GABAA and GABAB receptors differentially regulate striatal acetylcholine release in vivo

Anderson, Jeffrey J.; Kuo, Shirley; Chase, Thomas N.; Engber, Thomas M.

doi:10.1016/0304-3940(93)90395-2

Cited by 39 publications

(21 citation statements)

References 19 publications

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“…Evidence shows that LICI is mediated through long-lasting GABA B -dependent inhibitory postsynaptic potentials (IPSPs) and activation of pre-synaptic GABA B receptors on inhibitory interneurons (34). Interactions between cholinergic and GABA-ergic pathways may account for our finding (35). Cognitive functions were not only positively correlated with LICI measures but also with brain atrophy, specifically in the left IPL, an area which has been previously shown to be affected early and prominently in AD patients (36).…”

Section: Discussionmentioning

confidence: 64%

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Brem¹,

Atkinson²,

Seligson³

et al. 2013

Front. Psychiatry

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Acetylcholinesterase inhibitors (AChEIs) are the most commonly prescribed monotherapeutic medications for Alzheimer’s disease (AD). However, their underlying neurophysiological effects remain largely unknown. We investigated the effects of monotherapy (AChEI) and combination therapy (AChEI and memantine) on brain reactivity and plasticity. Patients treated with monotherapy (AChEI) (N = 7) were compared to patients receiving combination therapy (COM) (N = 9) and a group of age-matched, healthy controls (HCs) (N = 13). Cortical reactivity and plasticity of the motor cortex were examined using transcranial magnetic stimulation. Cognitive functions were assessed with the cognitive subscale of the Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), activities of daily living (ADLs) with the ADCS-ADL. In addition we assessed the degree of brain atrophy by measuring brain-scalp distances in seven different brain areas. Patient groups differed in resting motor threshold and brain atrophy, with COM showing a lower motor threshold but less atrophy than AChEI. COM showed similar plasticity effects as the HC group, while plasticity was reduced in AChEI. Long-interval intracortical inhibition (LICI) was impaired in both patient groups when compared to HC. ADAS-Cog scores were positively correlated with LICI measures and with brain atrophy, specifically in the left inferior parietal cortex. AD patients treated with mono- or combination-therapy show distinct neurophysiological patterns. Further studies should investigate whether these measures might serve as biomarkers of treatment response and whether they could guide other therapeutic interventions.

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Section: Discussionmentioning

confidence: 64%

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Brem¹,

Atkinson²,

Seligson³

et al. 2013

Front. Psychiatry

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“…This outcome indicates the existence of a D 1 -mediated inhibitory influence on striatal ACh output that is dependent on D 1 receptors located within the striatum. We hypothesize that this inhibition of striatal ACh efflux may be exerted via a direct D 1 -mediated activation of striatal GABA neurons that, in turn, can inhibit the cholinergic interneurons through GABA A receptors (Anderson et al, 1993;DeBoer and Westerink, 1994). In support of this hypothesis, the excitatory component of the cholinergic response to systemic D-amphetamine was enhanced by local application of the GABA A receptor antagonist bicuculline, indicating the removal of an offsetting GABAergic influence that normally is operative in this condition.…”

Section: Discussionmentioning

confidence: 68%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

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Dopamine release can regulate striatal acetylcholine efflux in vivo through at least two receptor mechanisms: (1) direct inhibition by dopamine D 2 receptors on the cholinergic neurons, and (2) excitation initiated by dopamine D 1 receptors. The neuroanatomical locus of the latter population of D 1 receptors and the pathway(s) involved in the expression of their influence are controversial issues. We have tested the hypothesis that D 1 receptors in substantia nigra pars reticulata are involved in the excitatory component of dopaminergic actions on striatal acetylcholine output. In vivo microdialysis was used in awake rats. Infusion of the selective D 1 receptor agonist R(ϩ)-1-Phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) hydrochloride into pars reticulata of substantia nigra elicited a significant increase in striatal acetylcholine efflux. Likewise, D-amphetamine applied into pars reticulata of substantia nigra by reverse dialysis produced an elevation in acetylcholine output measured at a second microdialysis probe in the striatum. Application of D-amphetamine in the striatum by reverse dialysis elicited a decrease in striatal acetylcholine efflux that could be reversed subsequently by local application of Damphetamine in substantia nigra pars reticulata. A 2 mg/kg intraperitoneal dose of D-amphetamine, which has no net effect on striatal acetylcholine output under control conditions, elicited a significant decrease in acetylcholine efflux when the D 1 receptor antagonist R(ϩ)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride was applied simultaneously via a second microdialysis probe in substantia nigra pars reticulata. Thus, an excitatory D 1 -mediated influence on striatal acetylcholine output is initiated in substantia nigra pars reticulata, and this influence contributes to the effects of indirect dopaminergic agonists such as D-amphetamine on striatal acetylcholine efflux. These results indicate an important role of somatodendritic dopamine release, in addition to nerve terminal dopamine release, in the regulation of activity in basal ganglia circuits.

