MNEMONIC DEFICITS IN THE DOUBLE Y-MAZE ARE RELATED TO THE EFFECTS OF NUCLEUS BASALIS INJECTIONS OF IBOTENIC AND QUISQUALIC ACID ON CHOLINE-ACETYLTRANSFERASE IN THE RAT AMYGDALA
Rj. Beninger et al., MNEMONIC DEFICITS IN THE DOUBLE Y-MAZE ARE RELATED TO THE EFFECTS OF NUCLEUS BASALIS INJECTIONS OF IBOTENIC AND QUISQUALIC ACID ON CHOLINE-ACETYLTRANSFERASE IN THE RAT AMYGDALA, Brain research bulletin, 35(2), 1994, pp. 147-152
Many researchers have reported that the magnitude of decrease in corti
cal choline acetyltransferase (ChAT) following excitotoxic lesions of
the nucleus basalis magnocellularis (nbm) is unrelated to the degree o
f cognitive impairment. Recently, an explanation has been offered for
this lack of correlation: different excitotoxins, when injected into t
he nbm, differentially affected cholinergic projections to the cortex
and amygdala, and those excitotoxins previously reported to produce th
e greatest mnemonic deficits produced the largest decreases in amygdal
oid ChAT. The present study evaluated the role of amygdalofugal cholin
ergic projections in memory by comparing the effects of intra-nbm ibot
enic and quisqualic acid on cortical and amygdaloid ChAT and on mnemon
ic performance in the double Y-maze. Rats were trained in the double Y
-maze until working and reference memory choice accuracy stabilized to
a criterion of greater than or equal to 78% correct. Rats then were g
iven either bilateral quisqualic acid (60 nmol in 0.5 mu l), bilateral
ibotenic acid (50 nmol in 0.5 mu l), or sham (0.9% saline in 0.5 mu l
) lesions of the nbm, and again were tested on the maze. Quisqualate p
roduced a selective impairment of working memory, a large (51%) decrea
se in cortical ChAT and a small (17%) decrease in amygdaloid ChAT; ibo
tenate, on the other hand, produced a greater impairment of working me
mory, an impairment of reference memory, a similar (51%) decrease in c
ortical ChAT, but a greater (30%) decrease in amygdaloid ChAT. These r
esults suggest that the cholinergic projections from the nbm to the co
rtex and amygdala play an important role in memory. They suggest that
excitotoxins producing greater depletions of amygdaloid ChAT produce g
reater mnemonic deficits.