Area:
superior colliculus, visual orientation, pain, basal ganglia
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High-probability grants
According to our matching algorithm, John G. McHaffie is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1995 — 1998 |
Mchaffie, John George |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Cns Mechanisms Involved in Orientation Behavior |
1 |
1999 — 2003 |
Mchaffie, John George |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Cortical-Subcortical Mechanisms Involved in Orientation @ Wake Forest University Health Sciences
Experiments in the 1980's established that the basal ganglia is critical to the expression of superior colliculus (SC)- mediated orientation behaviors. They physiology of the double inhibitory striato-nigro-tectal circuit mediating this interaction is well known: increased activity of striatal neurons suppresses the tonic inhibitory effects normally imposed by substantia nigra (SNr) neurons on SC tectospinal output neurons. The disinhibition of tectospinal neurons allows them to influence eye/head movements via their connections with regions of the brainstem and spinal cord. However, recent advances in unraveling the intrinsic circuitry of the basal ganglia have heightened our appreciation of the role played by inhibition in shaping motor behaviors. This has provided impetus to the emerging idea that the essential contribution of the basal ganglia to motor behavior is to coordinate selections of desired responses among competing, and often conflicting, behavioral needs. Thus, while desired motor behaviors are to be engaged (by disinhibition), competing sensory and/or motor responses that might otherwise interfere with the intended movements must be prevented (by inhibition). Indeed, contemporary models of the limb movement control by the globus pallidus, pars interna (the functional homologue of the SNr for limb movements have incorporated both processes. Nevertheless, despite the obvious implications that such synergistic processes would have in transforming our current understanding of the SC, no effort has been made to integrate such concepts into models of SC-mediated behaviors. Based on our observations made in the previous grant period, we propose a model wherein the basal ganglia uses three distinct populations of nigrotectal neurons, coupling focal disinhibition with widespread inhibition tot modulate SC activity. These influences are exerted via crossed and uncrossed nigrotectal neurons to coordinate activity in the colliculi on both sides of the brain. Specifically, phasic inhibition of GABAergic nigrotectal neurons in the ipsilateral SNr produces disinhibition of tectospinal neurons in the ipsilateral 'saccade zone' that specify the metrics of the desired eye/head movements. At the same time, phasic activation of GABAergic nigrotectal neurons in the rostral aspect of the same SNr inhibits both ipsilateral fixation neurons (to disengage fixation) and contralateral saccade neurons (that might initiate opposing movements). Thus, competing sensory stimuli and/or motor events are prevented from gaining access to the brainstem circuitry that could impair the accuracy of the specified movement. Experiments to test the predictions of this model will provide insights into the interplay that exists between cortical and subcortical structures and how such activity is coordinated by the basal ganglia.
|
0.96 |
2004 — 2012 |
Mchaffie, John George |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Cortical-Subcortical Mechanisms in Orientation Behavior @ Wake Forest University Health Sciences
DESCRIPTION (provided by applicant): The influence of visual cortex on the midbrain superior colliculus (SC) is essential for normal visual orientation behaviors, and the loss of such capabilities after unilateral cortical lesions has long been presumed to reflect the loss of excitatory cortico-colliculus inputs to the ipsilateral SC. Surprisingly, however, these lesion-induced deficits in visual orientation are ameliorated by a second lesion; one that eliminates basal ganglia inputs to the SC from the opposite side of the brain. This suggests that the basal ganglia is a critical but poorly understood factor, not only in the manifestation of this particular dysfunction, but also in the normal interhemispheric control of the subcortical processes that underlie visuomotor behavior. We suggest that visual cortex lesions produce visual hemineglect in part because cortical damage induces secondary alterations bilaterally within the basal ganglia. The most important of these changes in the present context are those in the basal ganglia output signals that reach the SC from the opposite side of the brain (i.e., the crossed nigro-colliculus pathway), which ultimately renders the SC ipsilateral to the cortical lesion nonfunctional. We suggest that cortical lesions that produce this dysfunction do so by inducing NMDA-mediated processes that act within the input structures of the basal ganglia on the opposite side of the brain and become, in turn, manifested in its crossed nigro-colliculus output signals. We propose to investigate how the basal ganglia is affected by cortical lesions and to evaluate whether pretreatment with NMDA antagonists can preclude these visuomotor deficits by preventing the normal sequelae of secondary events that normally follow visual cortical lesions. The proposed investigations will involve a multidisciplinary anatomical, behavioral, pharmacological, and physiological approach. The results of these experiments will provide insight into the delicate interplay between the basal ganglia and SC that is essential for SC-mediated visuomotor processes, examine how basal ganglia-SC control is orchestrated by inputs from visual cortex, and determine the changes in basal ganglia-SC processes that are induced by visual cortical lesions that disrupt the physiology of the SC and the visuomotor behaviors it controls. Understanding the strategic role of the basal ganglia in mediating visual hemineglect after visual cortical lesions may facilitate the development of therapeutic strategies for ameliorating this debilitating condition in human patients.
|
0.96 |