Imidazoleacetic acid-ribotide in the rodent striatum: a putative neurochemical link between motor and autonomic deficits in Parkinson's disease
| Autor: | J. Martir, O. Bozdagi, G. Martinelli, V. Friedrich, Gay Holstein |
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| Rok vydání: | 2012 |
| Předmět: |
Male
Calbindins Time Factors Stimulation Striatum Biology Neurotransmission Motor Activity Autonomic Nervous System Ligands Calbindin Synaptic Transmission General Biochemistry Genetics and Molecular Biology Basal Ganglia Rats Sprague-Dawley Glutamatergic S100 Calcium Binding Protein G medicine Animals heterocyclic compounds Rats Long-Evans GABA-A Receptor Antagonists Evoked Potentials gamma-Aminobutyric Acid General Environmental Science Neurons GABAA receptor Ventral striatum Glutamate receptor Imidazoles food and beverages Neural Inhibition Parkinson Disease Receptors GABA-A Electric Stimulation Rats medicine.anatomical_structure nervous system Neurology Microscopy Fluorescence Calbindin 1 Imidazoline Receptors Ribosemonophosphates Neuroscience Excitatory Amino Acid Antagonists |
| Zdroj: | Acta biologica Hungarica. 63 |
| ISSN: | 0236-5383 |
| Popis: | We have previously demonstrated that imidazole-4-acetic acid-ribotide (IAA-RP) is present in the mammalian brain and is an endogenous ligand at imidazoline binding sites. In the present study, we used a polyclonal antiserum to visualize IAA-RP-containing neurons in the rat caudoputamen. We observe IAA-RP-immunostained neurons scattered throughout the dorsal and ventral striatum. Most of these cells co-localize GABA, but none are parvalbumin-immunoreactive. In contrast, approximately 50% of the calbindin D28k-immunopositive striatal neurons co-localize IAA-RP. Electrophysiological studies using corticostriatal slices demonstrated that bath application of IAA-RP reversibly depresses the synaptically mediated component of field potentials recorded in the striatum by stimulation of cortical axons. Addition of competitive glutamate receptor antagonists completely blocks the response, confirming its association with glutamatergic transmission. Using paired-pulse stimuli, IAA-RP was shown to exert, at least in part, a presynaptic effect, but blockade of GABAA receptor-mediated transmission did not alter the response. Lastly, we show that this effect is attributable to imidazoline-1 receptors, and not to α2 adrenergic receptors. Since IAA-RP is an endogenous central regulator of blood pressure, and cardiovascular dysfunction is a common symptom associated with Parkinson's disease (PD), we speculate that IAA-RP-related abnormalities may underlie some of the autonomic dysfunction that occurs in PD. |
| Databáze: | OpenAIRE |
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