Acknowledgement
Introduction
Conclusions
Paper 1: Ursin, H., Jellestad, F. and Cabrera, I.G. The Amygdala, Exploration and Fear. In: The Amygdaloid Complex, edited by Y. Ben-Ari. Amsterdam: Elsevier North Holland, 1981, pp. 317-329. Summary
Paper 2: Jellestad, F.K. and Cabrera, I.G. Exploration and avoidance learning after ibotenic acid and radio frequency lesions in the rat amygdala. In press, Behavioral and Neural Biology, 1986. Summary
Paper 3: Jellestad, F.K. and Bakke, H.K. Passive avoidance after ibotenic acid and radio frequency lesions in the rat amygdala. Physiology & Behavior, 1965, 34. pp. 299-305. Summary
Paper 4: Jellestad, F.K., Markowska, A., Bakke, H.K. and Walther, B. Behavioral effects after ibotenic acid, 6-OHDA and electrolytic lesions in the central amygdala nucleus of the rat. Submitted to Physiology & Behavior, 1986. Summary
Paper 5: Jellestad, F.K. and Grahnstedt, 5. Electroencephalographic activity after kainic and ibotenic acid injections in the amygdaloid complex of rats. Brain Research, 1985, 340, pp. 229-234. Summary
Paper 6: Jellestad, F.K. and Murison, R.C.C. Stereotactic,
electrical and chemical lesions. To appear in: Advanced Methods
in Psychobiology, edited by J.N. Hingtgen, D. Hellhammer and G. Huppmann.
Toronto: Hogrefe. Summary
GENERAL SUMMARY
PAPER I
This paper gives a general review of the literature concerning the
amygdala complex and emotional behavior. Behavioral classifications of
fear-induced behavior and criteria for neuroethological localization are
discussed. It is concluded that both large amygdela lesions and small lesions
of the central nucleus seem to reduce fear motivation or the activation
effects of threat stimuli at least in rats. It is pointed out, however,
that the specific role of the various emygdala nuclei for emotional behavior
is difficult to evaluate since axons passing through the area are also
destroyed with conventional lesion techniques.
PAPER II
Paper II contains descriptions of different experiments. The experiments
were undertaken to evaluate the importance of amygdaloid neurons versus
axons of passage in fear-motivated behavior. Open-field and avoidance behavior
and plasma corticosterone levels were studied after intra-amygdala injections
of IBO (3.Oug) and radio frequency (AF) lesions in the amygdala complex
of male Wistar rats. The IBO lesions led to increased open-field activity,
but no impairments in avoidance learning, or changes in basal or experimental
levels of plasma corticosterone. In the one-way avoidance task the RF lesions,
in contrast to the IBO lesions, led to significant impairments in the acquisition
of the avoidance response and increased corticosterone levels. Even though
the long-term axon sparing effect of IBO is questioned since cavities were
detected eight weeks after the injections, the differences in avoidance
learning and in corticosterone levels between the RF and the IBO lesions
indicated that the axons were functionally active at the time of testing
(14-26 days post operatively). The increase in open field is attributed
to the destruction of amygdala neurons and neurons in the overlying cortex,
while the active-avoidance deficit seems to depend on the destruction of
axons. On the basis of the behavioral results and the corticosterone data
in these experiments, it is suggested that the behavioral changes are not
attributable to a general reduction in fear. However, since the IBO lesions
did not affect the most medial parts of the amygdala complex including
the central amygdala nucleus, it was suggested that the role of this nucleus
in the arousal of fear had to be investigated further.
PAPER III
Since the long-term axon sparing effect of ibotenic acid was questioned
in paper II, the effects of such lesions in the amygdala complex of rats
were compared to those of RF lesions on a passive avoidance task in paper
III. Both types of lesions impaired the acquisition of the passive avoidance
response. Plasma corticosterone levels were measured after a retention
test in which no electrical shocks were applied. None of the lesioned groups
showed reduced corticosterone levels, the IBO lesioned rats actually showed
significantly higher corticosterone levels than both RF lesioned and control
animals. The corticosterone results are not consistent with a general reduction
in fear. The slower passive avoidance learning may be a conditioning deficit
due to impaired information processing in the damaged amygdala complex.
PAPER IV
The amygdala lesions reported in paper II and III were relatively large
and the behavioral effects could be due to the destruction of the central
amygdala nucleus as suggested in paper I. The results showed that both
selective lesions of central amygdala neurons with ibotenic acid, and electrolytic
destruction of the nucleus, led to marked increases in open field activity
and general activity during passive avoidance conditioning. However, combined
destruction of neurons and axons of passage led to more pronounced passive
avoidance impairments and it was suggested that this effect should be attributed
to neurons located outside the central amygdala nucleus. The corticosterone
and the behavioral data indicated that general arousal of fear was not
critically dependent an intact central amygdala neurons or intact cortico-hypothalamic
fibers. The data were, however, still compatible with a hypothesis of temporary
reduction of fear-arousal in the initial phase of the passive avoidance
conditioning.
PAPER V
The most consistent findings in papers II, III and IV were a general
increase in locomotor activity in spite of different lesion sizes and localizations.
Since kainic acid (also a neuroexcitatory amino acid) is known to produce
severe epileptic activity, the increases in locomotor activity after ibotenic
acid injections could perhaps be due to subclinical epileptic discharges.
In paper V, long-term electroencephalographic (EEG) activity and neuropathological
effects were studied after unilateral amygdala injection of kainic (KA)
or ibotenic acid (IBO). Injections of 0.2 ug KA caused severe epileptic
activity which lasted up to post-operative day 49. Histological examination
revealed complete losses of neuronal and glial elements that appeared as
cavities within the injected areas. In contrast, the epileptiform activity
after injections of 3.Oug IBO was seen only as interictal spikes which
lasted for 2-4 h after surgery. Cavities within the lesion areas were also
evident in the IBO-injected rats. The results indicated that KA should
be avoided as a lesion method in behavioral studies of brain functions,
whereas IBO was judged to be a more suitable lesion tool, which produced
only minor and transitory epileptiform activity. However, neither KA nor
IBO seemed to have long-term axon sparing properties in the amygdala complex
within the range of the applied doses.
PAPER VI
This last paper is added to the thesis since it gives a general overview
and extensive description of the various surgical techniques and procedures
employed in paper II, III, IV and V. It gives a detailed description of
various anaesthetics, stereotaxic equipment and stereotaxic brain atlases.
Different procedures for calculating stereotaxic lesion coordinates are
also described. Advantages and disadvantages of different lesions methods
are discussed in addition to various factors like injection speed , volume
, needle size, diffusion time etc , factors that all should be taken into
consideration when producing chemical lesions.
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