Biomedical subjects

E A Wakeman

Publications and source records attributed to E A Wakeman.

6 recordsLinked to original sources

PubMed1999

Firing rate distributions and efficiency of information transmission of inferior temporal cortex neurons to natural visual stimuli.

The distribution of responses of sensory neurons to ecological stimulation has been proposed to be designed to maximize information transmission, which according to a simple model would imply an exponential distribution of spike counts in a given time window. We have used recordings from inferior temporal cortex neurons responding to quasi-natural visual stimulation (presented using a video of everyday lab scenes and a large number of static images of faces and natural scenes) to assess the validity of this exponential model and to develop an alternative simple model of spike count distributions. We find that the exponential model has to be rejected in 84% of cases (at the p < 0.01 level). A new model, which accounts for the firing rate distribution found in terms of slow and fast variability in the inputs that produce neuronal activation, is rejected statistically in only 16% of cases. Finally, we show that the neurons are moderately efficient at transmitting information but not optimally efficient.

Animals↗

PubMed1997

Responses of neurons in primary and inferior temporal visual cortices to natural scenes.

The primary visual cortex (V1) is the first cortical area to receive visual input, and inferior temporal (IT) areas are among the last along the ventral visual pathway. We recorded, in area V1 of anaesthetized cats and area IT of awake macaque monkeys, responses of neurons to videos of natural scenes. Responses were analysed to test various hypotheses concerning the nature of neural coding in these two regions. A variety of spike-train statistics were measured including spike-count distributions, interspike interval distributions, coefficients of variation, power spectra, Fano factors and different sparseness measures. All statistics showed non-Poisson characteristics and several revealed self-similarity of the spike trains. Spike-count distributions were approximately exponential in both visual areas for eight different videos and for counting windows ranging from 50 ms to 5 seconds. The results suggest that the neurons maximize their information carrying capacity while maintaining a fixed long-term-average firing rate, or equivalently, minimize their average firing rate for a fixed information carrying capacity.

Animals↗

PubMed1996

Orbitofrontal cortex neurons: role in olfactory and visual association learning.

1. The orbitofrontal cortex is implicated in the rapid learning of new associations between visual stimuli and primary reinforcers such as taste. It is also the site of convergence of information from olfactory, gustatory, and visual modalities. To investigate the neuronal mechanisms underlying the formation of odor-taste associations, we made recordings from olfactory neurons in the orbitofrontal cortex during the performance of an olfactory discrimination task and its reversal in macaques. 2. It was found that 68% of odor-responsive neurons modified their responses after the changes in the taste reward associations of the odorants. Full reversal of the neuronal responses was seen in 25% of these neurons. Extinction of the differential neuronal responses after task reversal was seen in 43% of these neurons. 3. For comparison, visually responsive orbitofrontal neurons were tested during reversal of a visual discrimination task. Seventy-one percent of these visual cells showed rapid full reversal of the visual stimulus to which they responded, when the association of the visual with taste was reversed in the reversal task. 4. These demonstrate that of many orbitofrontal cortex olfactory neurons on the taste with which the odor is associated. 5. This modification is likely to be important for setting the motivational value of olfactory for feeding and other rewarded behavior. However, it is less complete, and much slower, than the modifications found or orbit frontal visual during visual-taste reversal. This relative inflexibility of olfactory responses is consistent with the need for some stability is odor-taste associations to facilitate the formation and perception of flavors.

Acoustic Stimulation↗

PubMed1983

Development changes in pharmacological responsivity of the acoustic startle reflex: effects of picrotoxin.

Using the acoustic startle reflex as the behavioral measure, qualitatively different responses to the GABA antagonist picrotoxin were obtained in developing rats before and after 21 days postnatal (PN) age. Dose-dependent increases in acoustic startle were seen following picrotoxin in PN day 15-16 rat pups. In contrast, dose-dependent decreases in startle following picrotoxin were observed in adult rats. The switch from excitation to inhibition of startle was found to occur abruptly on PN day 21. Excitatory responses to picrotoxin were also found in adult rats following localized infusions of picrotoxin into lumbar spinal cord regions, but not into the forebrain. These results give evidence that picrotoxin-sensitive sites that modulate increases in startle reflex behavior mature first and are analogous to sites in the adult spinal cord, whereas picrotoxin-sensitive sites that modulate decreases in startle reflex behavior mature later (greater than or equal to PN day 21) and are localized in more rostral brain areas.

Acoustic Stimulation↗

PubMed1982

Prenatal exposure to electroconvulsive seizures and phenytoin: development of benzodiazepine binding sites, reflex behaviors and seizure thresholds in exposed offspring.

Electroconvulsive seizures administered during the period of fetal benzodiazepine (BZ) binding site proliferation (days 16, 18 and 20 in gestation) significantly decreased the density of cerebral cortical benzodiazepine binding sites in exposed pups up to 21 days postnatal age. Significant decreases in seizure threshold were also found in exposed offspring. However, decreases in BZ sites were not accompanied by significant alterations in RO5-4864-displaceable benzodiazepine binding as seen after in utero exposure to phenytoin (DPH). Neither prenatal treatment affected the ability of GABA to enhance BZ binding in vitro. Prenatal exposure to electroshock delayed the onset of acoustic startle and eye-opening during postnatal development; similar effects were not seen following in utero exposure to DPH. These data suggest that prenatal exposure to seizures and DPH decrease postnatal BZ site proliferation by different mechanisms.

Animals↗

PubMedDate not supplied

Responses of neurons in the primate taste cortex to the glutamate ion and to inosine 5'-monophosphate.

To investigate the neural encoding of glutamate taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex taste area, with a small number in adjacent taste areas. First, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. The correlation between the responses to these two tastants was higher than between any other pair of tastants, which included glucose (sweet), sodium chloride (salty), HCl (sour), and quinine HCl (bitter). Accordingly, the responsiveness to glutamic acid clustered with the response to monosodium glutamate in a cluster analysis with this set of stimuli, and glutamic acid was close to sodium glutamate in a space created by multidimensional scaling. Second, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5'-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Third, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fourth, neurons have not yet been found in this cortical region that showed synergism of monosodium glutamate and the nucleotide inosine 5'-monophosphate: it was shown that mixtures of 0.0001 M inosine 5'-monophosphate with different concentrations (0.001, 0.01, and 0.1 M) of monosodium glutamate did not have a greater effect than the monosodium glutamate alone. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety. In some cases this reduction was sensory-specific. These findings show that the taste neurons activated by monosodium glutamate can also be activated by other umami tastants, including glutamic acid and the nucleotide inosine 5'-monophosphate. The responses to these umami tastants were more similar to each other than to any of the other prototypical tastants, providing evidence that in this system umami is encoded differently from the other tastants. Moreover, the findings with these tastants provide additional evidence that the responses to monosodium glutamate are not due just to activation of a sodium taste channel.

Animals↗