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Electrophysiology of brain motor circuits in animal models of Parkinson’s disease

Domenii publicaţii > Ştiinţe medicale + Tipuri publicaţii > Tezã de doctorat (nepublicatã)

Autori: Cristian Voicu

Editorial: University of Otago, PhD Thesis, 2007.


The difficulty with movement initiation, or akinesia, is a cardinal debilitating symptom of Parkinson’s disease (PD). It is hypothesised that Parkinsonian akinesia is caused by impaired neuronal function in different brain areas that operate as a behavioural arrest control system, inside and outside the basal ganglia (Klemm, 2001).

The activity of this system is modulated by different neurotransmitters and the pathology of PD has shown, for many years, a loss of dopaminergic cells that may affect the function of basal ganglia nuclei, the thalamus and the motor cortex. In contrast, the involvement of adenosine has only recently emerged from studies suggesting that a blockade of adenosine receptors in the brain may be beneficial in Parkinson’s disease (Bara-Jimenez et al., 2003; Kanda et al., 2000; Pinna et al., 2005; Tanganelli et al., 2004).

Moreover, it seems that specific subtypes of dopamine and adenosine receptors are engaged in antagonistic interactions in the brain, during both normal and pathological neuronal activity s
This thesis examines the neural substrate of akinesia after acute dopamine depletion or specific adenosine stimulation.

No study has so far investigated the neural activity in the basal ganglia during akinesia induced by adenosine receptor stimulation and little is known about electrophysiological changes in Parkinsonian akinesia, although it is generally accepted that akinesia results from altered function in the cortico-basal ganglia-cortical loop.

The external segment of the globus pallidus and the substantia nigra pars reticulata were chosen as the recording sites because both nuclei are included into the behavioural arrest control system and seem to express somewhat complementary functions, as a key integrative station and a main output structure of the basal ganglia.

To induce a rat model of Parkinsonian akinesia, dopamine function was manipulated by an acute decrease in the availability of dopamine binding sites in the brain through dopamine D2 receptor blockade with raclopride. Conversely, movement was inhibited by specific adenosine A2A receptor stimulation with systemic injections of sodium2-p-carboxyethylphenylamino-5-N-carboxamidoadenosine (CGS21680).
In both situations, behaviour was assessed through specific catalepsy tests.
Single neuron activity, changes in the firing rates, firing patterns and synchronised firing between cell pairs have been assessed during periods of normal movement and akinesia.

The symptoms and pathology of Parkinson’s disease, as well as the main affected dopaminergic pathways are presented in the introductory chapter. This is followed by a review of the basal ganglia, the anatomy and physiology of the structures involved in general, and in particular the structures that we recorded from. Finally, neural activity under normal conditions and known neural changes in Parkinson’s disease are reviewed.

Cuvinte cheie: ganglioni bazali, globus pallidus, substantia nigra pars reticulata, akinezie, electrofiziologie unicelulara, inhibitori de dopamina, stimulante de adenozina // basal ganglia, globus pallidus, substantia nigra pars reticulata, akinesia, single unit extracellular recording, dopamine antagonists, adenosine agonists