Abnormal Functional Organization in the Dorsal Lateral Geniculate Nucleus of Mice Lacking the β2 Subunit of the Nicotinic Acetylcholine Receptor (original) (raw)
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Annals of the New York Academy of Sciences, 2002
dependent induction and expression of functional plasticity in the barrel cortex of the adult rat. J Neurophysiol 86: 422-437, 2001. Feller MB. The role of nAChR-mediated spontaneous retinal activity in visual system development. J Neurobiol 53: 556-567, 2002. Flores CM, Rogers SW, Pabreza LA, Wolfe BB and Kellar KJ. A subtype of nicotinic cholinergic receptor in rat brain is composed of alpha 4 and beta 2 subunits and is up-regulated by chronic nicotine treatment. Mol Pharmacol 41: 31-37, 1992.
Functional Nicotinic Acetylcholine Receptors Are Expressed in B Lymphocyte-Derived Cell Lines
Molecular Pharmacology, 2003
dependent induction and expression of functional plasticity in the barrel cortex of the adult rat. J Neurophysiol 86: 422-437, 2001. Feller MB. The role of nAChR-mediated spontaneous retinal activity in visual system development. J Neurobiol 53: 556-567, 2002. Flores CM, Rogers SW, Pabreza LA, Wolfe BB and Kellar KJ. A subtype of nicotinic cholinergic receptor in rat brain is composed of alpha 4 and beta 2 subunits and is up-regulated by chronic nicotine treatment. Mol Pharmacol 41: 31-37, 1992.
Postnatal development of two nicotinic cholinergic receptors in seven mouse brain regions
International Journal of Developmental Neuroscience, 1990
The developmental profiles for binding of ~-['~I]b~garotoxin and L-[3H]nicotine to putative nicotinic cholinergic receptors were determined in seven mouse brain regions. The overall pattern of development of a-bungarotoxin binding was similar in all of the regions. Neonatal binding values tended to be greater than those observed in adult brain regions. Maximal binding occurred within 10 days of birth and adult binding values were reached by 20 days of age. The patterns of development of nicotine binding in each of the seven brain regions differed according to re8ion. Gross similarities in developmental protiles for nicotine binding were found among the more caudal and among the more rostra1 regions. In hindbr~n and cerebellum, maxima1 nicotine binding was found at birth (5 days of age in cerebellum); binding declined approximately 4-fold by 20 days and remained relatively constant thereafter. In midbrain and hypothalamus, a less extensive decrease in nicotine binding occurred from birth to adulthood (midbrain, 25%; hypothalamus, 50%). Nicotine binding in hippocampus and cortex remained unchanged between birth and adulthood. The developmental pattern for nicotine binding in striatum differed from that found in the other brain repions. At 5 days of age, binding was about 65% of adult binding, which was reached at 30 days of age. In most of the brain regions the developmental profile for n-bungarotoxin binding was different from that of nicotine. This difference. was especially notable in striatum, where adult nicotine binding was higher than neonatal nicotine binding, whereas adult a-bungarotoxin binding was lower than neonatal a-bungarotoxin binding.
Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System
Annual Review of Pharmacology and Toxicology, 2007
Subtypes of neuronal nicotinic acetylcholine receptors (nAChRs) are constructed from numerous subunit combinations that compose channel-receptor complexes with varied functional and pharmacological characteristics. Structural and functional diversity and the broad presynaptic, postsynaptic, and nonsynaptic locations of nAChRs underlie their mainly modulatory roles throughout the mammalian brain. Presynaptic and preterminal nicotinic receptors enhance neurotransmitter release, postsynaptic nAChRs contribute a small minority of fast excitatory transmission, and nonsynaptic nAChRs modulate many neurotransmitter systems by influencing neuronal excitability. Nicotinic receptors have roles in development and synaptic plasticity, and nicotinic mechanisms participate in learning, memory, and attention. Decline, disruption, or alterations of nicotinic cholinergic mechanisms contribute to dysfunctions such as epilepsy, schizophrenia, Parkinson's disease, autism, dementia with Lewy bodies,...
