Biomedical subjects

Brian I Hyland

Publications and source records attributed to Brian I Hyland.

6 recordsLinked to original sources

PubMed2005

Motor preparation in a memorised delay task.

The effect on reaction time (RT) and movement time (MT) of remembering which one of several targets to move to was investigated in 18 participants who completed 416 trials in each task. On each trial, participants moved their index finger from a central, illuminated switch (the stimulus) to one of eight targets located on the circumference of a 6 cm radius circle. A visual cue (illumination of the target) informed the participant of the appropriate target. In the memorised delay task, the cued target was lit for 300 ms followed by a variable (450-750 ms) foreperiod during which the participant was required to remember the location of the target until the stimulus light was extinguished. In the non-memorised delay task, the target remained lit during the entire foreperiod (750-1050 ms) until the response was completed. At the "go" signal (stimulus light extinguished) participants moved as quickly and accurately as possible to the cued target. Both RT and MT were significantly (p<0.05) longer in the memorised delay task. The increase in RT shows that remembering which target imposed a greater load on motor preparation even though all the information needed for preparing the response was presented in the cue at the beginning of each trial. The increase in MT raises the possibility that movement execution was also programmed during motor preparation.

Adult↗

PubMed2005

Dopamine cells respond to predicted events during classical conditioning: evidence for eligibility traces in the reward-learning network.

Behavioral conditioning of cue-reward pairing results in a shift of midbrain dopamine (DA) cell activity from responding to the reward to responding to the predictive cue. However, the precise time course and mechanism underlying this shift remain unclear. Here, we report a combined single-unit recording and temporal difference (TD) modeling approach to this question. The data from recordings in conscious rats showed that DA cells retain responses to predicted reward after responses to conditioned cues have developed, at least early in training. This contrasts with previous TD models that predict a gradual stepwise shift in latency with responses to rewards lost before responses develop to the conditioned cue. By exploring the TD parameter space, we demonstrate that the persistent reward responses of DA cells during conditioning are only accurately replicated by a TD model with long-lasting eligibility traces (nonzero values for the parameter lambda) and low learning rate (alpha). These physiological constraints for TD parameters suggest that eligibility traces and low per-trial rates of plastic modification may be essential features of neural circuits for reward learning in the brain. Such properties enable rapid but stable initiation of learning when the number of stimulus-reward pairings is limited, conferring significant adaptive advantages in real-world environments.

Action Potentials↗

PubMed2005

Bradykinesia induced by dopamine D2 receptor blockade is associated with reduced motor cortex activity in the rat.

Disruption of motor cortex activity is hypothesized to play a major role in the slowed movement (bradykinesia) associated with reduced dopaminergic function. We recorded single neurons in the motor cortex of free-moving rats performing a forelimb-reaching task. The same neurons were examined before and after induction of bradykinesia with the D2 dopamine receptor antagonist haloperidol. Within-cell changes in the firing rate and firing pattern of individual cells and the correlation between simultaneously recorded cells after injection of haloperidol were statistically compared with vehicle-only control experiments. During haloperidol-induced bradykinesia (mean movement time increase, +231%), there was an average 11% decrease in baseline firing rate. Movement-related peaks in firing rate were more dramatically affected, with an overall reduction in peak amplitudes of 40%. Bradykinesia was also associated with decreased intensity of bursting and amplitude of cross-correlation peaks at rest. The results show for the first time that significant reductions can be detected in motor cortex activity at rest in animals with impaired ability to generate movements induced by reduced dopamine action and confirm that impaired movements are associated with reduced cortical activation. Together, these changes in neural activity may reduce recruitment and rate modulation of motor units in the spinal cord.

Animals↗

PubMed2005

Pedunculopontine tegmental nucleus controls conditioned responses of midbrain dopamine neurons in behaving rats.

Midbrain dopamine (DA) neurons respond to sensory cues that predict reward. We tested the hypothesis that projections from the pedunculopontine tegmental nucleus (PPTg) are involved in driving this DA cell activity. First, the activity of PPTg and DA neurons was compared in a cued-reward associative learning paradigm. The majority of PPTg neurons showed phasic responses to the onset of sensory cues, at significantly shorter latency than DA cells, consistent with a PPTg-to-DA transmission of information. However, unlike DA cells, PPTg responses were almost entirely independent of whether signals were associated with rewards. Second, DA neuron responses to the cues were recorded in free-moving rats during reversible inactivation of the PPTg by microinfusion of local anesthetic. The results showed clear suppression of conditioned sensory responses of DA neurons after PPTg inactivation that was not seen after saline infusion or in non-DA cells. We propose that the PPTg relays information about the precise timing of attended sensory events, which is integrated with information about reward context by DA neurons.

Acoustic Stimulation↗

PubMed2004

Modulation of an afterhyperpolarization by the substantia nigra induces pauses in the tonic firing of striatal cholinergic interneurons.

Striatal cholinergic interneurons, also known as tonically active neurons (TANs), acquire a pause in firing during learning of stimulus-reward associations. This pause response to a sensory stimulus emerges after repeated pairing with a reward. The conditioned pause is dependent on dopamine from the substantia nigra, but its underlying cellular mechanism is unknown. Using in vivo intracellular recording, we found that both subthreshold and suprathreshold depolarizations in cholinergic interneurons induced a prolonged after-hyperpolarization (AHP) associated with a pause in their tonic firing. The AHP duration was dependent on the level of depolarization, whether elicited by intracellular current injection or by activation of excitatory inputs from the cortex. High-frequency stimulation of the substantia nigra induced potentiation of the cortically evoked excitation and increased the prolonged AHP after the stimulus. These findings from anesthetized animals suggest that a substantia nigra-induced AHP produces stimulus-associated firing pauses in cholinergic interneurons. This mechanism may underlie the acquisition of the pause response in TANs recorded from behaving animals during learning.

Action Potentials↗

PubMed2003

Neural mechanisms of reward-related motor learning.

The analysis of the neural mechanisms responsible for reward-related learning has benefited from recent studies of the effects of dopamine on synaptic plasticity. Dopamine-dependent synaptic plasticity may lead to strengthening of selected inputs on the basis of an activity-dependent conjunction of sensory afferent activity, motor output activity, and temporally related firing of dopamine cells. Such plasticity may provide a link between the reward-related firing of dopamine cells and the acquisition of changes in striatal cell activity during learning. This learning mechanism may play a special role in the translation of reward signals into context-dependent response probability or directional bias in movement responses.

Animals↗