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“…Postsynaptic GABA responses, e.g., modulation of acetylcholine release in cholinergic neurons, are thought to be mediated by GABA A receptors (Anderson et al, 1993;DeBoer and Westerink, 1994;Ikarashi et al, 1999). Although anatomical data have confirmed that presynaptic GABA B R1 immunoreactivity is found in striatal axonal terminals that form asymmetrical synapses (Charara et al, 2000), intense GABA B R1 immunoreactivity is also found in cellular elements Charara et al, 2000).…”

Section: Functional Postsynaptic Gaba B Receptors In Striatal Neurons?mentioning

confidence: 95%

Differential expression of GABA_BR1 and GABA_BR2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum

Yung

2001

J of Comparative Neurology

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Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the neostriatum. Functions of GABA are known to mediate GABA(A) and GABA(B) receptors. A functional GABA(B) receptor is known to compose of heteromeric subunits, namely the GABA(B)R1 and GABA(B)R2 subunits. Our previous report (Yung et al. [1999] Brain Res. 830:345-352) has demonstrated that all major subpopulations of striatal neurons express GABA(B)R1 immunoreactivity. The cellular localization of the second subunit of GABA(B) receptor protein, i.e., GABA(B)R2 immunoreactivity, in the rat neostriatum is not yet known. By using a new commercially available specific antibody against GABA(B)R2, immunofluorescence was performed to investigate the cellular expression of GABA(B)R2 in neurochemically identified subpopulations of neurons in the rat neostriatum. Immunoreactivity for GABA(B)R2 was primarily found in the neuropil of the rat neostriatum. Double labeling revealed that those perikarya that expressed immunoreactivity for parvalbumin, choline acetyltransferase, nitric oxide synthase, glutamate receptor two, N-methyl-D-aspartate receptor one, or GABA(A)alpha1 receptor, respectively, did not express GABA(B)R2 immunoreactivity. In addition, perikarya and most of the neuropilar elements in the neostriatum that expressed glutamic acid decarboxylase 67 immunoreactivity were found to be GABA(B)R2-negative. In contrast, immunoreactivity for GABA(B)R1 was found to be expressed by all of the above neuronal subpopulations. Moreover, a vast number of SV2-immunoreactive profiles and a number of tyrosine hydroxylase-immunoreactive profiles in the neuropil of the neostriatum were found to display GABA(B)R2 immunoreactivity. The present results indicate that there is a differential expression of GABA(B)R2 and GABA(B)R1 immunoreactivity in different subpopulations of striatal neurons that are identified by their specific neurochemical markers. Immunoreactivity for GABA(B)R2 is likely to localize in neuropilar elements of the neostriatum that may belong to non-GABAergic elements. These findings provide anatomical evidence of GABA(B)R2 receptor localization in the neostriatum that may have an important functional implication of the GABA(B)-mediated functions in neurons of the neostriatum.

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GABAA and GABAB receptors differentially regulate striatal acetylcholine release in vivo

Cited by 39 publications

References 19 publications

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Differential expression of GABA_BR1 and GABA_BR2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum

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GABAA and GABAB receptors differentially regulate striatal acetylcholine release in vivo

Cited by 39 publications

References 19 publications

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Differential Pharmacological Effects on Brain Reactivity and Plasticity in Alzheimer’s Disease

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Differential expression of GABABR1 and GABABR2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum

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Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Differential expression of GABA_BR1 and GABA_BR2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum