Neuroscience
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Zinc plays an important role in synaptic signaling in the mammalian cerebral cortex. Zinc is sequestered into presynaptic vesicles of subpopulations of glutamatergic neurons and is released by depolarization, in a calcium-dependent manner. As the majority of mechanisms that have been suggested to participate in experience-dependent alterations in synaptic strength in the cerebral cortex implicate signaling by glutamate, it stands to reason that zincergic signaling might also be crucial. ⋯ In all age groups, levels of zinc staining returned to baseline by 21 days after whisker plucking. However, only in juvenile and adult mice did we observe that the level of zinc staining in deprived barrel hollows, was correlated with the length of whiskers as they regrew. Our data suggest that alterations in the regulation of synaptic zinc may be involved with decrements of synaptic plasticity that accompany senescence.
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Disruption of the glucocorticoid negative feedback system is observed in approximate one half of human depressives, and a similar condition is induced in animals by chronic stress. This disruption is thought to involve down-regulation of glucocorticoid receptors (GRs) in the feedback sites of the brain. However, the responsible site of the brain has not been well elucidated. ⋯ In addition, when DEX was injected systemically to the chronically stressed rats, the suppressive response to DEX was significantly attenuated. These results suggest that the abnormal changes in GRs in the higher centers of the hypothalamo-pituitary-adrenal axis are involved in the chronic stress-induced attenuation of the feedback. Since dysfunction of the PFC or hippocampus is implicated in the pathogenesis of depression, the present findings would help to understand the mechanisms underlying the disrupted feedback system and its relation to brain dysfunction in depression.
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Both endocannabinoids through cannabinoid receptor type I (CB1) receptors and dopamine through dopamine receptor type D1 receptors modulate postsynaptic inhibition in substantia nigra by changing GABA release from striatonigral terminals. By recording from visually identified pars compacta and pars reticulata neurons we searched for a possible co-release and interaction of endocannabinoids and dopamine. Depolarization of a neuron in pars reticulata or in pars compacta transiently suppressed evoked synaptic currents which were blocked by GABA(A) receptor antagonists (inhibitory postsynaptic currents [IPSCs]). ⋯ We conclude that endocannabinoids and dopamine can be co-released. Retrograde signaling through endocannabinoids and dopamine changes inhibition independently from each other. Activation of dopamine D1 receptors emphasizes extrinsic inhibition and activation of CB1 receptors promotes intrinsic inhibition.
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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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In vitro and in vivo electrophysiological studies were done to investigate the neuronal function of the hippocampus and prefrontal cortex in the amyloid precursor protein (APP) 23 transgenic mouse model for amyloidosis developed by Sturchler-Pierrat et al. [Proc Natl Acad Sci USA 94 (1997) 13287]. Brain slices were taken from 3, 6, 9, 12, 18 and 24 month old wildtype and hemizygous type APP23 mice. Extracellular field potentials were recorded from the CA1 region of the hippocampus while stimulating the Schaffer collaterals. ⋯ The present study shows that amyloidosis impairs basic synaptic function but not long-term potentiation in the hippocampus, however, does not alter any of the neurophysiological functions measured within the prefrontal cortex. These findings suggest that amyloidosis may be involved in altering some neurophysiological functions within only certain brain structures. Although APP23 mice have impaired cognitive performance, long-term plasticity, a cellular model for memory, is not affected, raising the question on the relationship between these processes.