Brain sites mediating cyclosomatostatin-induced catalepsy in Wistar rats: A specific role for the nigrostriatal system and locus coeruleus
•Antagonism of somatostatin receptors by cyclosomatostatin induces catalepsy in rats.•Administration into the nigrostriatal region and locus coeruleus initiates catalepsy.•Injections into the pedunculopontine nucleus and inferior colliculus are ineffective. A decrease in somatostatin activity is obs...
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Veröffentlicht in: | Brain research 2018-07, Vol.1691, p.26-33 |
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Sprache: | eng |
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Zusammenfassung: | •Antagonism of somatostatin receptors by cyclosomatostatin induces catalepsy in rats.•Administration into the nigrostriatal region and locus coeruleus initiates catalepsy.•Injections into the pedunculopontine nucleus and inferior colliculus are ineffective.
A decrease in somatostatin activity is observed in the Parkinsonian brain. In recent experiments on rats, we simulated this abnormality by intracerebroventricular injections of a somatostatin antagonist, cyclosomatostatin. The treated animals displayed catalepsy, a state that resembles the extrapyramidal signs of Parkinson’s disease. The neuroanatomical substrates mediating the catalepsy-inducing effect of cyclosomatostatin are unknown. To clarify this issue, we assessed here the action of cyclosomatostatin injected into the substantia nigra pars compacta (SNc), dorsal striatum (DS), locus coeruleus (LC), pedunculopontine tegmental nucleus (PPTg), and inferior colliculus (IC). The experiments were conducted with male Wistar rats of 270–290 g bw, catalepsy was evaluated by using the bar test. The injections into the PPTg and IC were without effect whereas the intra-SNc, intra-DS, and intra-LC administrations produced distinct cataleptic response. Thus, it was shown for the first time that the LC is a brain center capable of causing catalepsy. These data provide new insights into the neuroanatomical organization of the catalepsy-initiating mechanism and suggest the LC representing a potential target for therapeutic manipulations of extrapyramidal dysfunctions. |
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ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/j.brainres.2018.04.016 |