Table 1

Selective declines in striatal ¹²⁵I-α-conotoxin MII,¹²⁵I-epibatidine, and [¹²⁵I]A85380 receptor sites after MPTP treatment

Region	Radioligand	Control	MPTP	Percentage of Control
		fmol/mg of tissue
Striatum	[¹²⁵I]RTI-121	10.93 ± 0.64	1.63 ± 0.15***	15
	¹²⁵I-α-Conotoxin MII	0.77 ± 0.06	0.18 ± 0.03***	23
	¹²⁵I-Epibatidine	6.43 ± 0.09	4.70 ± 0.11***	73
	[¹²⁵I]A85380	7.84 ± 0.06	5.28 ± 0.06***	67
	¹²⁵I-α-Bungarotoxin	6.94 ± 0.28	6.38 ± 0.07	92
Cortex	[¹²⁵I]RTI-121	N.D.	N.D.
	¹²⁵I-α-Conotoxin MII	N.D.	N.D.
	¹²⁵I-Epibatidine	5.26 ± 0.16	5.34 ± 0.13	102
	[¹²⁵I]A85380	6.34 ± 0.06	6.23 ± 0.11	98
	¹²⁵I-α-Bungarotoxin	6.59 ± 0.14	6.38 ± 0.28	97
Septal Area	[¹²⁵I]RTI-121	N.D.	N.D.
	¹²⁵I-α-Conotoxin MII	N.D.	N.D.
	¹²⁵I-Epibatidine	2.85 ± 0.17	2.93 ± 0.06	103
	[¹²⁵I]A85380	3.84 ± 0.11	3.73 ± 0.06	97
	¹²⁵I-α-Bungarotoxin	2.29 ± 0.07	2.36 ± 0.14	103

In striatum, there were significant declines in¹²⁵I-α-conotoxin MII, ¹²⁵I-epibatidine, and [¹²⁵I]A85380 binding with lesioning, but no change in¹²⁵I-α-bungarotoxin sites. In contrast, there were no alterations in binding of any of the nAChR radioligands in the cortex or septal area of animals after MPTP treatment.¹²⁵I-α-Conotoxin MII sites were determined at 0.5 nM of the radioligand, ¹²⁵I-epibatidine at 0.03 nM, [¹²⁵I]A85380 at 0.095 nM, and¹²⁵I-α-bungarotoxin at 3.0 nM. These concentrations were selected to yield an optimal ratio of specific to nonspecific binding or were based on availability (¹²⁵I-epibatidine). Because these concentrations are not maximal, it is not possible to directly compare the density of sites measured with the different radioligands. Each value represents the mean ± S.E.M. of five to six animals.

N.D., not detected.
1-165 , P < 0.001 compared with control.