Glutamate Receptors and Xxxxxxxxx’x Disease Therapeutics Sample Clauses

Glutamate Receptors and Xxxxxxxxx’x Disease Therapeutics. Dopamine denervation of striatal neurons is the hallmark of PD, however equally relevant is the transformation of the glutamatergic innervation of the striatum. This system undergoes very interesting changes as part of PD pathology. There is an increased glutamatergic drive from the corticostriatal projection. However there is also a significantly decreased number of spines (Xxxxxxxx et al., 2005) in conjunction with a reduction in the size of the dendritic trees (Xxxxxxxx et al., 2005). Since the main input nucleus of the basal ganglia receives most of its input from glutamatergic sources and this input suffers a perturbation during PD, drugs that can target receptors in this system and restore some form of balance to the network would be of great value. Glutamate receptors are expressed both pre- and post-synaptically and serve as auto- and hetero-receptors in the basal ganglia. The iGluRs could serve as potential targets for mediation of the glutamatergic drive into the striatum and the effects looked promising in animal models. However, the activation of these receptors would lead to outcomes that were too strong and ubiquitous. In humans iGluR drugs caused sedative effects, impairment of learning, and psychotomimetic effects (Kristensen et al., 1992; Xxxx et al., 1959; Xxxx et al., 1994). The mGluRs, on the other hand, exhibit wide diversity and heterogeneous distribution of their subtypes. Thus the opportunity exists for developing highly selective drugs that affect a limited number of CNS functions. The mGluRs therefore provide a target for development of therapeutic agents that could impact our ability to treat a variety of psychiatric and neurologic disorders. Importantly, drugs acting at mGluRs would have more subtle effects on transmission at glutamatergic synapses than would iGluR agonists and antagonists and would probably have fewer side effects (Conn and Pin, 1997). Recent data have provided strong evidence for the potential antiparkinsonian effects of group III mGluR agonists and allosteric modulators in acute rodent models of parkinsonism. A good example are drugs acting on mGluR4. These drugs appear to selectively modulate striatopallidal transmission which raises the interesting possibility that activation of this receptor could decrease the excessive inhibition of the GP that has been postulated to occur in Xxxxxxxxx’x disease. Consistent with this, intracerebroventricular injections of L-AP4, an mGluR III agonist, produces therapeutic ...
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