Biomedical subjects

Catalin V Buhusi

Publications and source records attributed to Catalin V Buhusi.

9 recordsLinked to original sources

PubMed2006

Effect of clozapine on interval timing and working memory for time in the peak-interval procedure with gaps.

Previous research indicates that dopamine controls both the speed of an internal clock [Maricq, A.V., Church, R.M., 1983. The differential effects of haloperidol and methamphetamine on time estimation in the rat. Psychopharmacology 79, 10-15] and sharing of resources between the timer and other cognitive processes [Buhusi, C.V., 2003. Dopaminergic mechanisms of interval timing and attention. In: Meck, W.H. (Ed.), Functional and Neural Mechanisms of Interval Timing. CRC Press, Boca Raton, FL, pp. 317-338]. For example, dopamine agonist methamphetamine increases the speed of an internal clock and resets timing after a gap, while dopamine antagonist haloperidol decreases the speed of an internal clock and stops timing during a gap [Buhusi, C.V., Meck, W.H., 2002. Differential effects of methamphetamine and haloperidol on the control of an internal clock. Behav. Neurosci. 116, 291-297]. Using a 20-s peak-interval procedure with gaps we examined the acute effects of clozapine (2.0mg/kg i.p.), which exerts differential effects on dopamine and serotonin in the cortex and striatum, two brain areas involved in interval timing and working memory. Relative to saline, clozapine injections shifted the response functions leftward both in trials with and without gaps, suggesting that clozapine increased the speed of an internal clock and facilitated the maintenance of the pre-gap interval in working memory. These results suggest that clozapine exerts effects in different brain areas in a manner that allows for the pharmacological separation of clock speed and working memory as a function of peak trials without and with gaps.

Algorithms↗

PubMed2006

Time-sharing in pigeons: Independent effects of gap duration, position and discriminability from the timed signal.

Previous data suggest that in a peak-interval procedure with gaps, memory for the pre-gap interval varies with the discriminability of the gap from the to-be-timed signal. Here we extend this finding by manipulating the pre-gap and gap intervals as well as the visual contrast between the gap and the to-be-timed signal. The delay in response function after the gap was found to vary with the duration and position of the gap. However, for each gap duration and position, the delay in response increased with the gap-signal contrast: at 60% gap-signal contrast pigeons continued to accumulate time during the gap, at 80% gap-signal contrast pigeons stopped timing during the gap, and at 100% gap-signal contrast pigeons reset their timing after the gap. Data are accounted for by a time-sharing model assuming two concurrent processes during the gap--time accumulation and memory decay controlled by the salience of the gap--whose interplay results in a continuum of responses in the gap procedure.

Algorithms↗

PubMed2006

Time sharing in rats: A peak-interval procedure with gaps and distracters.

Four hypotheses (switch, instructional-ambiguity, memory decay, and time sharing) were evaluated in a reversed peak-interval procedure with gaps by presenting distracter stimuli during the uninterrupted timed signal. The switch, instructional-ambiguity, and memory-decay hypotheses predict that subjects should time through the distracter and delay responding during gaps. The time-sharing hypothesis assumes that the internal clock shares attentional and working-memory resources with other processes, so that both gaps and distracters delay timing by causing working memory to decay. We found that response functions were displaced both by gaps and by distracters. Computer simulations show that when combined, the memory-decay and time-sharing hypotheses can mechanistically address present data, suggesting that these two hypotheses may reflect different levels of analysis of the same phenomenon.

Animals↗

PubMed2006

Interval timing with gaps and distracters: evaluation of the ambiguity, switch, and time-sharing hypotheses.

