title: Inactivating the middle cerebellar peduncle abolishes the expression of short-latency conditioned eyeblinks.
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.
authors.affiliation: Biomedical Sciences, 2032 Vet Med, Iowa State University, Ames, IA 50011, USA.
authors.forename: Krystal L
authors.initials: KL
authors.lastname: Parker
authors.forename: Vlastislav
authors.initials: V
authors.lastname: Bracha
mesh_terms: D000818:Animals; D002525:Cerebellar Cortex / Q000166:cytology / Q000502:physiology*; D002529:Cerebellar Nuclei / Q000166:cytology / Q000502:physiology*; D003215:Conditioning, Eyelid / Q000187:drug effects / Q000502:physiology*; D003714:Denervation; D018756:GABA Antagonists / Q000494:pharmacology; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D011149:Pons / Q000166:cytology / Q000502:physiology*; D011689:Purkinje Cells / Q000502:physiology; D011724:Pyridazines / Q000494:pharmacology; D011817:Rabbits; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
chemical_list: D018756:GABA Antagonists; D011724:Pyridazines; D026941:Sodium Channel Blockers; D013779:Tetrodotoxin; C049853:gabazine