The Biological Bases of Behaviour

The Biological Bases of Behaviour

د. ثراء الجودي

Behavioural Neuro-Anatomy

The human nervous system consists of the central nervous system (CNS) and
the peripheral nervous system (PNS).

A. The CNS contains the brain and spinal cord, the brain contains the cerebral cortex and hemispheres:

1. The cerebral cortex of the brain can be divided

a. Anatomically into at least four sets of lobes: frontal, temporal, parietal, and occipital, as well as the limbic lobes (which contain medial parts of the frontal, temporal, and parietal lobes and include the hippocampus, amygdala,fornix, septum, parts of the thalamus, and cingulate gyrus and .related structures)

.b. By arrangement of neuron layers or cryo-architecture

.c. Functionally into motor, sensory, and association areas


Behavioural Neuro-Anatomy
The medial longitudinal fissure separates the human brain into two distinct cerebral hemispheres, connected by the corpus callosum.
The functions of the hemispheres are lateralized (The lateralization of brain function is the tendency for some neural functions or cognitive processes to be more dominant in one hemisphere than the other).

(1) The right, or non-dominant, hemisphere is associated primarily with perception (which is the organization, identification, and interpretation of sensory information in order to represent and understand the presented information, or the environment). ; it is also associated with spatial relations, body image, and musical and artistic ability.

(2) The left, or dominant, hemisphere is associated with language functions.

Behavioural Neuro-Anatomy
Brain lesions caused by accident, disease, surgery, or other insult are associated with particular neuropsychiatric effects.

Location of Lesion /Effects

Frontal lobes:
-Mood changes (e.g., depression with dominant lesions, elevation with non-dominant lesions)
-Difficulties with motivation, concentration, attention, orientation, and problem solving (dorsolateral convexity lesions)
-Difficulties with judgment, inhibitions, emotions, personality changes (orbitofrontal cortex lesions)
-Inability to speak fluently (i.e., Broca aphasia [dominant lesions])

Behavioural Neuro-Anatomy

Temporal lobes


Impaired memory (Impaired verbal memory in dominant side, and non-verbal memory in the non-dominant side)
-Psychomotor seizures
-Inability to understand language (i.e. Wernicke aphasia [dominant lesions])
-Impaired musical skills (non-dominant)

Behavioural Neuro-Anatomy

Limbic lobes
-Poor new learning

Hippocampus

Implicated specifically in Alzheimer disease (short-term memory .(loss and disorientation are included among the early symptoms

Amygdala

-Klüver-Bucy syndrome (decreased aggression, increased sexual behavior,
hyperorality)
-Decreased conditioned fear response
-Problems recognizing the meaningfulness of facial and vocal expressions of anger in others.

Behavioural Neuro-Anatomy

Parietal lobes

-Impaired processing of visual-spatial information (e.g., cannot copy a simple
line drawing or a clock face correctly [right-sided lesions])


-Impaired processing of verbal information (e.g., cannot tell left from right, do simple math, name fingers, or write [Gerstmann syndrome; dominant lesions])

Behavioural Neuro-Anatomy

Occipital lobes

-Visual hallucinations and illusions

-Inability to identify camouflaged objects
-Blindness

Behavioural Neuro-Anatomy

Hypothalamus

-Hunger leading to obesity (ventromedial nucleus damage);

loss of appetite leading to weight loss( lateral nucleus damage).
.-Effects on sexual activity and body temperature regulation

Behavioural Neuro-Anatomy

Reticular system

-Changes in sleep-wake mechanisms (e.g., decreased REM sleep)

-Loss of consciousness


Behavioural Neuro-Anatomy
Basal ganglia
Disorders of movement:
-Parkinson disease [substantia nigra],
-Huntington disease [caudate and putamen]
-Tourette syndrome [caudate])

Behavioural Neuro-Anatomy

The peripheral nervous system

The PNS contains all sensory, motor, and autonomic fibers outside of the CNS, including the spinal nerves, cranial nerves, and peripheral ganglia

Neuro-Transmission

Synapses and neurotransmitters

1. Information in the nervous system is transferred across the synaptic cleft (i.e., the space between the axon terminal of the pre-synaptic neuron and the dendrite of the postsynaptic neuron).

2. When the pre-synaptic neuron is stimulated, a neurotransmitter is released, travels across the synaptic cleft, and acts on receptors on the postsynaptic neuron.

Neurotransmitters are excitatory if they increase the chances that a neuron will fire and inhibitory if they decrease these chances.


Neuro-Transmission
Regulation of neurotransmitter activity

1. The concentration of neurotransmitters in the synaptic cleft is closely related to mood and behavior. A number
of mechanisms affect this concentration.

2. After release by the presynaptic neuron, neurotransmitters are removed from the synaptic cleft by mechanisms including:

a. Reuptake by the presynaptic neuron

b. Degradation by enzymes such as monoamine oxidase (MAO)

Neuro-Transmission

Dopamine

1. Dopamine, a catecholamine, is involved in the pathophysiology of schizophrenia and other psychotic disorders, Parkinson disease,
mood disorders, the conditioned fear response and the "rewarding" nature of drugs of abuse.