Gaps and distracters were presented during the timed signal to examine whether the stop/reset mechanism is activated by (a) changes in the timed signal (switch hypothesis), (b) ITI-like events (ambiguity hypothesis), or (c) processes concurrent with the timing process (time-sharing hypothesis). While the switch and ambiguity hypotheses predict that rats should time through (ignore) distracters, the time-sharing hypothesis predicts that extraneous events (e.g., gaps and distracters) delay timing by causing working memory to decay in proportion to the events' salience. The authors found that response functions were displaced by both gaps and distracters, in accord with the time-sharing hypothesis. Computer simulations show that the time-sharing and memory-decay hypotheses can mechanistically address present data, and reflect different levels of the same model.

Analysis of Variance↗

PubMed2005

Memory for timing visual and auditory signals in albino and pigmented rats.

The authors hypothesized that during a gap in a timed signal, the time accumulated during the pregap interval decays at a rate proportional to the perceived salience of the gap, influenced by sensory acuity and signal intensity. When timing visual signals, albino (Sprague-Dawley) rats, which have poor visual acuity, stopped timing irrespective of gap duration, whereas pigmented (Long-Evans) rats, which have good visual acuity, stopped timing for short gaps but reset timing for long gaps. Pigmented rats stopped timing during a gap in a low-intensity visual signal and reset after a gap in a high-intensity visual signal, suggesting that memory for time in the gap procedure varies with the perceived salience of the gap, possibly through an attentional mechanism.

Animals↗

PubMed2005

What makes us tick? Functional and neural mechanisms of interval timing.

Time is a fundamental dimension of life. It is crucial for decisions about quantity, speed of movement and rate of return, as well as for motor control in walking, speech, playing or appreciating music, and participating in sports. Traditionally, the way in which time is perceived, represented and estimated has been explained using a pacemaker-accumulator model that is not only straightforward, but also surprisingly powerful in explaining behavioural and biological data. However, recent advances have challenged this traditional view. It is now proposed that the brain represents time in a distributed manner and tells the time by detecting the coincidental activation of different neural populations.

Animals↗

PubMed2003

Interval timing as an emergent learning property.

Interval timing in operant conditioning is the learned covariation of a temporal dependent measure such as wait time with a temporal independent variable such as fixed-interval duration. The dominant theories of interval timing all incorporate an explicit internal clock, or "pacemaker," despite its lack of independent evidence. The authors propose an alternative, pacemaker-free view that demonstrates that temporal discrimination can be explained by using only 2 assumptions: (a) variation and selection of responses through competition between reinforced behavior and all other, elicited, behaviors and (b) modulation of the strength of response competition by the memory for recent reinforcement. The model departs radically from existing timing models: It shows that temporal learning can emerge from a simple dynamic process that lacks a periodic time reference such as a pacemaker.

Conditioning, Operant↗

PubMed2002

Differential effects of methamphetamine and haloperidol on the control of an internal clock.

Humans and animals process temporal information as if they were using an internal stopwatch that can be stopped and reset, and whose speed is adjustable. Previous data suggest that dopaminergic drugs affect the speed of this internal stopwatch. Using a paradigm in which rats have to filter out the gaps that (sometimes) interrupted timing, the authors found that methamphetamine and haloperidol also affect the stop and reset mechanism of the internal clock, possibly by modulating attentional components that are dependent on the content and salience of the timed events. This is the first report of both clock and attentional effects of dopaminergic drugs on interval timing in the same experimental setting.

Animals↗

PubMed2002

Temporal integration as a function of signal and gap intensity in rats (Rattus norvegicus) and pigeons (Columba livia).

Previous data suggest that rats (Rattus norvegicus) and pigeons (Columba livia) use different interval-timing strategies when a gap interrupts a to-be-timed signal: Rats stop timing during the gap, and pigeons reset their timing mechanism after the gap. To examine whether the response rule is controlled by an attentional mechanism dependent on the characteristics of the stimuli, the authors manipulated the intensity of the signal and gap when rats and pigeons timed in the gap procedure. Results suggest that both rats and pigeons stop timing during a nonsalient gap and reset timing after a salient gap. These results also suggest that both species use similar interval-timing mechanisms, influenced by nontemporal characteristics of the signal and gap.

Animals↗