Pharmacology & Therapeutics, 2001
Nicotinic acetylcholine receptors (nAChRs) in the muscle, autonomic ganglia, and brain are targets for pharmacologically administered nicotine. Several of the subunits that combine to form neuronal nicotinic receptors have been deleted by knockout or mutated by knockin in mice using homologous recombination. We will review the biochemical, pharmacological, anatomical, physiological, and behavioral phenotypes of mice with genetically altered neuronal nAChR subunits. Clinically relevant mutations in nAChR genes will also be discussed. In addition, some of the signal transduction pathways activated through nAChRs will be described in order to delineate the longer-term changes that might result from persistent activation or inactivation of nAChRs. Genetically manipulated mice have greatly increased our understanding of the subunit composition and physiological properties of nAChRs in vivo. In addition, these mice have provided a model system to determine the molecular basis for many of the pharmacological actions of nicotine on neurotransmitter release and behavior. Genetic manipulations in mice have also elucidated the role of nAChR subunits in various disease states, and suggest several avenues for drug development. D
Function of Mammalian Nicotinic Acetylcholine Receptors
Nicotinic Acetylcholine Receptor, 1986
This paper will briefly review the results of our studies of the function of the nicotinic acetylcholine receptors (AChRs) expressed by clonal mammalian BC3H-1 cells in vitro. The observations and interpretations will be compared with expectations based on the physiology of junctional transmission and with data obtained by others. BC3H-1 cells are a cell line which originated in a brain tumor of C3H mice (Schubert et al., 1974). These cells differentiate in culture and express a large number of AChR. A number of studies have established that the AChR are similar to skeletal muscle receptors biochemically (Boulter and Patrick, 1977), pharmacologically (Patrick et al., 1977; Sine and Taylor, 1981) and in the primary amino acid sequence of the subunits (LaPolla et al., 1984; Boulter et aI, 1985). The methods used have been described (Sine and Steinbach, 1984a,b; 1986a,b,c). The data discussed here were obtained at 11°C using cell attached patches. Cells
Immunohistochemical localization of a neuronal nicotinic acetylcholine receptor in mammalian brain
Proceedings of the National Academy of Sciences, 1987
A monoclonal antibody generated against purified acetylcholine receptor from Torpedo electric organ was used to immunohistochemically localize a neuronal nicotinic acetylcholine receptor. Regions of the rat brain stained with this antibody paralleled those areas of the brain exhibiting [3H]nicotine binding sites and corresponded to areas in which mRNAs encoding for alpha subunits of the neuronal nicotinic acetylcholine receptor are present. Thus, the anteroventral thalamus, cortex, hippocampus, medial habenula, interpeduncular nucleus, and substantia nigra/ventral tegmental area exhibited significant immunoreactivity. Neurons of the medial habenula and substantia nigra were densely stained, and processes were prominently delineated. Furthermore, in the projection areas of the medial habenula (interpeduncular nucleus and median raphe) axons were strongly immunoreactive and were distributed to distinct subdivisions of the target sites. The present data suggest that there are several d...
Journal of Chemical Neuroanatomy, 2010
We provide the first quantification and localization of the nicotinic acetylcholine receptors (nAChRs) a7 and b2 in the human adult and infant brainstem and hippocampus. After applying immunohistochemistry on formalin fixed and paraffin embedded human brain tissue, we qualitatively analyzed the staining to provide a comparison in expression amongst the brainstem nuclei and hippocampal regions, and between the infants and adults. Amongst the brainstem regions studied, the greatest protein expression for both a7 and b2 subunits was in the motor nuclei of the medulla and pons. Lowest expression for both subunits was in the midbrain nuclei, except for the oculomotor nucleus. Comparison between infants and adults showed greater expression in the infant brainstem nuclei of the dorsal motor nucleus of the vagus, hypoglossal, inferior olivary nucleus, nucleus of the solitary tract, abducens, and facial nuclei, for both a7 and b2 nAChRs. In the hippocampus, only the a7 subunit showed greater expression in infants compared to adults. We conclude that both a7 and b2 containing nAChRs play an important role in many nuclei of the human infant and adult brainstem, and that the a7 subunit may have a more prominent role in the infant than adult hippocampus. ß
FEBS letters, 1996
The tz31]~4 subtype of neuronal nicotinic acetylcholine receptor (nAChR) was stably expressed in human embryonic kidney (HEK) 293 cells that co-expressed a voltage-gated Ca 2+ channel. ¢z3/134-nAChR-expressing clones were identified using the fura-2 Ca 2÷ imaging technique, and were further characterised by single-cell and whole-cell patch-clamp studies. Acetylcholine (ACh) induced fast activating currents which showed desensitisation and inward rectification. The conductance of the ACh-activated channel was 29 pS. The order of potency of the nicotinic agonists tested was cytisine -=-nicotine > acetylcholine. The ECs0 value for ACh was 145 I~VI; the Hill coefficient was close to 2. The currents elicited by ACh were effectively blocked by nicotinic antagonists, but not by the muscarinic antagonist atropine. These properties are comparable to the pharmacological and physiological profile of ganglionic nicotinic receptors and type III currents of cultured Idppocampal neurons.