Neuronal activity in rabbit neostriatum during classical eyelid conditioning

Abstract

Extracellular multiple- and single-unit recordings were made from the neostriatum of rabbits during classical eyelid conditioning. Neostriatal neurons processed information regarding the conditioned auditory stimulus (CS) and conditioned eyelid response (CR) as well as the unconditioned stimulus/response (US/UR). These data are consistent with previous reports that neostriatal neurons respond to movement and movement-related sensory stimuli. In most cases, neostriatal neurons increased activity to the US during the early phase of training, but to the CR as training progressed. A close temporal correlation was found between neuronal activity and CR onset with unit discharges typically preceding CR onset by 10-50 ms. The activity of some multiple and single units was monitored after injection of haloperidol, a neuroleptic and dopamine antagonist known to disrupt neostriatal function. Interestingly, haloperidol caused a greater disruption of CRs at low-intensity than at high-intensity CSs, but conditioning-related neuronal activity was disrupted equally at both intensities. These data are discussed in terms of a possible role for the neostriatum in eyelid conditioning.

Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography.

“…Although some lesion and recording studies in the rabbit have suggested striatal involvement in eyeblink conditioning (14,15), the nature of that involvement has not been clarified and may be a fruitful area for investigation in rabbits and humans. However, the striatum has been implicated as critical for other procedural learning tasks in humans and other animals (42)(43)(44)(45).…”

“…In addition, lesions of the hippocampus, which do not interfere with acquisition of simple delay conditioning, do interfere with context conditioning and markedly impair learning in more complex paradigms (7)(8)(9)(10). Other forebrain areas, including basal ganglia, neocortex, and septal nuclei, have been less extensively studied but may also play a role in eyeblink conditioning (11)(12)(13)(14)(15)(16).-Human lesion studies are consistent with what is known about the organization of eyeblink conditioning in the rabbit brain. Several studies (17)(18)(19)(20)(21) have found that individuals with cerebellar damage show impaired eyeblink conditioning largely in the absence of motor deficits interfering with performance of unconditioned eyeblinks.…”

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

“…Thus, lesions of frontal cortex can alter CR latency (Fox et al 1982); lesions of prefrontal cortex and mediodorsal thalamic nuclei slow the rate of acquisition (Buchanan and Powell 1982;Buchanan 1991;Buchanan et al 1997a,b;Powell et al 2000; see below), as do medial septal lesions (Berry and Thompson 1979) neostriatal lesions (Kao and Powell 1988; see also recordings by Richardson and Thompson 1985;White et al 1994), and amygdala lesions (see below). A number of brain areas show the development of the learninginduced neuronal model of the CR in eyeblink conditioning.…”

Learning in Parkinson's disease: eyeblink conditioning, declarative learning, and procedural learning

“…This decreased firing rate does not occur when the striatum is depleted of dopamine with an infusion of 1-methy-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)2 or when dopamine receptors in the striatum are blocked 3. When White et al 4 studied eyeblink classical conditioning in rabbits, they found a shift in striatal cellular activity during the learning process, indicating the involvement of basal ganglia in conditioning. In their opinion, the neostriatum may modulate the timing of eyeblink classical conditioning.…”