whole brain [1] of rats. Gulya et al., [7] have suggested that

increase in AChE activity following aluminium exposure was due

to allosteric interaction between the cation in the brain and a

peripheral anionic site of the enzyme molecule. Bilkei-Gorzo [1]

has suggested the effect of aluminium on AChE activity was by a

direct action of aluminium. Since brain aluminium

accumulation

increased

decrease

exposure

with

increase

in

duration

of

treatment

[7]

days)

the

of

in

may

AChE

be

activity

at

longer

duration

(60

of

due

to

high

concentration

aluminium

accumulated. AChE activity in striatum is due to local circuit

interneurons [18] and does not receive cholinergic projections

as cortex and hippocampus brain regions receive

from

nucleus

basalis of Meynert [11]. Therefore AChE activity in striatum is

intrinsic and the observed changes in AChE activity in striatum

are

more

due

to

direct

effect

of

aluminium.

Therefore

the

increase in AChE activity after 4 and 14 days and the decrease

in AChE activity after 60 days of aluminium exposure may be due

to

the

slow

accumulation

of

of

aluminium

in

the

brain

reported

and

in

concentration dependent.

The

biphasic

effect

aluminium

has

been

diverse cell systems, including cell protein synthesis [13,14],

phosphorylation

of

neurofilament

sub

units

[8]

and

also

in

of

weight

gain

of

young

rabbits

[21].

The

biphasic

effect