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M E Lickey

Publications and source records attributed to M E Lickey.

10 recordsLinked to original sources
PubMed2000

Postnatal development of NR1, NR2A and NR2B immunoreactivity in the visual cortex of the rat.

N-Methyl-D-aspartate receptors (NMDARs) are critically involved in some types of synaptic plasticity. The NMDAR subunits NR1, NR2A and NR2B are developmentally regulated, and it has been proposed that developmental changes in their expression may underlie developmental changes in cortical plasticity. Age-dependent change in cortical plasticity is most commonly measured by the monocular deprivation effect, which occurs during a critical period between P22 and P50 in the rat. Although the development of NMDAR subunits has been studied from birth through the fourth postnatal week, there is only meager information from older ages when visual plasticity ends. We hypothesized that there will be significant age-dependent change in expression of NR1, NR2A or NR2B between P22, when the cortex is plastic, and P90, when it is not. We applied specific antibodies recognizing NR1, NR2A and NR2B to the primary visual cortex at P14, P22, P30, P45 and P90. We found age-dependent changes in NR1-IR that were negatively correlated with changes in NR2A-IR; these subunits are not regulated in unison. In contrast, NR2A-IR and NR2B-IR were positively correlated. NR2A-IR and NR2B-IR both passed through a developmental minimum around P45, then recovered to approximately their P22 level. NR1-IR passed through a maximum at P45. There were no significant differences between P22 and P90. These results do not support the simple hypothesis that the loss of plasticity corresponds to a simple transition from juvenile levels of NMDAR subunit proteins to new adult levels. On the other hand, the results do confirm the hypothesis that there are significant changes in processing of NMDAR proteins during the time that plasticity is lost. How these changes of IR relate to synaptic transmission and plasticity needs to be clarified.

Animals↗
PubMed1999

Critical period for the monocular deprivation effect in rats: assessment with sweep visually evoked potentials.

Rats and mice are the species most frequently used for cellular and biochemical studies of plasticity, but only a few studies have examined developmentally regulated visual plasticity in these species. Here we report a study of the critical period for monocular deprivation in Long-Evans rats in which visual pattern sweep evoked potentials (sweep VEP) was used. Successful recording of sweep VEPs depended on establishing a stable light plane of anesthesia. We found a mixture of halothane and NO2 to be suitable. During a single trial lasting 10 s, anesthetized rats (n = 28) viewed a sinusoidal contrast grating (spatial frequency of 0.13 cycles/deg) that reversed phase at 3 Hz. During the trial, the grating contrast increased logarithmically from 1 to 70%. Extracellular recording pipettes were placed bilaterally in layers II/III of the binocular regions of primary visual cortex. Stimulating the right and left eye on alternate trials, sweep VEP amplitudes were collected for 30 trials from each eye. In monocularly deprived animals, the right eyelid had been sutured for 5 days before recording. Age at suture varied from P19 to P86. In 12 of 13 rats sutured between P19 and P50, the crossed response from the deprived eye was smaller than the crossed response from the nondeprived eye. The same relation prevailed for the uncrossed responses in 11 of 13 animals. There was no significant monocular deprivation effect in animals sutured between P55 and P86 (n = 9). Dark rearing until approximately P90 followed by 5 days of eyelid suture resulted in a strong monocular deprivation effect in both crossed and uncrossed pathways (n = 3). There was little effect of dark rearing alone on the size the sweep VEPs (n = 3). The critical period reported here lasts at least 2 wk longer than reported for rats by Fagliolini et al. and for mice by Gordon and Stryker. Both previous studies used single unit recording rather than the sweep VEP method.

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PubMed1986

Regulation of the circadian clock in the Aplysia eye: mimicry of neural action by serotonin.

In Aplysia, activity of efferent fibers in the optic nerve can influence the circadian clock in the eye. In addition, serotonin (5-HT) is present in the eye and influences the function of the clock. Accordingly, we hypothesized that 5-HT is the transmitter of the optic efferents, and tested the prediction that exogenous 5-HT would mimic the action of the optic efferents on the clock. We also tested the prediction that the action of the efferents would be prevented by blocking synaptic secretions with high Mg2+, low Ca2+ (HMLC). Activity of the optic efferents enhances clock resetting in response to the onset of darkness. We used this neural enhancement as a measure of neural action on the eye clock. We found that HMLC blocked neural enhancement. Serotonin enhanced resetting to the same extent as efferent activity. Enhancement by 5-HT did not summate with neural enhancement. High concentrations of 5-HT ([5-HT] greater than or equal to 6 X 10(-4) did not cause enhancement. High concentrations of 5-HT also blocked neural enhancement. Enhancement by 5-HT depended on the phase of drug application, much as neural enhancement depends on the phase of neural activity. Enhancement by 5-HT depended on day length in a manner similar to the enhancement by neural activity. HMLC did not block the facilitatory action of 5-HT. Several other transmitters that may be active in the eye did not enhance resetting.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1981

In vitro resetting of the circadian clock in the Aplysia eye. I. Importance of efferent activity in optic nerve.

