Audiogenic seizures (AS) are a rodent model of generalized tonic-cloni
c seizures, induced in susceptible (S) animals by high intensity (110
dB) acoustic stimulation. Resistant (R) animals do not respond to the
sound with any seizure-related behavior, but they display facial autom
atisms and grooming clusters. Genetic selection and neuroethology are
the basic tools used in our laboratory to perform behavioral analysis
of AS S and R animals. Based upon selective lesion and microinjection
(GABA, clobazam, NMDA) studies of substantia nigra (SN), inferior coll
iculus (IC), superior colliculus (SC), and on specific knife cuts at m
idcollicular levels, we have suggested differential roles for these su
bstrates in the origin and spreading of AS. The IC central nucleus is
suggested to be the most critical area involved in the afferent pathwa
y whose activation is necessary for AS origin. IC cortical nuclei seem
to be the most important structures involved in the transduction of s
ensory to motor activity. SC, SN and other reticular subnuclei are sug
gested to be modulators or components of the efferent pathway. Althoug
h the midbrain is considered to be the only network necessary for acut
e AS origin, both emotion-linked acoustic memories and plastic changes
linked to audiogenic kindling involve midbrain-forebrain connections.
This paper reviews the behavioral manifestations of acute and chronic
AS, our contribuition to the knowledge of some AS neurobiological mid
brain substrates and the suggested implications of midbrain-forebrain
interactions typical of AS kindling.