primate and rodent PFC extending from the juvenile period well into the young adult period (Kalsbeek et al 1988;Benes et al 2000;Naneix et al 2012;Willing et al 2017;Hoops et al 2018). In mice, dopaminergic boutons in the PFC show greater activity-dependent plasticity in mid adolescence compared to adulthood (Mastwal et al 2014).…”
Section: Axonal Boutons In the Pfc Across Adolescent Development: Patmentioning
The maturation of the prefrontal cortex (PFC) during adolescence is thought to be important for cognitive and affective development and mental health risk. Whereas many summaries of adolescent development have focused on dendritic spine pruning and gray matter thinning in the PFC during adolescence, we highlight recent rodent data from our laboratory and others to call attention to continued synapse formation and plasticity in the adolescent period in specific cell types and circuits. In particular, we highlight changes in inhibitory neurotransmission onto intratelencephalic (IT-type) projecting cortical neurons and late expansion of connectivity between the amygdala and PFC and the ventral tegmental area and PFC. Continued work on these "late blooming" synapses in specific cell types and circuits, and their interrelationships, will illuminate new opportunities for understanding and shaping the biology of adolescent development. We also address which aspects of adolescent PFC development are dependent on pubertal processes.
“…Histological studies have also shown striking late growth of dopaminergic terminals into the primate and rodent PFC extending from the juvenile period well into the young adult period (Kalsbeek et al 1988;Benes et al 2000;Naneix et al 2012;Willing et al 2017;Hoops et al 2018). In mice, dopaminergic boutons in the PFC show greater activity-dependent plasticity in mid adolescence compared to adulthood (Mastwal et al 2014).…”
Section: Axonal Boutons In the Pfc Across Adolescent Development: Patmentioning
The maturation of the prefrontal cortex (PFC) during adolescence is thought to be important for cognitive and affective development and mental health risk. Whereas many summaries of adolescent development have focused on dendritic spine pruning and gray matter thinning in the PFC during adolescence, we highlight recent rodent data from our laboratory and others to call attention to continued synapse formation and plasticity in the adolescent period in specific cell types and circuits. In particular, we highlight changes in inhibitory neurotransmission onto intratelencephalic (IT-type) projecting cortical neurons and late expansion of connectivity between the amygdala and PFC and the ventral tegmental area and PFC. Continued work on these "late blooming" synapses in specific cell types and circuits, and their interrelationships, will illuminate new opportunities for understanding and shaping the biology of adolescent development. We also address which aspects of adolescent PFC development are dependent on pubertal processes.
“…The total DBH fibers length in each lamina of spinal dorsal horn were also calculated using a semi quantitative skeleton analysis adapted from Willing et al (2017). Briefly, after an adjustment of the threshold level as abovementioned, the images were converted to binary images, skeletonized using the skeleton macro from ImageJ and evaluated in terms of number of pixels occupied by skeletons.…”
Chemotherapy-induced peripheral neuropathy (CIPN) is a problem during cancer treatment and for cancer survivors but the central mechanisms underlying CIPN remain understudied. This study aims to determine if CIPN is associated with alterations of noradrenergic modulation of nociceptive transmission at the spinal cord. CIPN was induced in male Wistar rats by paclitaxel injections. One month after CIPN induction, the behavioral effects of the administration of reboxetine (noradrenaline reuptake inhibitor), clonidine (agonist of α 2 -adrenoreceptors; α 2− AR) and atipamezole (antagonist of α 2− AR) were evaluated using the von Frey and cold plate tests. Furthermore, we measured the expression of the noradrenaline biosynthetic enzyme dopamineβ-hydroxylase (DBH) and of α 2− AR in the spinal dorsal horn. Reboxetine and clonidine reversed the behavioral signs of CIPN whereas the opposite occurred with atipamezole. In the 3 pharmacological approaches, a higher effect was detected in mechanical allodynia, the pain modality which is under descending noradrenergic control. DBH expression was increased at the spinal dorsal horn of paclitaxel-injected animals. The enhanced noradrenergic inhibition during CIPN may represent an adaptation of the descending noradrenergic pain control system to the increased arrival of peripheral nociceptive input. A potentiation of the α 2− AR mediated antinociception at the spinal cord may represent a therapeutic opportunity to face CIPN.
“…7 The total volume of the tyrosine hydroxylase containing axons in the rat mPFC in males (a) and female (b). *p < .05 ( Willing et al, 2017 ). …”
Section: Changes Not Detectable With Mrimentioning
confidence: 97%
“…We quantified the growth of axons carrying tyrosine hydroxylase (the rate limiting step for dopamine synthesis) across adolescence with regard to both sexes and puberty. A definitive role for puberty was not apparent ( Willing et al, 2017 ) ( Fig. 7 ).…”
Section: Changes Not Detectable With Mrimentioning
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