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Inactivating the middle cerebellar peduncle abolishes the expression of short-latency conditioned eyeblinks
Journal article   Open access   Peer reviewed

Inactivating the middle cerebellar peduncle abolishes the expression of short-latency conditioned eyeblinks

Krystal L Parker and Vlastislav Bracha
Brain research, Vol.1303, pp.32-38
12/15/2009
DOI: 10.1016/j.brainres.2009.08.089
PMCID: PMC2823120
PMID: 19747462
url
https://doi.org/10.1016/j.brainres.2009.08.089View
Published (Version of record) Open Access

Abstract

The interposed nuclei (IN) of the cerebellum play a crucial role in the classically conditioned eyeblink circuit. It has previously been shown in well-trained animals that injecting the IN with GABA(A) antagonists produces short-latency conditioned responses (SLRs). The mechanism underlying SLR generation is not clear. According to one concept, SLRs originate in cerebellar nuclei in response to direct inputs from collaterals of mossy fibers. An alternate explanation is that SLRs are produced by extra-cerebellar circuits that are excited by increased tonic activity in cerebellar nuclei or by the combined action of inputs to cerebellar nuclei from mossy fiber collaterals and incompletely blocked Purkinje cells. In the present study, we examined whether cerebellar afferent axons in the middle cerebellar peduncle (MCP) participate in SLR expression. We hypothesized that if SLRs are evoked by the sensory mossy fiber input to the IN and cerebellar cortex, then blocking the MCP should abolish these responses. Well-trained animals, which had been implanted with dual injection cannulae in the left IN and the left MCP, were injected with gabazine (GZ) into the IN to produce SLRs followed by an injection of the sodium channel blocker tetrodotoxin (TTX) into the MCP. TTX infusions in the MCP suppressed both CRs and SLRs. These findings suggest that the expression of SLRs depends on both direct and cerebellar cortex-mediated sensory information from the mossy fiber system.
 Neural Pathways - drug effects Synaptic Transmission - physiology Cerebellar Nuclei - cytology Pons - physiology Male Pyridazines - pharmacology Neural Pathways - physiology Purkinje Cells - physiology Neural Inhibition - physiology Nerve Fibers - physiology Time Factors Reaction Time - drug effects Synaptic Transmission - drug effects Cerebellar Nuclei - physiology Tetrodotoxin - pharmacology Conditioning, Eyelid - drug effects Rabbits Cerebellar Cortex - cytology Nerve Fibers - drug effects Sodium Channel Blockers - pharmacology Reaction Time - physiology GABA Antagonists - pharmacology Conditioning, Eyelid - physiology Animals Neural Pathways - cytology Nerve Fibers - ultrastructure Cerebellar Cortex - physiology Neural Inhibition - drug effects Denervation Pons - cytology

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