Neuroscience
-
Comparative Study
Sparseness of coding in area 17 of the cat visual cortex: a comparison between pinwheel centres and orientation domains.
Optical imaging of intrinsic signals across the primary visual cortex in mammals has shown that neurons tuned to the same stimulus orientation are clustered together to form orientation domains, which converge on singularities called pinwheel centres. We used a combination of two gratings in different mutual relationships as in a plaid to study how visual cortical neurons differ in integrating these signals. Neurons in the centres of orientation domains responded to a smaller range of such composite stimuli than cells near pinwheel centres, even though orientation tuning for a single bar or grating did not differ significantly between the two locations. We believe that this difference between the two locations is related to the way local intracortical interactions generate a full complement of orientation preferences from a limited number of preferred stimulus orientations represented in the geniculate afferents to the striate cortex.
-
Goal of this manuscript is to investigate whether changes that exist in epileptic brain generating spontaneous seizures are reflected in the pattern of the UP-Down state (UDS) recorded from the neocortex and dentate gyrus. Experiments were carried out on naive and epileptic mice under urethane anesthesia. Local field potentials were recorded with chronically implanted microelectrodes and single unit activity was recorded with glass microelectrodes. ⋯ Changes in the duration of UP and Down phases as well increased time of recovery of excitability of epileptic brain after termination of UP phase suggest alterations in the homeostatic properties of neuronal network in epileptic brain. We suggest that the existence of UP-spikes in epileptic brain may be an additional electrographic pattern indicating epileptogenicity. Unraveling the neuronal substrates of UP-spikes may further improve our understanding of the mechanisms of epilepsy.
-
Calcium accumulation induces the breakdown of cytoskeleton and axonal fragmentation in the late stages of Wallerian degeneration. In the early stages there is no evidence for any long-lasting, extensive increase in intra-axonal calcium but there does appear to be some redistribution. We hypothesized that changes in calcium distribution could have an early regulatory role in axonal degeneration in addition to the late executionary role of calcium. ⋯ Calcium penetration and the early calcium increase in this system were indistinguishable between Wld(S) and wild-type axons. However, a significant difference was observed during the following hours, when calcium increased in wild-type neurites but not in Wld(S) neurites. We conclude that there is little relationship between calcium distribution and the early stages of Wallerian degeneration at the time points studied in vivo or in vitro but that Wld(S) neurites fail to show a later calcium rise that could be a cause or consequence of the later stages of Wallerian degeneration.
-
STriatal-Enriched protein tyrosine Phosphatase (STEP; PTPN5) is expressed in brain regions displaying adult neuroplasticity. STEP modulates neurotransmission by dephosphorylating regulatory tyrosine residues on its substrates. In this way, STEP inactivates extracellular-signal-regulated kinase 1/2 (ERK1/2), limiting the duration and spatial distribution of ERK signaling. ⋯ Here we demonstrate that STEP KO mice also display augmented fear conditioning as measured by an enhancement in conditioned suppression of instrumental response when a fear-associated conditioned stimulus was presented. Deletion of STEP also increases long-term potentiation and ERK phosphorylation in the lateral amygdala. The current experiments demonstrate that deletion of STEP can enhance experience-induced neuroplasticity and memory formation and identifies STEP as a target for pharmacological treatment aimed at improving the formation of long-term memories.
-
Chronic exposure to nicotine during the first postnatal week in rats, a developmental period that corresponds to the third trimester of human gestation, results in sexually dimorphic long-term functional defects in the adult hippocampus. One potential cause could be the sex-specific differences in the maturation of GABA(A) receptor-mediated responses from excitatory to inhibitory, which depends on the expression of the Na(2+)/K(+)/Cl(-) co-transporter 1 (NKCC1) and the K(+)/Cl(-) co-transporter 2 (KCC2). In the rat hippocampus, this switch occurs during the first and second postnatal week in females and males, respectively, and is regulated by nicotinic receptor activation. ⋯ Males also had higher expression of NR2A and lower expression of NR2B at P5 compared to females (p<0.05). At P8, there were neither sex nor treatment effects on mRNA expression, indicating the end of a critical period for sensitivity to nicotine. These results suggest that differential maturation of GABA(A)R-mediated responses result in sex-specific sensitivity to nicotine during early postnatal development, potentially explaining the differential long-term effects of CNN on hippocampal function.