Table 2.
Summary for the identification acetylcholine receptor abnormalities in the sudden infant death syndrome brainstem.
| Reference | Receptor | Samples | Results |
|---|---|---|---|
| (34) | nAChR | Procedure of all animal from National Institutes of Health Care | Calcineurin activation and reduced intracellular calcium by L-type channels |
| (34) | Neuronal nicotinic acetylcholine receptors (nAChR), α7, β2 | Rats | The existence of nicotine (10 M) in hypoxic insult secured a subpopulation |
| (35) | Nicotinic acetylcholine receptors, β2+/+ mice | Animals were used from the National Research Center | Modulate β2-nAChRs to the survival of infant brain cells |
| (36) | Nicotinic cholinergic receptor (nAChR) | Feminine rats | Reduced nAChR expression in dopaminergic areas in the duration of adolescence |
| (31) | Nicotine impairs breathing | Age-matched wild-mutant mice deficient the subunit β2 nAChR gene | The nAChRs are vital in breathing in the duration of sleeping and are important for the ordinary improvement in the mechanisms of arousal |
| (33) | Nicotine and preBotzinger complex | Medullary slice | Nicotinic acetylcholine receptors (nAChRs) activation improved the tonic synaptic excitatory input to inspiratory neurons |
| (37) | Nicotinic acetylcholine receptors (nAChRs) | The animals used were an adult male, age-matched | nAChRs with β2 contribute activity in REMS, NREMS, and the promoting effect of stress |