PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11482836

Critical flicker frequency responses in visual cortex.

E F Wells·G M Bernstein·B W Scott·P J Bennett·J R Mendelson
View original source ↗Export metadata ↓

Abstract

Critical flicker frequency (CFF) threshold is defined as the frequency at which a flickering light is indistinguishable from a steady, non-flickering light. CFF is useful for assessing the temporal characteristics of the visual system. While CFF responses are believed to reflect activity in the central visual system, little is known about how these temporal frequencies are processed in the visual cortex. The current paper estimated the CFF threshold for cells in the rat visual cortex by recording single unit responses to flickering stimuli. Results showed that: (1) there was a broad range of temporal tuning, (2) CFF threshold was lower in simple cells than in complex and hypercomplex cells, and (3) there was no significant difference in CFF threshold between areas 17 and 18.

Explore related subjects

Action PotentialsAnimalsFlicker FusionFourier AnalysisMaleNeuronsPhotic StimulationRatsRats, Long-EvansReaction TimeVisual CortexJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E F Wells, G M Bernstein, B W Scott, P J Bennett, J R Mendelson. 2001. Critical flicker frequency responses in visual cortex.. https://doi.org/10.1007/s002210100721

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Abnormal Na channel gating in murine cardiac myocytes deficient in myotonic dystrophy protein kinase.

DMPK is a serine/threonine kinase implicated in the human disease myotonic muscular dystrophy (DM). Skeletal muscle Na channels exhibit late reopenings in Dmpk-deficient mice and peak current density is reduced, implicating DMPK in regulation of membrane excitability. Since complete heart block and sudden cardiac death occur in the disease, we tested the hypothesis that cardiac Na channels also exhibit abnormal gating in Dmpk-deficient mice. We made whole cell and cell-attached patch clamp recordings of ventricular cardiomyocytes enzymatically isolated from wild-type, Dmpk+/-, and Dmpk-/- mice. Recordings from membrane patches containing one or a few Na channels revealed multiple Na channel reopenings occurring after the macroscopic Na current had subsided in both Dmpk+/- and Dmpk-/- muscle, but only rare reopenings in wild-type muscle (>3-fold difference, P < 0.05). This resulted in a plateau of non-inactivating Na current in Dmpk-deficient muscle. The magnitude of this plateau current was independent on the magnitude of the test potential from -40 to 0 mV and was also independent of gene dose. Macroscopic Na current density was similar in wild-type and Dmpk-deficient muscle, as was steady-state Na channel gating. Decay of macroscopic currents was slowed in Dmpk-/- muscle, but not in Dmpk+/- or wild-type muscle. Entry into, and recovery from, inactivation were similar at multiple test potentials in wild-type and Dmpk-deficient muscle. Resting membrane potential was depolarized, and action potential duration was significantly prolonged in Dmpk-deficient muscle. Thus in cardiac muscle, Dmpk deficiency results in multiple late reopenings of Na channels similar to those seen in Dmpk-deficient skeletal muscle. This is reflected in a plateau of non-inactivating macroscopic Na current and prolongation of cardiac action potentials.

Action Potentials↗
PubMed2003

Stable synchronized high-frequency signals from the main sensory and spinal nuclei of the pig activated by Abeta fibers of the maxillary nerve innervating the snout.

The primary somatosensory cortex of various species including man, monkey, pig and rat is capable of producing high-frequency signals in the 600 Hz range and above with very little latency jitter. We have recently observed such cortical signals for the trigeminal system of the swine. This study determined the projection of the maxillary nerve innervating the snout to the sensory trigeminal nuclear complex in the brain stem and stability of outputs of each nucleus receiving the projection. The snout stimulation activated large-caliber Abeta fibers in the trigeminal nerve with a mean velocity of 64.4+/-2.7 m/s (mean+/-1 S.E.M., six animals) comparable in velocity to the tooth pulp Abeta fibers (57.9+/-3.4 m/s) obtained from the same animals. These afferents activated the main sensory nucleus, and subnuclei oralis, interpolaris and caudalis of the spinal nucleus, as judged by evoked field potential maps superimposed on the histological maps of the trigeminal nuclei from the same animals. Inputs from these fast afferents arrived at all the four trigeminal nuclei almost simultaneously within a span of 0.7+/-0.2 ms (mean+/-1 S.D., seven animals). Evoked high-frequency signals were reproducible with a latency jitter of less than 0.2 ms during the first 4 ms of postsynaptic activity for each of main sensory and spinal nuclei. These results indicate that the snout stimulation activates fast-conducting peripheral afferents which project to all the sensory trigeminal nuclei and produces highly reproducible initial responses nearly simultaneously across the multiple trigeminal nuclei. These outputs from the trigeminal nuclei may play an important role in triggering the stable high-frequency signals in the cortex.

Action Potentials↗
PubMed2003

Estimating the number of release sites and probability of firing within the nerve terminal by statistical analysis of synaptic charge.

Investigating the function of individual synapses is essential to understanding the mechanisms that influence the efficacy of chemical synaptic transmission. The known simplicity of the synaptic structure at the crayfish neuromuscular junction (NMJ) and its quantal nature of release allows an assessment of discrete synapses within the motor nerve terminals. Our goal in this article is to investigate the effect of the stimulation frequency on the number of active release sites (n) and the probability of release (p) at those active sites. Because methods based on direct counts often provide unstable joint estimates of (n) and (p), we base our analysis on mixture modeling. In particular, the mixture modeling approach is used to estimate (n) and (p) for stimulation frequencies of 1 Hz, 2 Hz, and 3 Hz. Our results indicate that as the stimulation frequency increases, new sites are recruited (thus increasing n) and the probability of release (p) increases.

Action Potentials↗