Neuroscience
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Comparative Study
Selective mechanisms for complex visual patterns revealed by adaptation.
A great deal is known about the initial steps of visual processing. We know that humans have neural mechanisms selectively tuned to simple patterns of particular spatial frequencies and orientations. ⋯ Very little is known about intermediate levels of visual processing, where early visual signals are presumably combined to represent increasingly complex visual features. Here we show the existence of visual mechanisms in humans, tuned and selective to particular combinations of simple sinusoidal patterns, using a novel method of compound adaptation.
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Comparative Study
Gene expression in the rat cerebral cortex: comparison of recovery sleep and hypnotic-induced sleep.
Most hypnotic medications currently on the market target some aspect of GABAergic neurotransmission. Although all such compounds increase sleep, these drugs differentially affect the activity of the cerebral cortex as measured by the electroencephalogram. Whereas benzodiazepine medications such as triazolam tend to suppress slow wave activity in the cortex, the GABA(B) ligand gamma-hydroxybutyrate greatly enhances slow wave activity and the non-benzodiazepine, zolpidem, which binds to the omega1 site on the GABA(A) receptor/Cl(-) ionophore complex, is intermediate in this regard. ⋯ We find that, although each drug increases the expression of a subset of genes in the panel of biomarkers, no drug fully replicates the molecular changes in the cortex associated with recovery sleep. Furthermore, high levels of slow wave activity in the cortex are correlated with increased expression of fra-2 whereas the expression of grp94 is correlated with body temperature. These results demonstrate that sleep-related changes in gene expression may be affected by physiological covariates of sleep and wakefulness rather than by vigilance state per se.
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Comparative Study
Stereological estimation of Purkinje neuron number in C57BL/6 mice and its relation to associative learning.
Cerebellar Purkinje neurons are among the most vulnerable neurons in the CNS. Impairment in Purkinje neurons has consequences for cerebellar cortical-dependent forms of behavior. The primary aim of this study was to evaluate Purkinje neuron number over the lifespan of C57BL/6 mice. ⋯ Eliminating the hearing-impaired 18- and 24-month-old mice from the analysis, the correlation between Purkinje neuron number and rate of conditioning was -0.435 (P=0.053) in 15 younger mice aged 4-12 months. Purkinje neurons are one of the few types of neurons showing significant age-associated loss. Results indicate that individual variation in Purkinje neuron number is related to eyeblink conditioning in young organisms suggesting that reserves of neuron numbers against which individuals draw are defined early in life.
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Comparative Study
Inflammation increases the excitability of masseter muscle afferents.
Temporomandibular disorder is a major health problem associated with chronic orofacial pain in the masticatory muscles and/or temporomandibular joint. Evidence suggests that changes in primary afferents innervating the muscles of mastication may contribute to temporomandibular disorder. However, there has been little systematic study of the mechanisms controlling the excitability of these muscle afferents, nor their response to inflammation. ⋯ These changes in excitability and action potential waveform were associated with significant shifts in the voltage-dependence of activation and steady-state availability of voltage-gated K(+) current as well as significant decreases in the density of voltage-gated K(+) current subject to steady-state inactivation. These data suggest that K(+) channel subtypes may provide novel targets for the treatment of pain arising from inflamed muscle. These results also support the hypothesis that the underlying mechanisms of pain arising from specific regions of the body are unique suggesting that it may be possible, if not necessary to treat pain originating from different parts of the body with specific therapeutic interventions.
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Comparative Study
The tyrosine receptor kinase B ligand, neurotrophin-4, is not required for either epileptogenesis or tyrosine receptor kinase B activation in the kindling model.
The kindling model of epilepsy is a form of neuronal plasticity induced by repeated induction of pathological activity in the form of focal seizures. A causal role for the neurotrophin receptor, tyrosine receptor kinase B, in epileptogenesis is supported by multiple studies of the kindling model. Not only is tyrosine receptor kinase B required for epileptogenesis in this model but enhanced activation of tyrosine receptor kinase B has been identified in the hippocampus in multiple models of limbic epileptogenesis. ⋯ No differences were found between +/+ and -/- mice with respect to any facet of the development or persistence of kindling. Despite the absence of NT4, activation of the tyrosine receptor kinase B receptor in the mossy fiber pathway as assessed by phospho-trk immunohistochemistry was equivalent to that of +/+ mice. Together these findings demonstrate that NT4 is not required for limbic epileptogenesis nor is it required for activation of tyrosine receptor kinase B in hippocampus during limbic epileptogenesis.