Abstracts » Zoology and wildlife conservation

Loss of cerebellar Purkinje cells in aged mice homozygous for a disrupted PrP gene

Article Abstract:

Prion protein (PrP) appears to play a significant role in the long-term survival of cerebellar Purkinje neurons after the onset of neuronal cell death that occurs with aging. Mice whose PrP-coding sequence is replaced by a drug-resistant gene were found to be normal until about 70 weeks when the loss of cerebellar folia Purkinje cells began. The interaction of normal PrP with cell-death inhibitory synapses indicates excitotoxic mechanisms are responsible for the cell death. The symptoms are similar to those of mice with transmissible spongiform encephalopathies called prion diseases where PrP is believed to convert to a protease-resistant PrP isoform.

Prions, Prions (Proteins)

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Cerebellar complex spikes encode both destinations and errors in arm movements

Article Abstract:

Cerebellar Purkinje cells pick up two kinds of synaptic inputs: one climbing fibre synapse from the brain stem's inferior olive nuclear synapse and sevral parallel fibre inputs from cerebellar granule cells. Arousal of the climbing fibre synapse causes a massive response, called the complex spike, occurring at low frequency. A new study analyses the link between motor activity and complex spike firing during arm movements. It is suggested that complex spikes arising early in a reaching movement encode target location, while those at the end of the cycle encode final error as the movement is completed.

Animal mechanics, Animal biomechanics

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Facilitation of long-term potentiation and memory in mice lacking nociceptin receptors

Article Abstract:

Mice lacking the peptide nociceptin receptor show greater learning ability and better memory than control mice. These mice also show larger long-term potentiation in the hippocampal CA1 region, with no changes in presynaptic or postsynaptic electrophysiological properties noted. It appears that the nociceptin system has a negative impact on both memory and learning at whole-animal level and in CA1 long-term potentiation at the cellular level.

Mice, Mice (Rodents), Nociceptors

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