Neuroscience
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The pre-Bötzinger complex (preBötC) of the ventrolateral medulla is the kernel for inspiratory rhythm generation. However, it is not fully understood how inspiratory neural activity is generated in the preBötC and propagates to other medullary regions. We analyzed the detailed anatomical connectivity to and from the preBötC and functional aspects of the inspiratory information propagation from the preBötC on the transverse plane of the medulla oblongata. ⋯ Intra-preBötC imaging with high spatiotemporal resolution during a single spontaneous inspiratory cycle unveiled deterministic nonlinearities, i.e., chaos, in the population recruitment. Collectively, we comprehensively elucidated the anatomical pathways to and from the preBötC and dynamics of inspiratory neural information propagation: (1) From the preBötC in one side to the contralateral preBötC, which would synchronize the bilateral rhythmogenic kernels, (2) from the preBötC directly to the bilateral hypoglossal premotor and motor areas as well as to the nuclei tractus solitarius, and (3) from the hypoglossal premotor areas toward the hypoglossal motor nuclei. The coincidence of identified anatomical and functional connectivity between the preBötC and other regions in adult and neonatal rats, respectively, indicates that this fundamental connectivity is already well developed at the time of birth.
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Ketamine, a dissociative anesthetic most commonly used in many pediatric procedures, has been reported in many animal studies to cause widespread neuroapoptosis in the neonatal brain after exposure in high doses and/or for a prolonged period. This neurodegenerative change occurs most severely in the forebrain including the anterior cingulate cortex (ACC) that is an important brain structure for mediating a variety of cognitive functions. However, it is still unknown whether such apoptotic neurodegeneration early in life would subsequently impair the synaptic plasticity of the ACC later in life. ⋯ The LTP impairment was accompanied by an increase in the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated excitatory synaptic transmission and a decrease in GABA inhibitory synaptic transmission in neurons of the ACC. Thus, our present findings show that neonatal ketamine exposure causes a significant LTP impairment in the ACC. We suggest that the imbalanced synaptic transmission is likely to contribute to ketamine-induced LTP impairment in the ACC.
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We used FM imaging to identify neurons that receive sensory feedback from the body wall in a circuit for octopamine (OA)-evoked rhythmic locomotion in the earthworm, Eisenia fetida. We visualized synapses in which postsynaptic neurons receive the sensory feedback, by using FM1-43 dye to label the synapses of both motor and sensory pathways that are associated with locomotion, then clearing the motor pathway synapse labeling, and finally identifying the target synapses by distinguishing physiologically functional synapses through destaining using a high-K(+) solution. A pair of synaptic regions associated with the sensory feedback was found to be located two or three cell body-widths away from the midline, between the anterior parts of the roots of the second lateral nerves (LNs) at the segmental ganglia (SGs). ⋯ Current injection into an OPP caused firing in the ipsilateral first LNs, supporting the hypothesis that OPPs functionally project to the peripheral nerves. OPPs also sent neurites to the adjacent anterior and posterior SGs, suggesting connections with the adjacent segments. We conclude that FM imaging can be used to identify neurons involved in specific functions, and that OPPs are the first neurons to be associated with OA-induced locomotion in the earthworm.
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Abnormalities of mental status represent a severe complication and an important cause of death in acute pancreatitis (AP), which is characterized by a pattern of neurological signs and symptoms. As some of the symptoms of AP are also affected by catecholamine neurotransmitters, they cannot be ruled out of the pathophysiology of AP; however, little research has been performed exploring this hypothesis. Our study aimed to elucidate whether AP affects the metabolism of catecholamine neurotransmitters in rats. ⋯ The MAO-A and TH protein concentrations of the 6-h and 24-h groups also decreased. The other catecholamine concentration and enzyme activities fluctuated, but there was no statistically significant difference compared with the control group. Catecholamine neurotransmitter metabolic systems are widely affected in AP, and these fluctuations may play an important role in determining the symptomatology of AP.
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Depression is a common symptom in Parkinson's disease (PD), but its pathophysiology remains unclear. Several lines of studies have revealed that the prelimbic (PrL) sub-region of the ventral medial prefrontal cortex and 5-HT1A receptors are involved in the regulation of depression. In this study, we examined whether complete unilateral lesions of the medial forebrain bundle (MFB) using 6-hydroxydopamine in rats are able to induce depressive-like behaviors, the role of PrL 5-HT1A receptors in the regulation of these behaviors, and co-localization of 5-HT1A receptor and neuronal glutamate transporter EAAC1-immunoreactive (EAAC1-ir) neurons in the PrL. ⋯ Furthermore, the intra-PrL injection of 5HT1A receptor antagonist WAY-100635 (60, 120, and 240ng/rat) showed a decrease in sucrose consumption, and an increase in immobility time, indicating the induction of depressive-like responses. However, the effective doses in the lesioned rats were higher than those in sham-operated rats, which attribute to down-regulation of 5-HT1A receptor expression on EAAC1-ir neurons in the PrL of the lesioned rats. These findings suggest that unilateral lesions of the MFB in rats may induce depressive-like behaviors, and 5-HT1A receptors of the PrL play an important role in the regulation of these behaviors.