2. Synthesis: The amino acid tyrosine is converted to the precursor for dopamine by the enzyme tyrosine hydroxylase.

3. Receptor subtypes: At least five dopamine receptor subtypes (D1–D5) have been identified.
the major site of action is D2 for traditional antipsychotic agents and D1 and D4 as well as D2 for the newer "atypical" antipsychotic agents


Neuro-Transmission
Dopaminergic tracts
a. The nigrostriatal tract is involved in the regulation of muscle tone and movement.
This tract degenerates in Parkinson disease.
Treatment with antipsychotic drugs, which block postsynaptic dopamine receptors receiving input from the nigrostriatal tract,
can result in Parkinson-like symptoms.

b. Dopamine acts on the tuberoinfundibular tract to inhibit the secretion of prolactin from the anterior pituitary.
1. Blockade of dopamine receptors by antipsychotic drugs prevents the inhibition of prolactin release and results in elevated prolactin levels.
2. This elevation in turn results in symptoms such as breast
enlargement, galactorrhea, and sexual dysfunction.

Neuro-Transmission

The mesolimbic-mesocortical tract is associated
with psychotic disorders.

1. This tract may have a role in the expression of emotions since it projects into the limbic system and prefrontal cortex.

2. Hyperactivity of the meso-limbic tract is associated with the positive symptoms of schizophrenia;

hypoactivity of the meso-cortical tract is associated with .the negative symptoms of schizophrenia


Neuro-Transmission
Norepinephrine is a catecholamine, plays a role in mood, anxiety, arousal, learning, and memory.

Serotonin plays a role in mood, sleep, sexuality, and impulse control.

-Elevation of serotonin is associated with improved mood and sleep but decreased sexual function (particularly delayed orgasm).

-Very high levels are associated with psychotic symptoms.

-Decreased serotonin is associated with poor impulse control, depression, and poor sleep.

Neuro-Transmission

Antidepressants and serotonin.

Tricyclic antidepressants(TCAs), selective serotonin reuptake inhibitors (SSRIs), and monoamine oxidase inhibitors (MAOIs) ultimately increase the presence of serotonin and norepinephrine in the synaptic cleft.

a. TCAs block reuptake of serotonin and norepinephrine, but SSRIs such as fluoxetine (Prozac) selectively block reuptake of serotonin
by the presynaptic neuron.

b. MAOIs prevent the degradation of serotonin and norepinephrine by MAO.

Neuro-Transmission
Acetylcholine (Ach)
It is the transmitter used by nerve-skeleton muscle junctions.


1. Degeneration of cholinergic neurons is associated with Alzheimer disease, Down syndrome, and movement and sleep disorders (e.g.,decreased REM sleep).

2. Cholinergic neurons synthesize Ach from acetyl coenzyme A and choline using choline acetyltransferase(AchE).

3. The nucleus basalis of Meynert is a brain area involved in production of Ach.

Neuro-Transmission
4. Acetylcholinesterase (AchE) breaks Ach down into choline and acetate.

5. Blocking the action of AchE with AchE Inhibitor drugs such as donepezil , rivastigmine, and galantamine may delay the progression of Alzheimer disease but cannot reverse function already lost.

6. Blockade of muscarinic Ach receptors with drugs such as antipsychotics and tricyclic antidepressants results in the classic "anticholinergic" adverse effects seen with use of these drugs, including dry mouth, blurred vision, urinary hesitancy, and constipation.

7. Anticholinergic agents are commonly used to treat the Parkinson-like symptoms caused by antipsychotic agents.

Neuro-Transmission

Glutamate

1. Glutamate is an excitatory neurotransmitter that may be toxic to neurons (exitotoxicity) and thereby contribute to the pathophysiology of disorders such as schizophrenia, Alzheimer disease, and other neurodegenerative illnesses.

2. Memantine, a blocker of the N-methyl-d-aspartate (NMDA) receptor, a type of glutamate receptor, has been approved to treat Alzheimer disease and may prove useful also in the treatment of schizophrenia.


Neuro-Transmission
GABA
GABA is the principal inhibitory neurotransmitter in the CNS.
Benzodiazepines (e.g., diazepam) and barbiturates increase the affinity of GABA for its GABA A-binding site, allowing more chloride to enter the neuron. The chloride-laden neurons become hyperpolarized and inhibited, decreasing neuronal firing and ultimately decreasing anxiety.
Anticonvulsants also potentiate the activity of GABA.

Neuro-Transmission

Neuro-Transmission
NEUROPEPTIDES

Endogenous opioids

1. Enkephalins, endorphins, dynorphins, and endomorphins are opioids produced by the brain itself that decrease pain and anxiety and have a role in addiction and mood.

2. Placebo effects may be mediated by the endogenous opioid system. Prior treatment with an opioid receptor blocker such as naloxone may block placebo effects.

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