A transition from constant light (LL) to constant darkness (DD) will reset the circadian rhythms of most organisms to a phase that normally occurs near dusk. We tested the circadian oscillator in the Aplysia eye for this property. The test was run in vitro under two conditions. Using the two eyes of a single animal, one eye was left attached to the cerebral ganglion by its intact optic nerve and the other was detached by cutting its nerve. The amount of LL preceding LL/DD was the independent variable; the phase of the two eyes was the measured variable. When LL less than 12 hr, neither the cut nor the attached eye was reset by LL/DD. When 12 less than or equal to LL less than or equal to 24 hr, the attached eye was reset but the detached eye was not. Thus, for these durations of LL, resetting by LL/DD was found to be dependent on the integrity of optic nerve. When LL was about 21 hr, the differential response of the two eyes caused them to be about 12 hr out of phase. When LL was between 27 and 75 hr, LL/DD reset both eyes but there was a low amplitude cyclic modulation of about +/- 3 hr in the phase to which they were reset by LL/DD. This modulation shows that LL did not stop the eye clock but rather that LL/DD reset its phase while it was free running in LL.

Animals↗
PubMed1981

In vitro resetting of the circadian clock in the Aplysia eye. II. The critical period for optic nerve activity.

When constant light is 18, 21, or 24 hr, a constant light to constant darkness (LL/DD) transition in vitro results in a phase difference (delta psi) between an eye that is attached to the cerebral ganglion and its partner that is detached by cutting its optic nerve just prior to the LL/DD. This delta psi develops during the first 24 hr after LL/DD as the result of efferent activity in the optic nerve of the attached eye. By cutting the nerve of the original attached eye at various times after LL/DD, we determined when the phase resetting nerve activity occurs. This experiment was carried out following LL = 18, 21, and 24 hr. Optic nerve activity at the time of and for several hours after LL/DD did not produce nerve-dependent resetting (NDR). Instead, there was a restricted critical period, 2 to 3 hr long during which the effective nerve activity occurred. Following 24 hr of LL, a 2-hr window of optic nerve activity during the critical period could produce NDR, but a 2-hr window outside of the critical period was ineffective. The resetting effect of nerve activity was produced suddenly as if NDR were an all-or-nothing event. Following 18, 21, and 24 hr of LL, the critical period occurred 10, 7, and 4 hr, respectively, after LL/DD. In each case, this was about 28 hr after the last dawn of the light cycles to which the animal had been exposed prior to LL. We conclude that the critical period is timed by a mechanism that is not reset by LL/DD.

Action Potentials↗
PubMed1981

In vitro resetting of the circadian clock in the Aplysia eye. III. Location of photoreceptors that signal continuous light to continuous darkness.

As shown in the previous two papers (Prichard, R.G., and M.E. Lickey (1981 a, b) J. Neurosci. 1: 835-839; 840-845), the circadian rhythm of compound action potentials (CAPs) from the Aplysia eye can be reset in vitro by single transitions from continuous light to continuous darkness (LL/DD). The magnitude of the reset depends on the duration of LL that precedes the LL/DD. When LL duration is 18, 21, or 24 hr, the magnitude of the reset is different if the eye is neurally attached to the brain than if it is neurally detached. The brain gives rise to optic efferent fibers that terminate in the retina. In the present paper, we explore how the optic efferents contribute to resetting by asking whether LL/DD is sensed by the photoreceptors known to exist in the brain or those in the eye. Eye-brain preparations were placed in a special recording chamber in which the eye and brain could be isolated photically from each other while one optic nerve remained intact. The LL/DD then was delivered to the eyes and to the brain at different times. During the separate illumination, neural communication between the eyes and brain was prevented by reversible nerve blockade. The magnitude of the resulting resets always corresponded to the duration of LL that was delivered to the eyes. Photoreceptors in the brain did not contribute effectively to resetting. Also, resetting was not disturbed by nerve blockade that began before LL/DD and lasted for more than 6 hr after LL/DD. This implies that information about the timing of LL/DD was stored in the eye for more than 6 hr before it was expressed in the form of a reset. We conclude that the efferent fibers in the optic nerve do not instruct the eye about the magnitude of the reset. Instead, they activate or modulate circadian functions that are latent in the eye itself.

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