Behavioral and neuronal reorganization after unilateral substantia nigra lesions: Evidence for increased interhemispheric nigrostriatal projections
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N-acetylcysteine decreases dopamine transporter availability in the non-lesioned striatum of the 6-OHDA hemiparkinsonian rat
2022, Neuroscience LettersCitation Excerpt :Another possible mechanism by which NAC could potentially modulate DAT activity and dopamine transport, is by direct interaction with sensitive cysteine residues in the transporter [15], as NAC possesses disulphide breaking activity [25]. We reject the possibility of a higher degree of degeneration after NAC treatment in the interhemispheric connections [4,5] as this reduction appears to be transitional, and at 4 weeks the BPND values are almost normalized again. When striatal levels of TH at 4 weeks post-lesion were analyzed by immunohistochemistry, we could demonstrate the loss of dopaminergic nerve fibers in the injected striatum, confirming the dopamine denervation induced by 6-OHDA.
The cross-hemispheric nigrostriatal pathway prevents the expression of levodopa-induced dyskinesias
2021, Neurobiology of DiseaseCitation Excerpt :Similarly, ~80% of A9 dopaminergic neurons in one hemisphere are affected by stimulation of the contralateral SN (Castellano and Rodriguez Diaz, 1991). Further, the unilateral lesioning of the nigrostriatal pathway is shown to induce compensatory increases in; the interhemispheric nigrostriatal neurons (Pritzel et al., 1983a), the contralateral SN dopaminergic cell counts (Zhao et al., 2003), contralateral striatal TH expression (Schlachetzki et al., 2014), DA release (Nieoullon et al., 1977; Zhang et al., 1988), DA turnover (Garris et al., 1997; Rodriguez et al., 1990) and the firing rates of the contralateral SN (Breit et al., 2008). Rats with bilateral intra-striatal dopaminergic lesioning show more behavioral deficits compared to those with a unilateral lesion.
Cortical slow wave activity correlates with striatal synaptic strength in normal but not in Parkinsonian rats
2018, Experimental NeurologyCompensatory mechanisms in Parkinson's disease: Circuits adaptations and role in disease modification
2017, Experimental NeurologyCitation Excerpt :Although an old issue, the role of inter-hemispheric mechanism's in compensation and indeed in the general scheme of PD pathophysiology has not been addressed formally. There are many studies suggesting there can be inter-hemispheric compensatory processes trying to restore dopaminergic balance in the striatum, for example controlling the ratio of DA receptors or changing the number of synaptic terminals (Altar et al., 1983; Blesa et al., 2011; Frohna et al., 1997; Giardino, 1996; Golden et al., 2013; Jaeger et al., 1983; Joyce, 1991a, 1991b; Lawler et al., 1995; Mejias et al., 2016; Pritzel et al., 1983; Rodriguez et al., 1994; Roedter et al., 2001; Vernaleken et al., 2007). We believe that this should be considered and mentioned, even if in a rather limited manner here, because it is highly likely that inter-hemispheric compensation at the level of cortico-BG activity does take place in early PD.
GABA<inf>A</inf>-receptor activation in the subthalamic nucleus compensates behavioral asymmetries in the hemiparkinsonian rat
2013, Behavioural Brain ResearchCitation Excerpt :Also, these authors did not report on an ipsiversive motor-bias associated with the 6-OHDA lesion, indicative of a less severe lesion, as compared to ours. Furthermore, we applied 6-OHDA into the MFB, whereas Mehta et al. [34] injected it directly into the substantia nigra, a protocol known to spare interhemispheric nigro-striatal projections (unlike lesions in the MFB), which are known to account for compensatory processes in the dopamine denervated striatum [50,51]. Such differences related to the lesion procedure may also account for the contradictory results observed and display a valuable new finding in the context of 6-OHDA models of PD.
The interhemispheric connections of the striatum: Implications for Parkinson's disease and drug-induced dyskinesias
2012, Brain Research BulletinCitation Excerpt :To our knowledge, we are unaware of any studies that have examined the relative density of intrahemispheric and interhemispheric corticostriatal connections in response to dopamine denervation in animal models of PD. It has been suggested that lesions to the nigrostriatal dopaminergic pathway can induce a short-term compensatory increase of interhemispheric nigrostriatal neurons [50]. In this study using kainic acid or 6-OHDA before unilateral labeling with HRP in rats, an increase in interhemispheric nigrostriatal neurons at 7 and 21 days was found when compared to controls.