Neuroscience
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Comparative Study
Glutamic acid decarboxylase immunoreactivity in callosal projecting neurons of cat and rat somatic sensory areas.
The distribution of GABAergic callosally projecting neurons was analysed in the somatic sensory areas of cat and rat cerebral cortex by combining retrograde tracing of nerve cell bodies and glutamic acid decarboxylase (GAD) immunocytochemistry. A retrograde tracer (colloidal gold- labelled wheat germ agglutinin conjugated to enzymatically inactive horseradish peroxidase) was injected in the first or second somatic sensory area. ⋯ Their proportion was similar in both species (0.8% of all retrogradely-labelled neurons in cat, 0.7% in rat). These results: 1) confirm the existence of a small proportion of GABAergic callosally projecting neurons in rat somatic sensory cortices; 2) indicate the presence of a small but significant proportion of GAD-positive callosally projecting neurons in cat somatic sensory cortices; and 3) show that the proportion of GAD-positive callosal neurons is similar in the two species.
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Although there has been growing interest in the neuroanatomical and physiological mechanisms underlying aggressive behavior, little work has focused on possible mechanisms controlling natural plasticity in aggression. In the current study, we used naturally occurring changes in aggression level displayed by female Peromyscus californicus across the estrous cycle and parallel changes in c-fos expression to examine possible brain regions involved in mediating this plasticity. We found that c-fos expression was increased in females exposed to a conspecific female intruder compared with control females in numerous brain regions thought to be involved in the control of aggression. ⋯ Conversely, c-fos increased in the medial amygdala (MeA) across all stages of estrus compared with controls, suggesting the MeA is not involved in mediating changes in individual levels of aggression. Moreover, we found correlations between several measures of aggression and c-fos expression in the BNST and LSv but not the MeA, again suggesting a role in mediating aggression plasticity for the former two but not the latter brain region. We further hypothesize that the BNST and the LSv may be involved more generally in mediating natural changes in aggression, such as increases often observed after individuals win aggressive interactions against conspecifics.
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Comparative Study
Delayed onset of Huntington's disease in mice in an enriched environment correlates with delayed loss of cannabinoid CB1 receptors.
Huntington's disease (HD) is a late onset progressive genetic disorder characterised by motor dysfunction, personality changes, dementia and premature death. The disease is caused by an unstable expanded trinucleotide (CAG) repeat encoding a polyglutamine stretch in the IT15 gene for huntingtin, a protein of unknown function. Transgenic mice expressing exon one of the human HD gene with an expanded polyglutamine region develop many features of human HD. ⋯ In the brains of humans diagnosed with HD cannabinoid CB1 receptors are selectively lost from the basal ganglia output nuclei prior to the development of other identifiable neuropathology [Neuroscience 97 (2000) 505]. Our results therefore show that an enhanced environment slows the rate of loss of one of the first identifiable neurochemical deficits of HD. This suggests that delaying the loss of CB1 receptors, either by environmental stimulation or pharmacologically, may be beneficial in delaying disease progression in HD patients.
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Comparative Study
Modulation of activator protein 1/DNA binding activity by acoustic overstimulation in the guinea-pig cochlea.
Changes in gene expression are part of the homeostatic machinery with which cells respond to external stimuli or assaults. The activity of the early response transcriptional factor activator protein-1 (AP-1) can be modulated by a variety of environmental stimuli including those that alter the cellular oxidation/reduction status. This study investigates the activation of AP-1/DNA binding in the guinea-pig cochlea in response to acoustic overstimulation which produces reactive oxygen species. ⋯ Incubation of nuclear extracts with antibodies against Fos/Jun family proteins prior to a supershift assay showed Fra-2 as a major component of the AP-1 complex immediately after the noise exposure. In the organ of Corti, Fra-2 immunoreactivity was localized to the middle turn, i.e. the region which is most affected by the 4-kHz octave band exposure. The results suggest the modulation of gene expression via the activation of AP-1 as a consequence of noise trauma but also demonstrate differential responses in cochlear tissues.
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Comparative Study
Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function.
Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. ⋯ In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed.