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PubMed1999

The role of nucleus accumbens dopamine in motivated behavior: a unifying interpretation with special reference to reward-seeking.

Studies addressing behavioral functions of dopamine (DA) in the nucleus accumbens septi (NAS) are reviewed. A role of NAS DA in reward has long been suggested. However, some investigators have questioned the role of NAS DA in rewarding effects because of its role in aversive contexts. As findings supporting the role of NAS DA in mediating aversively motivated behaviors accumulate, it is necessary to accommodate such data for understanding the role of NAS DA in behavior. The aim of the present paper is to provide a unifying interpretation that can account for the functions of NAS DA in a variety of behavioral contexts: (1) its role in appetitive behavioral arousal, (2) its role as a facilitator as well as an inducer of reward processes, and (3) its presently undefined role in aversive contexts. The present analysis suggests that NAS DA plays an important role in sensorimotor integrations that facilitate flexible approach responses. Flexible approach responses are contrasted with fixed instrumental approach responses (habits), which may involve the nigro-striatal DA system more than the meso-accumbens DA system. Functional properties of NAS DA transmission are considered in two stages: unconditioned behavioral invigoration effects and incentive learning effects. (1) When organisms are presented with salient stimuli (e.g., novel stimuli and incentive stimuli), NAS DA is released and invigorates flexible approach responses (invigoration effects). (2) When proximal exteroceptive receptors are stimulated by unconditioned stimuli, NAS DA is released and enables stimulus representations to acquire incentive properties within specific environmental context. It is important to make a distinction that NAS DA is a critical component for the conditional formation of incentive representations but not the retrieval of incentive stimuli or behavioral expressions based on over-learned incentive responses (i.e., habits). Nor is NAS DA essential for the cognitive perception of environmental stimuli. Therefore, even without normal NAS DA transmission, the habit response system still allows animals to perform instrumental responses given that the tasks take place in fixed environment. Such a role of NAS DA as an incentive-property constructor is not limited to appetitive contexts but also aversive contexts. This dual action of NAS DA in invigoration and incentive learning may explain the rewarding effects of NAS DA as well as other effects of NAS DA in a variety of contexts including avoidance and unconditioned/conditioned increases in open-field locomotor activity. Particularly, the present hypothesis offers the following interpretation for the finding that both conditioned and unconditioned aversive stimuli stimulate DA release in the NAS: NAS DA invigorates approach responses toward 'safety'. Moreover, NAS DA modulates incentive properties of the environment so that organisms emit approach responses toward 'safety' (i.e., avoidance responses) when animals later encounter similar environmental contexts. There may be no obligatory relationship between NAS DA release and positive subjective effects, even though these systems probably interact with other brain systems which can mediate such effects. The present conceptual framework may be valuable in understanding the dynamic interplay of NAS DA neurochemistry and behavior, both normal and pathophysiological.

Animals↗

PubMed2000

Role of primary sensorimotor cortices in generating inhibitory motor response in humans.

To clarify the mechanism by which inhibitory motor responses such as cortical negative myoclonus are generated in humans, three patients with medically intractable partial epilepsy (two with frontal lobe epilepsy and one with parietal lobe epilepsy) were studied by means of direct cortical stimulation with a single electric pulse through subdural electrodes. All underwent chronic long-term video/EEG monitoring, cortical mapping by 50 Hz electric cortical stimulation and recording of cortical somatosensory evoked potentials with chronically implanted subdural grid electrodes (3 mm in diameter and centre-to-centre distance of 1 cm) to map both epileptogenic and functional zones. After these clinical evaluations, cortical stimulation by single electric pulse (0.3 ms duration, 1 Hz) was carried out through pairs of subdural electrodes located at the primary sensorimotor area (MI-SI), pre-supplementary motor area (pre-SMA) and lateral negative motor area (lateral NMA), while surface EMG was recorded from the muscles of the contralateral hand. The results showed that (i) in all subjects, single pulse stimulation of MI-SI elicited a motor evoked potential (MEP) followed by a silent period (SP) in the contralateral distal hand muscles, the latter lasting 300 ms after the stimulus. The duration of SP was proportional to the size of the preceding MEP. In one subject, SP without any preceding MEP was elicited, and, in another subject, there was a short SP immediately before MEP in the contralateral thenar muscle. (ii) Following the stimulation of either pre-SMA or lateral NMA, no SP was observed. It is concluded that the inhibitory mechanism within the MI-SI, but probably not in the non-primary motor areas, either closely linked to or completely independent of excitation, most likely plays an important role in eliciting brief negative motor phenomena such as cortical negative myoclonus or SP.

Adult↗

PubMed2002

Analysis of fMRI and finger tracking training in subjects with chronic stroke.

Hand movement recovery and cortical reorganization were studied in 10 subjects with chronic stroke using functional MRI (fMRI) before and after training with an intensive finger movement tracking programme. Subjects were assigned randomly to a treatment or control group. The treatment group received 18-20 sessions of finger tracking training using target waveforms under variable conditions. The control group crossed over to receive the same treatment after the control period. For comparison with a healthy population, nine well elderly females were also studied; however, the well elderly controls did not cross over after the control period. The dependent variables consisted of a Box and Block score to measure prehensile ability (subjects with stroke only), a tracking accuracy score and quantification of active cortical areas using fMRI. For the tracking tests, the subjects tracked a sine wave target on a computer screen with extension and flexion movements of the paretic index finger. Functional brain images were collected from the frontal and parietal lobes of the subject with a 4 tesla magnet. Areas of interest included the sensorimotor cortex (SMC), primary motor area (M1), primary sensory area (S1), premotor cortex (PMC) and supplementary motor area (SMA). Comparison between all subjects with stroke and all well elderly subjects at pre-test was analysed with two-sample t-tests. Change from pre-test to post-test within subjects was analysed with paired t-tests. Statistical significance was set at P < 0.05. Stroke treatment subjects demonstrated significant improvement in tracking accuracy, whereas stroke control subjects did not until after crossover treatment. At pre-test, the cortical activation in the subjects with stroke was predominantly ipsilateral to the performing hand, whereas in the well elderly subjects it was contralateral. Activation for the stroke treatment group following training switched to contralateral in SMC, M1, S1 and PMC. The stroke control group's activation remained ipsilateral after the control period, but switched to contralateral after crossover to receive treatment. All well elderly subjects maintained predominantly contralateral activation throughout. Transfer of skill to functional activity was shown in significantly improved Box and Block scores for the stroke treatment group, with no such improvement in the stroke control group until after crossover. We concluded that individuals with chronic stroke receiving intensive tracking training showed improved tracking accuracy and grasp and release function, and that these improvements were accompanied by brain reorganization.

Adult↗

PubMed2005

Evolutionary autonomous agents and the nature of apraxia.

BACKGROUND: Evolutionary autonomous agents are robots or robot simulations whose controller is a dynamical neural network and whose evolution occurs autonomously under the guidance of a fitness function without the detailed or explicit direction of an external programmer. They are embodied agents with a simple neural network controller and as such they provide the optimal forum by which sensorimotor interactions in a specified environment can be studied without the computational assumptions inherent in standard neuroscience. METHODS: Evolutionary autonomous agents were evolved that were able to perform identical movements under two different contexts, one which represented an automatic movement and one which had a symbolic context. In an attempt to model the automatic-voluntary dissociation frequently seen in ideomotor apraxia, lesions were introduced into the neural network controllers resulting in a behavioral dissociation with loss of the ability to perform the movement which had a symbolic context and preservation of the simpler, automatic movement. RESULTS: Analysis of the changes in the hierarchical organization of the networks in the apractic EAAs demonstrated consistent changes in the network dynamics across all agents with loss of longer duration time scales in the network dynamics. CONCLUSION: The concepts of determinate motor programs and perceptual representations that are implicit in the present day understanding of ideomotor apraxia are assumptions inherent in the computational understanding of brain function. The strength of the present study using EAAs to model one aspect of ideomotor apraxia is the absence of these assumptions and a grounding of all sensorimotor interactions in an embodied, autonomous agent. The consistency of the hierarchical changes in the network dynamics across all apractic agents demonstrates that this technique is tenable and will be a valuable adjunct to a computational formalism in the understanding of the physical basis of neurological disorders.

Apraxias↗

PubMed1984

Behavioural effects of manipulation of basal ganglia neurotransmitters.

Topographically organized dopaminergic projections from the extrapyramidal structures of the ventral mesencephalon (substantia nigra and ventral tegmental area) to the dorsal (body of caudate-putamen) and ventral (anterior-ventral caudate, nucleus accumbens, tuberculum olfactorium) striatum subserve sensorimotor integration in the rat. Selective depletion of DA impairs the animal's ability to integrate sensory input with motor output; in the dorsal striatum the exteroceptive sensory input and in the ventral or limbic striatum the interoceptive input principally related to motivation and affect. Grafts of fetal DA neurons to the damaged dorsal striatum reverse sensorimotor asymmetry and sensory neglect. A large number of other excitatory and inhibitory neurotransmitters, including recently discovered neuropeptides, contribute to the functional balance afforded by the DA neurons. This chemical heterogeneity of the basal ganglia offers the possibility that novel therapeutic approaches with drugs could be used to control the chemical imbalances in basal ganglia that are associated with a number of neurological and psychiatric conditions.

Acetylcholine↗

PubMed2006

Modulation of excitability as an early change leading to structural adaptation in the motor cortex.

The excitability of the motor cortex is a function of single cell excitability, synaptic strength, and the balance between excitatory cells and inhibitory cells. Sustained periods of sensory stimulation enhance the excitability in the motor cortex. This adaptation, which represents an early change in cortical network function effective in motor learning and recovery from a motor deficit, is followed by longer-lasting changes, such as modifications in cortical somatotopy, and by structural plasticity. Interventions aiming at increasing excitability also positively affect learning processes. Recent studies highlight that the cerebellum, especially the interpositus nucleus, plays a key function in the adaptation of the motor cortex to repeated trains of peripheral stimulation. Interpositus neurons, which receive inputs from the sensorimotor cortex and the spinal cord, are involved in somesthetic reflex behaviors and assist the cerebral cortex in transforming sensory signals to motor-oriented commands by acting via the cerebello-thalamo-cortical projections. Moreover, climbing fibers originating in the inferior olivary complex and innervating the nucleus interpositus mediate highly integrated sensorimotor information derived from spinal modules. The intermediate cerebellum allows the motor cortex to tune the gain of polysynaptic responses originating from the spinal cord after repetitive trains of peripheral stimulation, allowing an online calibration of cutaneo-muscular responses.

Adaptation, Physiological↗

PubMed2002

Dystonia: a disorder of motor programming or motor execution?

For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H-reflex examination, long-latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration.

Cerebral Cortex↗

PubMed2000

Coordination of prehensile forces during precision grip in Huntington's disease.

The present study examined the coordination of prehensile forces during precision grip in subjects with Huntington's disease (HD). Fingertip forces were measured in 12 subjects with HD and 12 age-matched controls during the lifting of an instrumented object whose weight and surface texture were varied. The results indicate that subjects with HD have impaired initiation and delayed transitions between movement sequences and produce excessive and variable forces. However, subjects with HD demonstrated anticipatory scaling of force development based on the object's expected physical properties (planning) and adjustment of the force to the object's actual physical properties (sensorimotor integration). The observed findings generally were unrelated to the overall disease severity. However, the variability in forces was correlated with functional capacity and motor performance suggesting that variability is a key feature of the motor deficit. These results provide insights into the impaired hand function observed in individuals with HD.

Adult↗

PubMed2001

Neural circuit regulation of prepulse inhibition of startle in the rat: current knowledge and future challenges.

RATIONALE: Sensorimotor gating of the startle reflex can be assessed across species, using similar stimuli to elicit similar responses. Prepulse inhibition (PPI), a measure of sensorimotor gating, is reduced in patients with some neuropsychiatric disorders, and in rats after manipulations of limbic cortex, striatum, pallidum or pontine tegmentum ("CSPP" circuitry). OBJECTIVE: To review the current knowledge of the neural circuit regulation of PPI in rats, and to anticipate the future challenges facing this line of inquiry. METHODS: The published literature was reviewed and critically evaluated. RESULTS: Limbic CSPP circuitry has been studied in rats to reveal the neurochemical and neuroanatomical substrates regulating PPI at a high level of resolution. In translational cross-species research, this detailed circuit information is used as a "blueprint" to identify substrates that may lead to PPI deficits in psychiatrically disordered humans. Some human disorders with identifiable, localized lesions in CSPP circuitry may provide direct validation for the contribution of CSPP circuitry to this cross-species model. The rapid collection of experimental data supporting this cross-species PPI circuit "blueprint" has supported continuing advances in the development of theoretical models for understanding how this circuitry normally functions to regulate PPI. Such models are needed for building a conceptual framework for understanding the role of this circuitry in the regulation of sensorimotor gating in normal humans, and in the relative loss of sensorimotor gating, and the resulting clinical consequences, in individuals with particular neuropsychiatric disorders. CONCLUSIONS: Our understanding of the neural regulation of PPI has increased tremendously over the past 15 years. Progress has come in "broad strokes", and a number of important details and complex questions remain to be addressed. It is anticipated that this is a "work in progress", and that the precise models for the neural regulation of PPI will evolve substantially in the coming years.

Animals↗

PubMed2006

Neonatal hippocampal Tat injections: developmental effects on prepulse inhibition (PPI) of the auditory startle response.

The current estimate of children (<15 years) living with HIV and AIDS is 2.2 million. The major source of infection occurs through vertical transmission of the virus from mother to child during delivery [UNAIDS/WHO, 2005. AIDS Epidemic Update. UNAIDS, Geneva]. Recent studies have shown that timing of HIV-1 infection might be related to the onset and rate of progression of CNS disease. The effects of HIV on the brain are thought to be mediated indirectly through the viral toxins Tat and gp120. This study characterized developmental effects on PPI following intrahippocampal administration of Tat. On postnatal day (P)1, one male and one female pup from each of eight Sprague-Dawley litters were bilaterally injected with 50 microg Tat or saline (1 microl volume). Animals were tested for PPI of the auditory startle response (ASR) (ISIs of 0, 8, 40, 80, 120, and 4000 ms, six trial blocks, Latin-square design) on days 30, 60 and 90. Tat altered PPI and the pattern of alterations was different for males and females. For males, a leftward shift was evident in the ISI for maximal inhibition of the response on day 30 and on day 60 (chi(2)(1)=4.7, p< or =.03, and chi(2)(1)=5.3, p< or =.02, respectively), but not on day 90. For females, Tat altered peak ASR latency across PPI trials (8-120 ms) at all days of testing (30, 60, and 90 days of age), as indexed by orthogonal component analyses, indicating less modulation of PPI by ISI. Data collected from a second group that were tested only once at 90 days of age, suggested that the observed adverse Tat effects for males and females early in development were maintained with age. Thus, the diminishing TAT effect on PPI at day 90 in a longitudinal study design was attributed to repeated testing, rather than 'recovery of function'. Collectively, the data suggested that hippocampal Tat injections in neonatal rats produced alterations in the pre-attentive process of sensorimotor gating, as indexed by PPI.

Acoustic Stimulation↗

PubMed2004

Facilitation of motor skill learning by callosal denervation or forced forelimb use in adult rats.

Unilateral forelimb sensorimotor cortex lesions in adult rats produce a compensatory hyper-reliance on the forelimb ipsilateral to the lesion and temporally related glial and neural plasticity in the contralateral homotopic cortex. Recently, we found that these lesions enhance acquisition of a motor skills task with the ipsilateral, non-impaired, forelimb in comparison to shams. This effect might be related to a denervation-induced facilitation of neuroplastic changes in the motor cortex opposite the lesion and/or to the lesion-induced hyper-reliance on the non-impaired forelimb. The present study assessed whether increased forelimb use, denervation of motor cortical callosal afferents, or a combination of the two influences acquisition of a skilled reaching task. Adult rats with partial corpus callosum transections or sham procedures were either forced to rely on one forelimb or permitted normal forelimb use for 8 days. Rats were then trained for 14 days with their previously non-preferred forelimb (and the forced-use limb) on a unilateral pellet retrieval task. Compared to shams, transections produced a greater acquisition rate and asymptotic performance level on the task. Forced-use improved reaching performance relative to controls, but this effect was less enduring than the improvements produced by transections alone. The addition of forced-use to transections did not further enhance performance. These findings suggest that denervation-induced changes are likely to be a major contributor to the enhanced learning observed after unilateral sensorimotor cortex lesions.

Animals↗

PubMed1999

Structure-activity studies of conantokins as human N-methyl-D-aspartate receptor modulators.

The activities of conantokin-G (con-G), conantokin-T (con-T), and several novel analogues have been studied using polyamine enhancement of [3H]MK-801 binding to human glutamate-N-methyl-D-aspartate (NMDA) receptors, and their structures have been examined using CD and 1H NMR spectroscopy. The potencies of con-G[A7], con-G, and con-T as noncompetitive inhibitors of spermine-enhanced [3H]MK-801 binding to NMDA receptor obtained from human brain tissue are similar to those obtained using rat brain tissue. The secondary structure and activity of con-G are found to be highly sensitive to amino acid substitution and modification. NMR chemical shift data indicate that con-G, con-G[D8, D17], and con-G[A7] have similar conformations in the presence of Ca2+. This consists of a helix for residues 2-16, which is kinked in the vicinity of Gla10. This is confirmed by 3D structure calculations on con-G[A7]. Restraining this helix in a linear form (i.e., con-G[A7,E10-K13]) results in a minor reduction in potency. Incorporation of a 7-10 salt-bridge replacement (con-G[K7-E10]) prevents helix formation in aqueous solution and produces a peptide with low potency. Peptides with the Leu5-Tyr5 substitution also have low potencies (con-G[Y5,A7] and con-G[Y5,K7]) indicating that Leu5 in con-G is important for full antagonist behavior. We have also shown that the Gla-Ala7 substitution increases potency, whereas the Gla-Lys7 substitution has no effect. Con-G and con-G[K7] both exhibit selectivity between NMDA subtypes from mid-frontal and superior temporal gyri, but not between sensorimotor and mid-frontal gyri. Asn8 and/or Asn17 appear to be important for the ability of con-G to function as an inhibitor of polyamine-stimulated [3H]MK-801 binding, but not in maintaining secondary structure. The presence of Ca2+ does not increase the potencies of con-G and con-T for NMDA receptors but does stabilize the helical structures of con-G, con-G[D8,D17], and, to a lesser extent, con-G[A7]. The NMR data support the existence of at least two independent Ca2+-chelating sites in con-G, one involving Gla7 and possibly Gla3 and the other likely to involve Gla10 and/or Gla14.

Amino Acid Sequence↗

PubMed2005

Structural-metabolic organization of field 4 of the cat brain in normal conditions and after unilateral enucleation of the eye.

Comparative data on the structural-metabolic organization of field 4 of the cat brain in normal conditions and after unilateral enucleation of the eye are presented. Cytochrome oxidase was detected histochemically. Data were processed by a computerized method using an original video capture system. Data were obtained demonstrating the uneven distribution of enzyme along sublayer IlIb of field 4 in animals with unilateral enucleation. A hypothesis based on published data is suggested whereby the alternation of high- and low-reactive areas is evidence for the ordering of the retinal representations of the right and left eyes in the sensorimotor cortex.

Animals↗

PubMed1986

Rats given dopamine-depleting brain lesions as neonates do not respond to acute homeostatic imbalances as adults.

Rats given near-total dopamine-depleting brain lesions as neonates exhibit none of the severe sensorimotor or ingestive dysfunctions that result when adult rats are given comparable lesions. These experiments showed that the apparent sparing of function is incomplete; when tested as adults, the brain-damaged animals did not eat in response to acute glucoprivation, nor did they drink water and saline in response to hypovolemia. Indeed, after receiving these homeostatic challenges, the animals became much less able to simply move about. In contrast to these marked effects, the dopamine-depleted rats ate normally after glucoprivation when they were handled hourly instead of being left alone. Similarly, administration of caffeine permitted them to drink while hypovolemic. These and other observations suggest that some central neurons other than those containing dopamine are responsible for maintaining behavioral activation in rats after neonatal destruction of dopaminergic fiber systems in the brain and that the homeostatic challenges compromise their function and thereby disrupt behavior.

Adaptation, Physiological↗

PubMed2005

Activation of D1, but not D2 receptors potentiates dizocilpine-mediated disruption of prepulse inhibition of the startle.

Although substantial evidence has shown interactions between glutamatergic and dopaminergic systems play a cardinal role in the regulation of attentional processes, their involvement in informational filtering has been poorly investigated. Chiefly, little research has focused on functional correlations between the dopaminergic system and the mechanism of action of N-methyl-D-aspartate (NMDA) receptor antagonists on sensorimotor gating. The present study was targeted at evaluating whether the activation of D1 and D2 receptors is able to interact with the disruption of prepulse inhibition (PPI) of startle mediated by dizocilpine, a selective, noncompetitive NMDA receptor antagonist. We tested the effects of SKF 38393 ((+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol) (10 mg/kg, s.c.), a selective D1 agonist, and quinpirole (0.3, 0.6 mg/kg, s.c.), a D2 agonist, in rats, per se and in cotreatment with different doses of dizocilpine, ranging from 0.0015 to 0.15 mg/kg (s.c.). Subsequently, the effect of the D1 antagonist SCH 23390 ((R)-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine) (0.05, 0.1 mg/kg, s.c.) on PPI disruptions mediated by dizocilpine and by combination of dizocilpine and SKF 38393 was tested. Two further experiments were performed to verify whether the synergic effect of the D1 agonist with dizocilpine was counteracted by effective doses of haloperidol (0.1, 0.5 mg/kg, i.p.) and clozapine (5, 10 mg/kg, i.p.). All experiments were carried out using standard procedures for the assessment of PPI of the acoustic startle reflex. SKF 38393, while unable to impair sensorimotor gating alone, induced PPI disruption in cotreatment with 0.05 and 0.15 mg/kg of dizocilpine, both ineffective per se. Furthermore, this effect was reversed by SCH 23390, but not by haloperidol or clozapine. Conversely, no synergistic effect was exhibited between quinpirole and dizocilpine, at any given dose. These findings suggest that D1, but not D2 receptors, enhance the disruptive effect of dizocilpine on PPI.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1998

Behavioral studies of hallucinogenic drugs in animals: implications for schizophrenia research.

Schizophrenic and schizotypal patients exhibit deficits in the habituation and prepulse inhibition (PPI) of startle responses, providing operational measures of the sensorimotor gating or filtering deficits suggested to contribute to cognitive disorganization in these patients. In rats, hallucinogens, entactogens, and NMDA antagonists share the ability to both retard startle habituation and disrupt PPI. Extensive pharmacological studies in rats have indicated that the effects of hallucinogens on habituation are mediated by direct agonist actions at 5-HT2 receptors. The effects of the entactogens on both habituation and PPI reflect indirect agonist actions due to the stimulation of presynaptic serotonin release. These observations in rats have supported the development of 5-HT2A antagonists for the treatment of schizophrenia. Animal studies have shown that PPI is modulated by multiple interacting neurotransmitters, including dopaminergic, serotonergic, cholinergic, GABAergic, and glutamatergic systems within cortical, limbic, striatal, and brainstem structures. The effects of PCP and other NMDA antagonists on PPI are insensitive to either dopaminergic or serotonergic antagonists, but are reduced by atypical antipsychotics such as clozapine, olanzapine, and Seroquel. Thus, the PCP model of schizophrenia-like deficits in sensorimotor gating offers promise for the identification and neurobiological investigation of atypical antipsychotics. The cross-species study of homologous gating functions, such as habituation and PPI, in animal models and psychiatric patients provides novel opportunities for the exploration of neurobiological substrates relevant to the group of schizophrenias.

Animals↗

PubMed1994

Selection-based learning in bird song development.

Bird song is a model system for study of the neurobiology, development, and functions of learned vocal communication signals. Research on avian song learning has been dominated by an instructive model of learning--the sensorimotor model. Developmental plasticity is assumed to be based on the incorporation of novel material into the song repertoire. Experimental evidence now indicates an alternative form of plasticity operating in harmony with sensorimotor learning, based on principles of selection, rather than instruction. Song dialects, a common consequence of vocal learning, can be achieved by overproduction of previously memorized songs and selective attrition of those that fail to match the dialect of interacting males. These distinct processes of learning have important implications for study of the neural substrates underlying song production and perception and for efforts to interpret patterns of geographic variation in song.

Aging↗

PubMed2004

Functional anatomy of motor recovery after early brain damage.

Functional magnetic resonance imaging and transcranial magnetic stimulation were used to examine a 34 year-old right-handed patient, who, at the age of 6 years, had experienced sudden right hemiplegia, seizures, and stupor during a bout of measles encephalitis, followed by incomplete distal right motor recovery. Morphological MRI showed massive unilateral enlargement of the left ventricle, associated with extreme thinning of the white and gray matter,with partial preservation of the pyramidal tract. Functional MRI and transcranial magnetic stimulation revealed reorganization of the motor cortices, and integrity of the corticospinal pathway, respectively. Our findings indicate that complete hand motor recovery may require functional connections between the motor cortical areas and cortical-subcortical structures, in addition to the retained integrity of the primary sensorimotor area and pyramidal tract.

Adult↗

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