Yarreiphang (UGC Junior Research Fellow) presented a paper by M. Sonia Angeline et al.in the journal Neuroscience(2012) titled 'Rotenone-induced parkinsonism elicits behavioral impairments and differential expression of parkin, heat shock protein and caspases in the rats"
Abstract—Rotenone is a pesticide that inhibits mitochondrial complex I activity, thus creating an environment of oxidative stress in the cell. Many studies have employed rotenone to generate an experimental animal model of Parkinson’s disease (PD) that mimics and elicits PD-like symptoms, such as motor and cognitive decline. Cytoprotective proteins including parkin and heat shock proteins (HSPs) play major roles in slowing PD progression. Moreover, evidence suggests that mitochondrial dysfunction and oxidative stress-dependent apoptotic pathways contribute to dopaminergic neuron degeneration In PD. Here, rats were chronically exposed to rotenone to confirm that it causes a debilitating phenotype and various behavioral defects. We also performed histopathological examinations of nigrostriatal, cortical and cerebellar regions of rotenone-treated brain to elucidate a plausible neurodegenerative mechanism. The results of silver, tyrosine hydroxylase (TH), park in, ubiquitin and caspase staining of brain tissue sections further validated our findings. The stress response is known to trigger HSP In response to pharmacological insult. These protective proteins help maintain cellular homeostasis and may be capable of rescuing cells from death. Therefore, we assessed the levels of different HSPs in the rotenone-treated animals. Collectively, our studies indicated the following findings in the striatum and substantia nigra following chronic rotenone exposure in an experimental PD model: (i) behavioral deficit that correlated with histopathological changes and down regulation of TH signaling, (ii) decreased levels of the cytoprotective proteins parkin, DJI and Hsp7O and robust expression of mitochondrial chaperone Hsp6O according to Western blot, (iii) increased immunoreactivity for caspase 9, caspase 3 and ubiquitin and decreased parkin immunoreactivity.
The presentation was neat and drew in valuable discussion among the listeners. The paper tried to emphasize that rotenone-induced Parkinson's disease model in rats, brings out the role of molecular mechanisms like that of HSPs (Heat shock proteins), which could be a potential target for therapeutic interventions.
Some interesting thoughts were:
Anshu Kumari (2nd year PhD Scolar) presented her seminar titled "Plasticity in Amygdala and Anxiety".
She gave a clear introduction to Anxiety disorders in terms of a psychiatric disorder as well as its neurobiology. From human studies to molecular mechanisms, the evidences seemed to show that anxiety is associated with an over active Amygdala which possibly have a detrimental effect on the hippocampus mediated cognitive network.
Some of the interesting thoughts during the seminar were:
1) As anxiety prone individuals show increased Amygdala activity during presentation of happy as well as fearful images, Amygdala should not only be related to anxiety but stress response as a whole.
2) Do Amygdala on both sides act differently during anxiety.
3) Pre-exposure to mild stressors or exogenous cortisone could be benificial during a subsequent exposure.
4) Does BDNF get differentially elevated in different brain regions in response to stress?
Please share your comments
Merlin Flaura (1st year MPhil Scholar) presented a paper from the journal Behavioural Brain Research (2012) titled "Histamine Promotes rat motor performances by activation of H2 receptors in the cerebellar fastigial nucleus"
The cerebellar fastigial nucleus (FN), together with the interpositus nucleus (IN), constitutes the two ﬁnal output nuclei of the spinocerebellum and plays an important role in body and limb movements. Previous studies have revealed a direct histaminergic projection from the hypothalamus to the cerebellar nuclei and an excitatory effect of histamine on the IN neurons. However, role of hypothalamic histaminergic projection in the FN has been still little known. Here we show that histamine elicited the FN neurons of rats a concentration-dependent excitatory response in vitro. The histamine-induced excitation on FN neurons was mediated by postsynaptic histamine H2 rather than H1 receptors. In behavioral tests, microinjection of histamine into bilateral FNs remarkably improved motor performances of rats on both accelerating rota-rod and balance beam. Selective H2 receptor antagonist ranitidine considerably declined thosemotor performances and selective H2 receptor agonist dimaprit mimicked the facilitation effect of histamine on themovements. But selective H1 receptor antagonisttriprolidine and agonist 2-pyridylethylamine had no effect. Furthermore, microinjection of histamine into bilateral FNs narrowed stride width of footprint but did notinﬂuence wire suspension, whereas microinjection of histamine into bilateral INs increased stride length and promoted suspension. These results demonstrate that histamine enhances rat motor balance and coordination through modulation of both proximal and distal muscles by activation of histamine H2 receptors in the cerebellar FN and IN, and suggest that the hypothalamocerebellar histaminergic projections may modulate the ﬁnal outputs of the spinocerebellum and participate in the cerebellum mediated motor control.
The presentation was simple and clear.
Some interesting thoughts that arose from the presentation: