Neuroscience
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Comparative Study
Impaired long-term potentiation in obese zucker rats: possible involvement of presynaptic mechanism.
Electrophysiological investigation of basal synaptic transmission and synaptic plasticity in the CA1 region of the hippocampus was carried out in anesthetized obese Zucker rats (OZR). Comparison of the input/output curves of basal field excitatory postsynaptic potential indicates that these are similar in both the OZR and its lean counterpart suggesting that basal synaptic transmission is intact in the OZR. ⋯ Since post-tetanic potentiation and paired pulse facilitation, forms of short-term potentiation of presynaptic origin, are also severely impaired in the OZR, the results imply that impairment of CA1 hippocampal LTP in these obese rats may be due, in part, to impaired presynaptic function. The results emphasize the potential deleterious effect of obesity on learning and memory functions of the CNS.
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Since metabolic activity is accompanied by heat release, measurement of brain temperatures offers a method for assessing behavior-associated changes in neural activity. To explore this possibility, we monitored local brain (nucleus accumbens, medial-preoptic hypothalamus, and hippocampus) and body (temporal muscle) temperature in an experienced male rat during sexual behavior with a sexually receptive female. Placement of the female into a neighboring compartment increased the male's temperature and additional increases occurred when rats were allowed to see and partially interact with the female through a Plexiglas barrier with dime-size holes. ⋯ These data generally match single-unit and other physiological findings, suggesting that male sexual behavior is accompanied by sustained and generalized neural activation. This activation is triggered by sexually relevant stimuli (arousal), maintained during repeated mounts and intromissions, and peaked at ejaculation. These findings suggest brain temperature fluctuations not only as a sensitive index of functional neural activation, but as a powerful factor affecting various neural functions and an important part of brain mechanisms underlying motivated behavior.
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Comparative Study
Exacerbated status epilepticus and acute cell loss, but no changes in epileptogenesis, in mice with increased brain-derived neurotrophic factor signaling.
Several studies suggest that brain-derived neurotrophic factor (BDNF) can exacerbate seizure development during status epilepticus (S. E.) and subsequent epileptogenesis in the adult brain. On the other hand, evidence exists for the protective effect of BDNF. ⋯ Our data support the role of BDNF and trkB signaling in seizure generation and acute cellular damage after S. E. Long-term outcome was not, however, exacerbated by trkB overexpression.
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Historical Article
Where are the perirhinal and parahippocampal cortices? A historical overview of the nomenclature and boundaries applied to the primate medial temporal lobe.
Strong evidence has emerged over the last 15 years showing that the perirhinal and parahippocampal cortices play an important role in normal memory function. Despite our progress in understanding the mnemonic functions of these areas, controversy still exists concerning the precise location of the boundaries of these areas in the primate brain. ⋯ We describe how the boundaries and the names applied to these regions have evolved over time, starting with the classic cytoarchitectonisists working in the early 1900s, and ending with the various schemes being used in the contemporary literature. We show that the current controversies concerning the boundaries of the perirhinal and parahippocampal cortices can be traced directly to the classic cytoarchitectonic literature.
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Glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN) and their receptors (GFRalpha1, GFRalpha2 and Ret) play an important role in the survival of neurons in the central and peripheral nervous system. For example, GDNF as well as other trophic factors promotes photoreceptor survival during retinal degeneration. Recent studies have proposed that part of neurotophic rescue of photoreceptors may be indirect, mediated by interaction of the neurotrophic factors with other cell types, that in turn release secondary factors that act directly on photoreceptors. ⋯ Exogenous GDNF increased brain-derived neurotrophic factor, basic fibroblast growth factor and GDNF, but not NTN mRNA production. On the other hand, NTN increased NTN, but not GDNF mRNA production in cultured Müller cells. These observations suggest that GDNF, NTN and their receptors are involved in the regulation of trophic factor production in retinal glial cells, and that functional glia-neuron network may utilize GDNF family for the protection of neural cells during retinal degeneration.