Table 1.

Several Examples of Neuronal Plasticity Paradigms That Are Altered in Models of Fetal Alcohol Spectrum Disorders

		Type of Neuronal Plasticity	Timing of Exposurea	Speciesb	Region Affected	References
		Long-term potentiation	I-II, III, I-III	R, GP	Hippocampus	1,2,3
		Long-term depression	I-II, III	M	Hippocampus, cerebellum	4,5
		Ocular dominance plasticity	III	F, M	Visual cortex	6,7
		Barrel cortex plasticity	I-II	R	Somatosensory cortex	8
		Eyeblink conditioning	III	R	Hippocampus, cerebellum, inferior olivary nucleus	9
		Water maze performance	III	R, GP	Hippocampus	3,10,11
		Fear conditioning	I-III, III	R, M	Hippocampus, amygdala	12,13,14
		Lesion-induced plasticity	I-II	R	Olfactory tubercle, hippocampus	15,16
		Olfactory response to alcohol	I-II	R	Olfactory bulb, trigeminal system	17

^aEquivalents to trimesters of human gestation.

^bR = rats; M = mice; GP = guinea pig; F = ferret.

Downward arrows = Decrease of function. Upward arrows = Increase of function. Gray star = Servais and others (2007) showed that LTD at the parallel fiber-Purkinje cell synapses was converted to LTP.

References: 1 = Puglia and Valenzuela (2010); 2 = Sutherland and others (1997); 3 = Richardson and others (2002); 4 = Servais and others (2007); 5 = Izumi and others (2005); 6 = Medina and others (2003); 7 = Medina and Ramoa (2005); 8 = Rema and Ebner (1999); 9 = Stanton and Goodlett (1998); 10 = Goodlett and Johnson (1997); 11 = Girard and others (2000); 12 = Ieraci and Herrera (2006); 13 = Murawski and Stanton (2010); 14 = Savage and others (2010); 15 = Gottesfeld and others (1989); 16 = West and others (1984); 17 = Youngentob and Glendinning (2009).